FTO Facilitates Cervical Cancer Malignancy Through Inducing m6A‐Demethylation of PIK3R3 mRNA
ABSTRACT Background The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6‐methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity‐associated gene (FTO) works as the m6A demethylase. Aims Our study aimed to narr...
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Published in | Cancer medicine (Malden, MA) Vol. 13; no. 24; pp. e70507 - n/a |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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United States
John Wiley & Sons, Inc
01.12.2024
John Wiley and Sons Inc Wiley |
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Abstract | ABSTRACT
Background
The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6‐methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity‐associated gene (FTO) works as the m6A demethylase.
Aims
Our study aimed to narrate the biological function and potential mechanisms for FTO in cervical cancer malignancy.
Materials & Methods
We analyzed potential clinical value of FTO in cervical cancer patients. The relative protein levels of FTO in cervical cancerous tissue and paracancerous tissue were verified by IHC. After changing the FTO expression level by lentivirus transfection, the proliferation and metastasis ability of cervical cancer cells were detected both in vitro and in vivo. Further, Merip‐seq and Merip‐qPCR are used to profile m6A transcriptome‐wide. Finally, western blot were performed to identify the regulatory mechanism.
Results
Based on TCGA‐CESC cohort and GEO dataset, FTO expression levels in HPV‐positive cancer patients were significantly higher than those in HPV‐negative cancer patients and could predict advanced FIGO stage. The protein level of FTO in cervical cancerous tissue was higher than that in paracancerous tissue. Functional assays indicated that FTO promoted the proliferation, migration and invasion of cervical cancer cells both in vitro and in vivo. The Merip‐seq and Merip‐qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer.
Conclusion
All in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer. |
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AbstractList | ABSTRACT Background The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6‐methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity‐associated gene (FTO) works as the m6A demethylase. Aims Our study aimed to narrate the biological function and potential mechanisms for FTO in cervical cancer malignancy. Materials & Methods We analyzed potential clinical value of FTO in cervical cancer patients. The relative protein levels of FTO in cervical cancerous tissue and paracancerous tissue were verified by IHC. After changing the FTO expression level by lentivirus transfection, the proliferation and metastasis ability of cervical cancer cells were detected both in vitro and in vivo. Further, Merip‐seq and Merip‐qPCR are used to profile m6A transcriptome‐wide. Finally, western blot were performed to identify the regulatory mechanism. Results Based on TCGA‐CESC cohort and GEO dataset, FTO expression levels in HPV‐positive cancer patients were significantly higher than those in HPV‐negative cancer patients and could predict advanced FIGO stage. The protein level of FTO in cervical cancerous tissue was higher than that in paracancerous tissue. Functional assays indicated that FTO promoted the proliferation, migration and invasion of cervical cancer cells both in vitro and in vivo. The Merip‐seq and Merip‐qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer. Conclusion All in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer. The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6-methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity-associated gene (FTO) works as the m6A demethylase. Our study aimed to narrate the biological function and potential mechanisms for FTO in cervical cancer malignancy. We analyzed potential clinical value of FTO in cervical cancer patients. The relative protein levels of FTO in cervical cancerous tissue and paracancerous tissue were verified by IHC. After changing the FTO expression level by lentivirus transfection, the proliferation and metastasis ability of cervical cancer cells were detected both in vitro and in vivo. Further, Merip-seq and Merip-qPCR are used to profile m6A transcriptome-wide. Finally, western blot were performed to identify the regulatory mechanism. Based on TCGA-CESC cohort and GEO dataset, FTO expression levels in HPV-positive cancer patients were significantly higher than those in HPV-negative cancer patients and could predict advanced FIGO stage. The protein level of FTO in cervical cancerous tissue was higher than that in paracancerous tissue. Functional assays indicated that FTO promoted the proliferation, migration and invasion of cervical cancer cells both in vitro and in vivo. The Merip-seq and Merip-qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer. All in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer. ABSTRACT Background The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6‐methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity‐associated gene (FTO) works as the m6A demethylase. Aims Our study aimed to narrate the biological function and potential mechanisms for FTO in cervical cancer malignancy. Materials & Methods We analyzed potential clinical value of FTO in cervical cancer patients. The relative protein levels of FTO in cervical cancerous tissue and paracancerous tissue were verified by IHC. After changing the FTO expression level by lentivirus transfection, the proliferation and metastasis ability of cervical cancer cells were detected both in vitro and in vivo. Further, Merip‐seq and Merip‐qPCR are used to profile m6A transcriptome‐wide. Finally, western blot were performed to identify the regulatory mechanism. Results Based on TCGA‐CESC cohort and GEO dataset, FTO expression levels in HPV‐positive cancer patients were significantly higher than those in HPV‐negative cancer patients and could predict advanced FIGO stage. The protein level of FTO in cervical cancerous tissue was higher than that in paracancerous tissue. Functional assays indicated that FTO promoted the proliferation, migration and invasion of cervical cancer cells both in vitro and in vivo. The Merip‐seq and Merip‐qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer. Conclusion All in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer. The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6-methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity-associated gene (FTO) works as the m6A demethylase.BACKGROUNDThe incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6-methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity-associated gene (FTO) works as the m6A demethylase.Our study aimed to narrate the biological function and potential mechanisms for FTO in cervical cancer malignancy.AIMSOur study aimed to narrate the biological function and potential mechanisms for FTO in cervical cancer malignancy.We analyzed potential clinical value of FTO in cervical cancer patients. The relative protein levels of FTO in cervical cancerous tissue and paracancerous tissue were verified by IHC. After changing the FTO expression level by lentivirus transfection, the proliferation and metastasis ability of cervical cancer cells were detected both in vitro and in vivo. Further, Merip-seq and Merip-qPCR are used to profile m6A transcriptome-wide. Finally, western blot were performed to identify the regulatory mechanism.MATERIALS & METHODSWe analyzed potential clinical value of FTO in cervical cancer patients. The relative protein levels of FTO in cervical cancerous tissue and paracancerous tissue were verified by IHC. After changing the FTO expression level by lentivirus transfection, the proliferation and metastasis ability of cervical cancer cells were detected both in vitro and in vivo. Further, Merip-seq and Merip-qPCR are used to profile m6A transcriptome-wide. Finally, western blot were performed to identify the regulatory mechanism.Based on TCGA-CESC cohort and GEO dataset, FTO expression levels in HPV-positive cancer patients were significantly higher than those in HPV-negative cancer patients and could predict advanced FIGO stage. The protein level of FTO in cervical cancerous tissue was higher than that in paracancerous tissue. Functional assays indicated that FTO promoted the proliferation, migration and invasion of cervical cancer cells both in vitro and in vivo. The Merip-seq and Merip-qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer.RESULTSBased on TCGA-CESC cohort and GEO dataset, FTO expression levels in HPV-positive cancer patients were significantly higher than those in HPV-negative cancer patients and could predict advanced FIGO stage. The protein level of FTO in cervical cancerous tissue was higher than that in paracancerous tissue. Functional assays indicated that FTO promoted the proliferation, migration and invasion of cervical cancer cells both in vitro and in vivo. The Merip-seq and Merip-qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer.All in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer.CONCLUSIONAll in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer. ABSTRACT Background The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6‐methyladenosine (m6A) always plays an important role in tumor progression, and fat mass and obesity‐associated gene (FTO) works as the m6A demethylase. Aims Our study aimed to narrate the biological function and potential mechanisms for FTO in cervical cancer malignancy. Materials & Methods We analyzed potential clinical value of FTO in cervical cancer patients. The relative protein levels of FTO in cervical cancerous tissue and paracancerous tissue were verified by IHC. After changing the FTO expression level by lentivirus transfection, the proliferation and metastasis ability of cervical cancer cells were detected both in vitro and in vivo. Further, Merip‐seq and Merip‐qPCR are used to profile m6A transcriptome‐wide. Finally, western blot were performed to identify the regulatory mechanism. Results Based on TCGA‐CESC cohort and GEO dataset, FTO expression levels in HPV‐positive cancer patients were significantly higher than those in HPV‐negative cancer patients and could predict advanced FIGO stage. The protein level of FTO in cervical cancerous tissue was higher than that in paracancerous tissue. Functional assays indicated that FTO promoted the proliferation, migration and invasion of cervical cancer cells both in vitro and in vivo. The Merip‐seq and Merip‐qPCR evoked that relative PIK3R3 m6A level was significantly increased after FTO knockdown, which effected the activation of FoxO pathway. After knocking down FTO, upregulation of PIK3R3 can restore the malignancy of cervical cancer. Conclusion All in all, these data suggest a vital role for FTO in occurrence and development of cervical cancer. |
Author | Chen, Bingxin Wang, Hui Ding, Wencheng Li, Xiaomin Wang, Liming Ren, Ci Gao, Chun |
AuthorAffiliation | 1 Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China 2 Department of Gynecologic Oncology, Women's Hospital Zhejiang University School of Medicine Hangzhou China |
