Bioinformatic analysis of the clinicopathological and prognostic significance of oocyte-arresting BTG4 mRNA expression in gynecological cancers
BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian canc...
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Published in | Journal of obstetrics and gynaecology Vol. 43; no. 1; p. 2182672 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
England
Taylor & Francis
01.12.2023
Taylor & Francis Ltd Taylor & Francis Group |
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Online Access | Get full text |
ISSN | 0144-3615 1364-6893 1364-6893 |
DOI | 10.1080/01443615.2023.2182672 |
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Abstract | BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.
Impact Statement
What is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells.
What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers.
What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways. |
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AbstractList | BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact Statement What is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells. What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers. What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways. BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of expression. expression was downregulated in breast cancer compared with normal tissues ( < .05), but the opposite was observed in cervical, endometrial and ovarian cancers ( < .05). methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers ( < .05). mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. expression was negatively correlated with the survival of ovarian cancer patients ( < .05), but positively for breast, cervical and endometrial cancers ( < .05). expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact Statement Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells. BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers. Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways. BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers. Impact Statement What is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells. What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers. What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways. BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact StatementWhat is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells.What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers.What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways.BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact StatementWhat is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells.What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers.What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways. BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was downregulated in breast cancer compared with normal tissues (p < .05), but the opposite was observed in cervical, endometrial and ovarian cancers (p < .05). BTG4 methylation was negatively correlated with its mRNA expression in breast, cervical and endometrial cancers (p < .05). BTG4 mRNA expression was negatively correlated with T staging and distant metastasis of breast cancer; and with tumor invasion, clinical stage, low weight and BMI, low histological grade and no diabetes in endometrial cancer but positively with T stage and non-keratinizing squamous carcinoma in endometrial cancer. BTG4 expression was negatively correlated with the survival of ovarian cancer patients (p < .05), but positively for breast, cervical and endometrial cancers (p < .05). BTG4 expression is thus a potential marker reflecting the carcinogenesis, aggressiveness and prognosis in gynecological cancers.Impact StatementWhat is already known on this subject? Previous studies have revealed the structure and location of BTG4. BTG4 inhibit cell proliferative, promote apoptosis, induce G1 cell cycle arrest. BTG4 promotes the development of mouse embryos from cell stage 1 to 2. The methylation and biological function of BTG4 were clarified in gastric and/or colorectal cancer cells.What do the results of this study add? BTG4 is found to closely link to reflect the carcinogenesis, histogenesis, aggressive behaviors and prognosis of gynecological cancers, and involved in ligand-receptor interaction, microtubule motor activity, dynein light chain binding, cilium organization, assembly, and movement in endometrial and ovarian cancers.What are the implications of these finding for clinical practice and/or further research? Aberrant BTG4 mRNA expression can be employed as a marker of the tumorigenesis, histogenesis, aggressiveness and prognosis of gynecological cancers in the future practice and guide the investigation of BTG4-related signal pathways. |
Author | Xue, Hang Zheng, Hua-chuan Zhang, Cong-yu Zhang, Rui |
Author_xml | – sequence: 1 givenname: Hua-chuan surname: Zheng fullname: Zheng, Hua-chuan organization: Department of Oncology, The Affiliated Hospital of Chengde Medical University – sequence: 2 givenname: Hang surname: Xue fullname: Xue, Hang organization: Department of Oncology, The Affiliated Hospital of Chengde Medical University – sequence: 3 givenname: Cong-yu surname: Zhang fullname: Zhang, Cong-yu organization: Cancer Center, The First Affiliated Hospital of Jinzhou Medical University – sequence: 4 givenname: Rui surname: Zhang fullname: Zhang, Rui organization: Department of Colorectal Surgery, Liaoning Cancer Hospital |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36880525$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.3389/fonc.2022.830570 10.1016/j.gore.2016.09.004 10.1158/0008-5472.CAN-08-0325 10.1095/biolreprod.105.041574 10.1016/j.cryobiol.2011.09.134 10.1016/j.theriogenology.2012.01.015 10.1007/s10815-021-02340-9 10.1098/rsob.160184 10.3390/healthcare10091605 10.1006/geno.2000.6288 10.1016/j.ogc.2022.08.008 10.1093/jmcb/mjw023 10.1016/j.ajhg.2020.05.010 10.1002/gcc.20159 10.3390/genes11020217 10.1016/j.bbrc.2009.06.140 10.1038/nsmb.3204 10.1080/09168451.2015.1008976 10.1002/jcp.21919 10.1530/ERC-11-0083 10.1016/j.ejogrb.2022.09.029 10.18632/oncotarget.10337 10.1097/MD.0000000000024485 10.1186/s40001-022-00952-0 10.1186/s12860-017-0130-3 10.1136/ijgc-2020-001640 10.1177/1933719117715126 10.1007/s00404-019-05358-8 10.1038/nmeth.2956 10.1186/1471-2164-9-110 |
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Keywords | BTG4 carcinogenesis bioinformatic analysis prognosis aggressiveness gynecological cancer |
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References | e_1_3_4_4_1 e_1_3_4_3_1 e_1_3_4_2_1 e_1_3_4_9_1 e_1_3_4_8_1 Laganà A.S. (e_1_3_4_14_1) 2015; 36 e_1_3_4_7_1 e_1_3_4_20_1 e_1_3_4_6_1 e_1_3_4_5_1 e_1_3_4_23_1 e_1_3_4_24_1 e_1_3_4_21_1 e_1_3_4_22_1 e_1_3_4_27_1 e_1_3_4_28_1 e_1_3_4_25_1 e_1_3_4_26_1 e_1_3_4_29_1 e_1_3_4_31_1 e_1_3_4_30_1 e_1_3_4_12_1 e_1_3_4_13_1 e_1_3_4_10_1 e_1_3_4_11_1 e_1_3_4_32_1 e_1_3_4_16_1 e_1_3_4_17_1 e_1_3_4_15_1 e_1_3_4_18_1 e_1_3_4_19_1 |
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Snippet | BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of BTG4 expression. BTG4 expression was... BTG4 arrests the cell cycle and suppresses oocyte and embryonic development. We performed a bioinformatic analysis of expression. expression was downregulated... |
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StartPage | 2182672 |
SubjectTerms | aggressiveness Animals bioinformatic analysis Breast cancer BTG4 Carcinogenesis Cell cycle Cell Cycle Proteins Colorectal cancer Computational Biology Endometrial cancer Endometrial Neoplasms Female Gynecological cancer Humans Medical prognosis Mice Ovarian cancer Ovarian Neoplasms - genetics Pregnancy Prognosis RNA, Messenger |
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Title | Bioinformatic analysis of the clinicopathological and prognostic significance of oocyte-arresting BTG4 mRNA expression in gynecological cancers |
URI | https://www.tandfonline.com/doi/abs/10.1080/01443615.2023.2182672 https://www.ncbi.nlm.nih.gov/pubmed/36880525 https://www.proquest.com/docview/3087538099 https://www.proquest.com/docview/2784385460 https://doaj.org/article/befb70ad65de4b56ae265f3a84fb7d23 |
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