A novel protein encoded by circFNDC3B inhibits tumor progression and EMT through regulating Snail in colon cancer

Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. We used Sanger sequence and RNase R digestion assay to con...

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Published inMolecular cancer Vol. 19; no. 1; pp. 71 - 15
Main Authors Pan, Zihao, Cai, Jianye, Lin, Jiatong, Zhou, Huinian, Peng, Jingwen, Liang, Jinliang, Xia, Long, Yin, Qi, Zou, Baojia, Zheng, Jun, Qiao, Liang, Zhang, Lei
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 02.04.2020
BioMed Central
BMC
Subjects
Animal experimentation
Animal research
Animals
Apoptosis
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Cancer treatment
Carcinogenesis
Cell migration
Cell Proliferation
circFNDC3B
circRNA
Colon cancer
Colonic Neoplasms - genetics
Colonic Neoplasms - metabolism
Colonic Neoplasms - pathology
Colorectal cancer
Cytoplasm
Development and progression
DNA sequencing
Epithelial-Mesenchymal Transition
Ethics
FBP1
Female
Fibronectins - genetics
Fluorescence in situ hybridization
Gene Expression Regulation, Neoplastic
Glucose metabolism
Health aspects
Humans
Hybridization
Immunoglobulins
Male
Mice
Mice, Inbred BALB C
Mice, Nude
Middle Aged
Peptides
Prognosis
Proteins
Ribonuclease
Ribonucleic acid
RNA
RNA, Circular - genetics
Snail Family Transcription Factors - genetics
Snail Family Transcription Factors - metabolism
Studies
Survival Rate
Therapeutic applications
Tumor Cells, Cultured
Tumors
Wound healing
Xenograft Model Antitumor Assays
China
United States > US
Japan
Germany
circFNDC3B
Colon cancer
circRNA
FBP1
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Abstract Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA's expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa. CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC. The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.
AbstractList Abstract Background Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. Methods We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA’s expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa. Results CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC. Conclusions The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.
Background Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. Methods We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA's expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa. Results CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC. Conclusions The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC. Keywords: circRNA, circFNDC3B, FBP1, Colon cancer
Background Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. Methods We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA’s expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa. Results CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC. Conclusions The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.
Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC.BACKGROUNDColon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC.We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA's expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa.METHODSWe used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA's expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa.CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC.RESULTSCircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC.The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.CONCLUSIONSThe novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.
Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA's expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa. CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC. The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.
Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA's expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa. CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC. The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.
ArticleNumber 71
Audience Academic
Author Cai, Jianye
Yin, Qi
Pan, Zihao
Lin, Jiatong
Xia, Long
Qiao, Liang
Liang, Jinliang
Peng, Jingwen
Zhou, Huinian
Zou, Baojia
Zhang, Lei
Zheng, Jun
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/32241279$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1038/cr.2017.31
10.3322/caac.21551
10.1080/15384101.2016.1191706
10.1016/j.canlet.2015.06.003
10.1038/s41419-018-0454-8
10.1002/jcp.29316