AuthorAffiliation_xml | – name: 2 Department of Gynecologic Oncology, Women's Hospital Zhejiang University School of Medicine Hangzhou China – name: 1 Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan China |
Author_xml | – sequence: 1 givenname: Bingxin surname: Chen fullname: Chen, Bingxin organization: Zhejiang University School of Medicine – sequence: 2 givenname: Liming surname: Wang fullname: Wang, Liming organization: Zhejiang University School of Medicine – sequence: 3 givenname: Xiaomin surname: Li fullname: Li, Xiaomin organization: Huazhong University of Science and Technology – sequence: 4 givenname: Ci surname: Ren fullname: Ren, Ci organization: Huazhong University of Science and Technology – sequence: 5 givenname: Chun surname: Gao fullname: Gao, Chun organization: Huazhong University of Science and Technology – sequence: 6 givenname: Wencheng surname: Ding fullname: Ding, Wencheng organization: Huazhong University of Science and Technology – sequence: 7 givenname: Hui orcidid: 0000-0001-6789-5185 surname: Wang fullname: Wang, Hui email: huit71@sohu.com organization: Zhejiang University School of Medicine |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39692250$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1038/ng.3178 10.1007/978‐1‐0716‐3052‐5_22 10.1016/j.ccell.2020.02.004 10.1101/gad.269415.115 10.1002/mc.22782 10.1016/j.ygyno.2013.10.003 10.1038/ncomms2822 10.1016/j.ygyno.2013.10.014 10.1016/j.ypmed.2019.04.010 10.1186/s12967‐024‐05242‐3 10.1038/nature11112 10.1016/j.ccell.2016.11.017 10.1016/j.ygyno.2016.11.011 10.1016/j.stem.2017.11.016 10.1038/onc.2008.244 10.1038/s41419‐022‐04672‐5 10.1038/nmeth.2089 10.1093/annonc/mdx220 10.1136/ijgc‐2021‐003140 10.1016/j.cell.2017.11.031 10.1038/s41594‐023‐00981‐1 10.1038/s41556‐018‐0174‐4 10.1038/nature14169 10.1016/j.tig.2023.11.003 10.3322/caac.21660 10.1016/j.jgg.2016.12.004 10.1016/S0140‐6736(13)60022‐7 10.1038/nature12730 10.1016/j.cell.2006.12.029 10.1002/cam4.6068 10.1186/s13046‐021‐02096‐1 10.1093/nar/gks9 10.1158/1535‐7163.MCT‐14‐0049 10.1002/mc.22243 10.1080/15384047.2017.1416936 10.1038/nrc2664 10.1016/0092‐8674(75)90158‐0 10.1038/nature21386 10.1016/j.cell.2011.08.019 10.1016/j.cell.2012.05.003 10.1016/j.cell.2020.05.012 10.1038/s41422‐018‐0040‐8 10.1016/j.ccell.2022.10.004 10.3389/fonc.2022.763341 10.1186/s13046‐020‐01799‐1 10.1038/nchembio.1432 10.1016/j.molcel.2017.09.024 10.1038/s41586‐023‐06323‐x 10.3389/fonc.2023.1087644 10.1186/s12943‐020‐01216‐3 10.1016/j.molcel.2012.10.015 |
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Copyright | 2024 The Author(s). published by John Wiley & Sons Ltd. 2024 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd. 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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Keywords | FTO PIK3R3 m6A malignancy cervical carcinoma |
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Notes | Funding This study was funded by grants from the National Natural Science Foundation of China (81830074) and the Natural Science Foundation of Zhejiang Province (No. LQ23H160033). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Funding: This study was funded by grants from the National Natural Science Foundation of China (81830074) and the Natural Science Foundation of Zhejiang Province (No. LQ23H160033). |