10.1016/j.canlet.2017.03.019
10.1016/j.ccr.2013.01.022
10.1038/s41598-017-17931-9
10.1016/j.molcel.2017.02.021
10.1186/s12943-019-1010-6
10.1038/cr.2017.70
10.1186/s12943-018-0908-8
10.1093/nar/gkw027
10.1038/ncomms11215
10.18632/oncotarget.22349
10.1038/nrd.2017.59
10.1021/pr300736v
10.1016/j.molcel.2017.02.017
10.1126/science.7536344
10.1002/jcp.28588
10.1016/j.jbiotec.2016.09.011
10.1016/j.virol.2015.02.046
10.1053/j.gastro.2015.07.050
10.1261/rna.043687.113
10.1038/onc.2009.332
10.1038/s41419-018-1165-x
10.1093/jnci/djx166
10.1038/s41388-017-0019-9
10.1111/febs.14756
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Issue 1
Keywords circFNDC3B
Colon cancer
circRNA
FBP1
Language English
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References P Lunetti (1179_CR29) 2019; 286
F Wang (1179_CR5) 2016; 6
NR Pamudurti (1179_CR23) 2017; 66
C Dong (1179_CR18) 2013; 23
1179_CR25
S Qu (1179_CR3) 2015; 365
S Peppicelli (1179_CR30) 2016; 15
S Halldorsson (1179_CR28) 2017; 396
FR Kulcheski (1179_CR4) 2016; 238
P Glazar (1179_CR6) 2014; 20
X Liu (1179_CR16) 2017; 7
Q Dai (1179_CR20) 2017; 7
Z Qiu (1179_CR32) 2015; 149
M Zhang (1179_CR26) 2018; 37
CY Chen (1179_CR22) 1995; 268
I Legnini (1179_CR24) 2017; 66
1179_CR14
H Liu (1179_CR13) 2018; 17
Y Hong (1179_CR15) 2019; 234
X Zheng (1179_CR27) 2019; 18
K Zeng (1179_CR8) 2018; 9
L Teng (1179_CR9) 2017; 8
T Schneider (1179_CR11) 2017; 27
X Liu (1179_CR31) 2010; 29
S Cassidy (1179_CR1) 2017; 16
D Power (1179_CR17) 2015; 481
Q Zheng (1179_CR7) 2016; 7
WW Du (1179_CR10) 2016; 44
Y Yang (1179_CR12) 2017; 27
GM Liu (1179_CR19) 2018; 9
RL Siegel (1179_CR2) 2019; 69
AT Qattan (1179_CR21) 2012; 11
References_xml – volume: 27
  start-page: 626
  issue: 5
  year: 2017
  ident: 1179_CR12
  publication-title: Cell Res
  doi: 10.1038/cr.2017.31
– volume: 69
  start-page: 7
  issue: 1
  year: 2019
  ident: 1179_CR2
  publication-title: CA Cancer J Clin
  doi: 10.3322/caac.21551
– volume: 7
  start-page: 2121
  issue: 11
  year: 2017
  ident: 1179_CR20
  publication-title: Am J Cancer Res
– volume: 6
  start-page: 1167
  issue: 6
  year: 2016
  ident: 1179_CR5
  publication-title: Am J Cancer Res
– volume: 15
  start-page: 1908
  issue: 14
  year: 2016
  ident: 1179_CR30
  publication-title: Cell Cycle
  doi: 10.1080/15384101.2016.1191706
– volume: 365
  start-page: 141
  issue: 2
  year: 2015
  ident: 1179_CR3
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2015.06.003
– volume: 9
  start-page: 417
  issue: 4
  year: 2018
  ident: 1179_CR8
  publication-title: Cell Death Dis
  doi: 10.1038/s41419-018-0454-8
– ident: 1179_CR14
  doi: 10.1002/jcp.29316
– volume: 396
  start-page: 117
  year: 2017
  ident: 1179_CR28
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2017.03.019
– volume: 23
  start-page: 316
  issue: 3
  year: 2013
  ident: 1179_CR18
  publication-title: Cancer Cell
  doi: 10.1016/j.ccr.2013.01.022
– volume: 7
  start-page: 17571
  issue: 1
  year: 2017
  ident: 1179_CR16
  publication-title: Sci Rep
  doi: 10.1038/s41598-017-17931-9
– volume: 66
  start-page: 9
  issue: 1
  year: 2017
  ident: 1179_CR23
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2017.02.021
– volume: 18
  start-page: 47
  issue: 1
  year: 2019
  ident: 1179_CR27
  publication-title: Mol Cancer
  doi: 10.1186/s12943-019-1010-6
– volume: 27
  start-page: 724
  issue: 6
  year: 2017
  ident: 1179_CR11
  publication-title: Cell Res
  doi: 10.1038/cr.2017.70
– volume: 17
  start-page: 161
  issue: 1
  year: 2018
  ident: 1179_CR13
  publication-title: Mol Cancer
  doi: 10.1186/s12943-018-0908-8
– volume: 44
  start-page: 2846
  issue: 6
  year: 2016
  ident: 1179_CR10
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkw027
– volume: 7
  start-page: 11215
  year: 2016
  ident: 1179_CR7
  publication-title: Nat Commun
  doi: 10.1038/ncomms11215
– volume: 8
  start-page: 107125
  issue: 63
  year: 2017
  ident: 1179_CR9
  publication-title: Oncotarget
  doi: 10.18632/oncotarget.22349
– volume: 16
  start-page: 525
  issue: 8
  year: 2017
  ident: 1179_CR1
  publication-title: Nat Rev Drug Discov
  doi: 10.1038/nrd.2017.59
– volume: 11
  start-page: 6080
  issue: 12
  year: 2012
  ident: 1179_CR21
  publication-title: J Proteome Res
  doi: 10.1021/pr300736v
– volume: 66
  start-page: 22
  issue: 1
  year: 2017
  ident: 1179_CR24
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2017.02.017
– volume: 268
  start-page: 415
  issue: 5209
  year: 1995
  ident: 1179_CR22
  publication-title: Science.
  doi: 10.1126/science.7536344
– volume: 234
  start-page: 19895
  issue: 11
  year: 2019
  ident: 1179_CR15
  publication-title: J Cell Physiol
  doi: 10.1002/jcp.28588
– volume: 238
  start-page: 42
  year: 2016
  ident: 1179_CR4
  publication-title: J Biotechnol
  doi: 10.1016/j.jbiotec.2016.09.011
– volume: 481
  start-page: 142
  year: 2015
  ident: 1179_CR17
  publication-title: Virology.
  doi: 10.1016/j.virol.2015.02.046
– volume: 149
  start-page: 1587
  issue: 6
  year: 2015
  ident: 1179_CR32
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2015.07.050
– volume: 20
  start-page: 1666
  issue: 11
  year: 2014
  ident: 1179_CR6
  publication-title: RNA
  doi: 10.1261/rna.043687.113
– volume: 29
  start-page: 442
  issue: 3
  year: 2010
  ident: 1179_CR31
  publication-title: Oncogene
  doi: 10.1038/onc.2009.332
– volume: 9
  start-page: 1132
  issue: 11
  year: 2018
  ident: 1179_CR19
  publication-title: Cell Death Dis
  doi: 10.1038/s41419-018-1165-x
– ident: 1179_CR25
  doi: 10.1093/jnci/djx166
– volume: 37
  start-page: 1805
  issue: 13
  year: 2018
  ident: 1179_CR26
  publication-title: Oncogene
  doi: 10.1038/s41388-017-0019-9
– volume: 286
  start-page: 688
  issue: 4
  year: 2019
  ident: 1179_CR29
  publication-title: FEBS J
  doi: 10.1111/febs.14756
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Snippet Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear...
Background Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was...
Abstract Background Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However,...
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StartPage 71
SubjectTerms Animal experimentation
Animal research
Animals
Apoptosis
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Cancer treatment
Carcinogenesis
Cell migration
Cell Proliferation
circFNDC3B
circRNA
Colon cancer
Colonic Neoplasms - genetics
Colonic Neoplasms - metabolism
Colonic Neoplasms - pathology
Colorectal cancer
Cytoplasm
Development and progression
DNA sequencing
Epithelial-Mesenchymal Transition
Ethics
FBP1
Female
Fibronectins - genetics
Fluorescence in situ hybridization
Gene Expression Regulation, Neoplastic
Glucose metabolism
Health aspects
Humans
Hybridization
Immunoglobulins
Male
Mice
Mice, Inbred BALB C
Mice, Nude
Middle Aged
Peptides
Prognosis
Proteins
Ribonuclease
Ribonucleic acid
RNA
RNA, Circular - genetics
Snail Family Transcription Factors - genetics
Snail Family Transcription Factors - metabolism
Studies
Survival Rate
Therapeutic applications
Tumor Cells, Cultured
Tumors
Wound healing
Xenograft Model Antitumor Assays
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Title A novel protein encoded by circFNDC3B inhibits tumor progression and EMT through regulating Snail in colon cancer
URI https://www.ncbi.nlm.nih.gov/pubmed/32241279
https://www.proquest.com/docview/2391505273
https://www.proquest.com/docview/2386279272
https://pubmed.ncbi.nlm.nih.gov/PMC7114813
https://doaj.org/article/05c8955b461640daa98ffa4c468e7a34
Volume 19
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