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References | 2023; 30 2012; 485 2013; 4 2017; 44 2021; 71 2019; 123 2020; 19 2017; 31 2015; 47 2018; 172 2022; 40 2008; 27 2014; 13 2024; 22 2022; 32 2023; 619 2021; 40 1975; 4 2014; 10 2018; 28 2023; 13 2023; 2644 2013; 49 2007; 128 2023; 12 2017; 28 2020; 181 2017; 68 2015; 54 2013; 41 2020; 39 2020; 37 2013; 382 2018; 22 2012; 149 2018; 20 2018; 19 2011; 146 2014; 505 2015; 29 2022; 12 2022; 13 2024; 40 2009; 9 2015; 518 2013; 131 2017; 144 2017; 543 2012; 9 2018; 57 e_1_2_10_23_1 e_1_2_10_46_1 e_1_2_10_21_1 e_1_2_10_44_1 e_1_2_10_42_1 e_1_2_10_40_1 e_1_2_10_2_1 e_1_2_10_4_1 e_1_2_10_18_1 e_1_2_10_53_1 e_1_2_10_6_1 e_1_2_10_16_1 e_1_2_10_39_1 e_1_2_10_8_1 e_1_2_10_14_1 e_1_2_10_37_1 e_1_2_10_13_1 e_1_2_10_34_1 e_1_2_10_11_1 e_1_2_10_32_1 e_1_2_10_30_1 e_1_2_10_51_1 e_1_2_10_29_1 e_1_2_10_27_1 e_1_2_10_25_1 e_1_2_10_48_1 e_1_2_10_24_1 e_1_2_10_45_1 e_1_2_10_22_1 e_1_2_10_43_1 e_1_2_10_20_1 e_1_2_10_41_1 e_1_2_10_52_1 e_1_2_10_3_1 e_1_2_10_19_1 e_1_2_10_5_1 e_1_2_10_17_1 e_1_2_10_38_1 e_1_2_10_7_1 e_1_2_10_15_1 e_1_2_10_36_1 e_1_2_10_12_1 e_1_2_10_35_1 e_1_2_10_9_1 e_1_2_10_10_1 e_1_2_10_33_1 e_1_2_10_31_1 e_1_2_10_50_1 e_1_2_10_28_1 e_1_2_10_49_1 e_1_2_10_26_1 e_1_2_10_47_1 |
References_xml | – volume: 128 start-page: 309 issue: 2 year: 2007 end-page: 323 article-title: FoxOs Are Lineage‐Restricted Redundant Tumor Suppressors and Regulate Endothelial Cell Homeostasis publication-title: Cell – volume: 32 start-page: 239 issue: 3 year: 2022 end-page: 245 article-title: Prognostic Factors in Locally Advanced Cervical Cancer With Pelvic Lymph Node Metastasis publication-title: International Journal of Gynecological Cancer – volume: 619 start-page: 868 issue: 7971 year: 2023 end-page: 875 article-title: Complementary Alu Sequences Mediate Enhancer‐Promoter Selectivity publication-title: Nature – volume: 40 start-page: 294 issue: 1 year: 2021 article-title: RNA m6A Demethylase FTO‐Mediated Epigenetic Up‐Regulation of LINC00022 Promotes Tumorigenesis in Esophageal Squamous Cell Carcinoma publication-title: Journal of Experimental & Clinical Cancer Research – volume: 505 start-page: 117 year: 2014 end-page: 120 article-title: N6‐Methyladenosine‐Dependent Regulation of Messenger RNA Stability publication-title: Nature – volume: 39 start-page: 283 issue: 1 year: 2020 article-title: CircRNA_0000392 Promotes Colorectal Cancer Progression Through the miR‐193a‐5p/PIK3R3/AKT Axis publication-title: Journal of Experimental & Clinical Cancer Research – volume: 382 start-page: 889 issue: 9895 year: 2013 end-page: 899 article-title: Human Papillomavirus and Cervical Cancer publication-title: Lancet – volume: 149 start-page: 1635 issue: 7 year: 2012 end-page: 1646 article-title: Comprehensive Analysis of mRNA Methylation Reveals Enrichment in 3' UTRs and Near Stop Codons publication-title: Cell – volume: 71 start-page: 209 issue: 3 year: 2021 end-page: 249 article-title: Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries publication-title: A Cancer Journal for Clinicians – volume: 22 start-page: 191 issue: 2 year: 2018 end-page: 205 article-title: METTL14 Inhibits Hematopoietic Stem/Progenitor Differentiation and Promotes Leukemogenesis Via mRNA M 6 A Modification publication-title: Cell Stem Cell – volume: 9 start-page: 550 issue: 8 year: 2009 end-page: 562 article-title: Targeting PI3K Signalling in Cancer: Opportunities, Challenges and Limitations publication-title: Nature Reviews. Cancer – volume: 20 start-page: 1074 issue: 9 year: 2018 end-page: 1083 article-title: m6A mRNA Methylation Regulates AKT Activity to Promote the Proliferation and Tumorigenicity of Endometrial Cancer publication-title: Nature Cell Biology – volume: 543 start-page: 378 year: 2017 end-page: 384 article-title: Integrated Genomic and Molecular Characterization of Cervical Cancer publication-title: Nature – volume: 28 issue: suppl_4 year: 2017 article-title: Cervical Cancer: ESMO Clinical Practice Guidelines for Diagnosis, Treatment and Follow‐Up publication-title: Annals of Oncology – volume: 12 year: 2022 article-title: YTHDF2 Inhibits the Migration and Invasion of Lung Adenocarcinoma by Negatively Regulating the FAM83D‐TGFβ1‐SMAD2/3 Pathway publication-title: Frontiers in Oncology – volume: 518 start-page: 495 issue: 7540 year: 2015 end-page: 501 article-title: Whole Genomes Redefine the Mutational Landscape of Pancreatic Cancer publication-title: Nature – volume: 146 start-page: 669 issue: 5 year: 2011 end-page: 670 article-title: A New FOXO Pathway Required for Leukemogenesis publication-title: Cell – volume: 37 start-page: 270 issue: 3 year: 2020 end-page: 288 article-title: m6A Modification in Coding and Non‐Coding RNAs: Roles and Therapeutic Implications in Cancer publication-title: Cancer Cell – volume: 47 start-page: 158 issue: 2 year: 2015 end-page: 163 article-title: Genome‐Wide Profiling of HPV Integration in Cervical Cancer Identifies Clustered Genomic Hot Spots and a Potential Microhomology‐Mediated Integration Mechanism publication-title: Nature Genetics – volume: 12 start-page: 14413 issue: 13 year: 2023 end-page: 14425 article-title: PIK3R3 Is Upregulated in Liver Cancer and Activates Akt Signaling to Control Cancer Growth by Regulation of CDKN1C and SMC1A publication-title: Cancer Medicine – volume: 41 start-page: D970 year: 2013 end-page: D976 article-title: TSGene: A Web Resource for Tumor Suppressor Genes publication-title: Nucleic Acids Research – volume: 68 start-page: 566 issue: 3 year: 2017 end-page: 580.e10 article-title: PTEN Regulates PI(3,4)P2 Signaling Downstream of Class I PI3K publication-title: Molecular Cell – volume: 57 start-page: 590 issue: 5 year: 2018 end-page: 597 article-title: FTO Regulates the Chemo‐Radiotherapy Resistance of Cervical Squamous Cell Carcinoma (CSCC) by Targeting β‐Catenin Through mRNA Demethylation publication-title: Molecular Carcinogenesis – volume: 144 start-page: 40 issue: 1 year: 2017 end-page: 45 article-title: Prediction Model for Para‐Aortic Lymph Node Metastasis in Patients With Locally Advanced Cervical Cancer publication-title: Gynecologic Oncology – volume: 27 start-page: 5486 issue: 41 year: 2008 end-page: 5496 article-title: Class I PI3K in Oncogenic Cellular Transformation publication-title: Oncogene – volume: 40 start-page: 160 issue: 2 year: 2024 end-page: 174 article-title: Time Will Tell: Comparing Timescales to Gain Insight Into Transcriptional Bursting publication-title: Trends in Genetics – volume: 123 start-page: 316 year: 2019 end-page: 323 article-title: Trends in Cervical Cancer Incidence Rates by Age, Race/Ethnicity, Histological Subtype, and Stage at Diagnosis in the United States publication-title: Preventive Medicine – volume: 40 start-page: 1566 issue: 12 year: 2022 end-page: 1582.e10 article-title: The m6A Reader IGF2BP2 Regulates Glutamine Metabolism and Represents a Therapeutic Target in Acute Myeloid Leukemia publication-title: Cancer Cell – volume: 4 start-page: 379 year: 1975 end-page: 386 article-title: Methylated Nucleotides Block 5′ Terminus of HeLa Cell Messenger RNA publication-title: Cell – volume: 13 start-page: 1837 issue: 7 year: 2014 end-page: 1847 article-title: PIK3R3 Induces Epithelial‐to‐Mesenchymal Transition and Promotes Metastasis in Colorectal Cancer publication-title: Molecular Cancer Therapeutics – volume: 131 start-page: 650 issue: 3 year: 2013 end-page: 654 article-title: Genetic Profiling to Predict Recurrence of Early Cervical Cancer publication-title: Gynecologic Oncology – volume: 2644 start-page: 349 year: 2023 end-page: 359 article-title: Transwell in Vitro Cell Migration and Invasion Assays publication-title: Methods in Molecular Biology – volume: 30 start-page: 692 issue: 5 year: 2023 end-page: 702 article-title: Dynamic Epistasis Analysis Reveals How Chromatin Remodeling Regulates Transcriptional Bursting publication-title: Nature Structural & Molecular Biology – volume: 28 start-page: 616 year: 2018 end-page: 624 article-title: Dynamic Transcriptomic m (6) a Decoration: Writers, Erasers, Readers and Functions in RNA Metabolism publication-title: Cell Research – volume: 131 start-page: 701 issue: 3 year: 2013 end-page: 707 article-title: A Novel Diagnostic Criterion for Lymph Node Metastasis in Cervical Cancer Using Multi‐Detector Computed Tomography publication-title: Gynecologic Oncology – volume: 19 start-page: 104 issue: 1 year: 2020 article-title: Mechanism of RNA Modification N6‐Methyladenosine in Human Cancer publication-title: Molecular Cancer – volume: 19 start-page: 222 issue: 3 year: 2018 end-page: 229 article-title: PIK3R3 Promotes Chemotherapeutic Sensitivity of Colorectal Cancer Through PIK3R3/NF‐kB/TP Pathway publication-title: Cancer Biology & Therapy – volume: 44 start-page: 119 issue: 2 year: 2017 end-page: 121 article-title: ONGene: A Literature‐Based Database for Human Oncogenes publication-title: Journal of Genetics and Genomics – volume: 13 year: 2023 article-title: Targeting Fat Mass and Obesity‐Associated Protein Mitigates Human Colorectal Cancer Growth In Vitro and in a Murine Model publication-title: Frontiers in Oncology – volume: 172 start-page: 90 issue: 1–2 year: 2018 end-page: 105 article-title: R‐2HG Exhibits Anti‐Tumor Activity by Targeting FTO/m6A/MYC/CEBPA Signaling publication-title: Cell – volume: 9 start-page: 671 year: 2012 end-page: 675 article-title: NIH Image to ImageJ: 25 Years of Image Analysis publication-title: Nature Methods – volume: 31 start-page: 127 issue: 1 year: 2017 end-page: 141 article-title: FTO Plays an Oncogenic Role in Acute Myeloid Leukemia as a N6‐Methyladenosine RNA Demethylase publication-title: Cancer Cell – volume: 4 year: 2013 article-title: FTO‐Mediated Formation of N6‐Hydroxymethyladenosine and N6‐Formyladenosine in Mammalian RNA publication-title: Nature Communications – volume: 29 start-page: 2037 issue: 19 year: 2015 end-page: 2053 article-title: A Majority of m6A Residues Are in the Last Exons, Allowing the Potential for 3' UTR Regulation publication-title: Genes & Development – volume: 10 start-page: 93 year: 2014 end-page: 95 article-title: A METTL3‐METTL14 Complex Mediates Mammalian Nuclear RNA N6‐Adenosine Methylation publication-title: Nature Chemical Biology – volume: 49 start-page: 18 issue: 1 year: 2013 end-page: 29 article-title: ALKBH5 Is a Mammalian RNA Demethylase That Impacts RNA Metabolism and Mouse Fertility publication-title: Molecular Cell – volume: 22 start-page: 442 issue: 1 year: 2024 article-title: Choline Metabolism Reprogramming Mediates an Immunosuppressive Microenvironment in Non‐Small Cell Lung Cancer (NSCLC) by Promoting Tumor‐Associated Macrophage Functional Polarization and Endothelial Cell Proliferation publication-title: Journal of Translational Medicine – volume: 54 start-page: E162 issue: Suppl 1 year: 2015 end-page: E171 article-title: TGF‐β Regulates the Proliferation of Lung Adenocarcinoma Cells by Inhibiting PIK3R3 Expression publication-title: Molecular Carcinogenesis – volume: 181 start-page: 1582 issue: 7 year: 2020 end-page: 1595.e18 article-title: A Unified Model for the Function of YTHDF Proteins in Regulating m6A‐Modified mRNA publication-title: Cell – volume: 13 start-page: 230 issue: 3 year: 2022 article-title: YTHDF1 Promotes Breast Cancer Cell Growth, DNA Damage Repair and Chemoresistance publication-title: Cell Death & Disease – volume: 485 start-page: 201 year: 2012 end-page: 206 article-title: Topology of the Human and Mouse m6A RNA Methylomes Revealed by m6A‐Seq publication-title: Nature – ident: e_1_2_10_10_1 doi: 10.1038/ng.3178 – ident: e_1_2_10_41_1 doi: 10.1007/978‐1‐0716‐3052‐5_22 – ident: e_1_2_10_27_1 doi: 10.1016/j.ccell.2020.02.004 – ident: e_1_2_10_14_1 doi: 10.1101/gad.269415.115 – ident: e_1_2_10_52_1 doi: 10.1002/mc.22782 – ident: e_1_2_10_46_1 doi: 10.1016/j.ygyno.2013.10.003 – ident: e_1_2_10_18_1 doi: 10.1038/ncomms2822 – ident: e_1_2_10_6_1 doi: 10.1016/j.ygyno.2013.10.014 – ident: e_1_2_10_3_1 doi: 10.1016/j.ypmed.2019.04.010 – ident: e_1_2_10_36_1 doi: 10.1186/s12967‐024‐05242‐3 – ident: e_1_2_10_12_1 doi: 10.1038/nature11112 – ident: e_1_2_10_24_1 doi: 10.1016/j.ccell.2016.11.017 – ident: e_1_2_10_8_1 doi: 10.1016/j.ygyno.2016.11.011 – ident: e_1_2_10_49_1 doi: 10.1016/j.stem.2017.11.016 – ident: e_1_2_10_31_1 doi: 10.1038/onc.2008.244 – ident: e_1_2_10_21_1 doi: 10.1038/s41419‐022‐04672‐5 – ident: e_1_2_10_40_1 doi: 10.1038/nmeth.2089 – ident: e_1_2_10_4_1 doi: 10.1093/annonc/mdx220 – ident: e_1_2_10_7_1 doi: 10.1136/ijgc‐2021‐003140 – ident: e_1_2_10_50_1 doi: 10.1016/j.cell.2017.11.031 – ident: e_1_2_10_43_1 doi: 10.1038/s41594‐023‐00981‐1 – ident: e_1_2_10_25_1 doi: 10.1038/s41556‐018‐0174‐4 – ident: e_1_2_10_33_1 doi: 10.1038/nature14169 – ident: e_1_2_10_42_1 doi: 10.1016/j.tig.2023.11.003 – ident: e_1_2_10_45_1 – ident: e_1_2_10_2_1 doi: 10.3322/caac.21660 – ident: e_1_2_10_47_1 doi: 10.1016/j.jgg.2016.12.004 – ident: e_1_2_10_5_1 doi: 10.1016/S0140‐6736(13)60022‐7 – ident: e_1_2_10_20_1 doi: 10.1038/nature12730 – ident: e_1_2_10_28_1 doi: 10.1016/j.cell.2006.12.029 – ident: e_1_2_10_35_1 doi: 10.1002/cam4.6068 – ident: e_1_2_10_26_1 doi: 10.1186/s13046‐021‐02096‐1 – ident: e_1_2_10_48_1 doi: 10.1093/nar/gks9 – ident: e_1_2_10_39_1 doi: 10.1158/1535‐7163.MCT‐14‐0049 – ident: e_1_2_10_38_1 doi: 10.1002/mc.22243 – ident: e_1_2_10_37_1 doi: 10.1080/15384047.2017.1416936 – ident: e_1_2_10_30_1 doi: 10.1038/nrc2664 – ident: e_1_2_10_11_1 doi: 10.1016/0092‐8674(75)90158‐0 – ident: e_1_2_10_9_1 doi: 10.1038/nature21386 – ident: e_1_2_10_29_1 doi: 10.1016/j.cell.2011.08.019 – ident: e_1_2_10_13_1 doi: 10.1016/j.cell.2012.05.003 – ident: e_1_2_10_23_1 doi: 10.1016/j.cell.2020.05.012 – ident: e_1_2_10_16_1 doi: 10.1038/s41422‐018‐0040‐8 – ident: e_1_2_10_51_1 doi: 10.1016/j.ccell.2022.10.004 – ident: e_1_2_10_22_1 doi: 10.3389/fonc.2022.763341 – ident: e_1_2_10_34_1 doi: 10.1186/s13046‐020‐01799‐1 – ident: e_1_2_10_15_1 doi: 10.1038/nchembio.1432 – ident: e_1_2_10_32_1 doi: 10.1016/j.molcel.2017.09.024 – ident: e_1_2_10_44_1 doi: 10.1038/s41586‐023‐06323‐x – ident: e_1_2_10_53_1 doi: 10.3389/fonc.2023.1087644 – ident: e_1_2_10_17_1 doi: 10.1186/s12943‐020‐01216‐3 – ident: e_1_2_10_19_1 doi: 10.1016/j.molcel.2012.10.015 |
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Background
The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6‐methyladenosine (m6A) always plays an... The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6-methyladenosine (m6A) always plays an important role in... ABSTRACT Background The incidence rate and mortality of cervical cancer rank the fourth in the global female cancer. N6‐methyladenosine (m6A) always plays an... |
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SubjectTerms | Adenosine - analogs & derivatives Adenosine - metabolism Alpha-Ketoglutarate-Dependent Dioxygenase FTO - genetics Alpha-Ketoglutarate-Dependent Dioxygenase FTO - metabolism Animals Antibodies Body fat Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cells Cervical cancer cervical carcinoma Cloning Demethylation Epigenetics Ethanol Female Females Fluorides Forkhead protein FTO Gene expression Gene Expression Regulation, Neoplastic Human papillomavirus Humans Kinases Lymphatic system m6A Malignancy Metastases Metastasis Mice Mice, Nude N6-methyladenosine PIK3R3 Proteins RNA, Messenger - genetics RNA, Messenger - metabolism Transcriptomes Transfection Uterine Cervical Neoplasms - genetics Uterine Cervical Neoplasms - metabolism Uterine Cervical Neoplasms - pathology |
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Title | FTO Facilitates Cervical Cancer Malignancy Through Inducing m6A‐Demethylation of PIK3R3 mRNA |
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