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Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration

BACKGROUND: Colon cancer is highly prevalent, and cell proliferation and migration are major reasons for its progression to malignancy. The upregulation of INHBA, a glycoprotein hormone that regulates the secretion of pituitary hormones, is documented to be oncogenic in numerous cancers, consisting...

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Autores principales: Wang, Jianan, Li, Bo, Yang, Shaohui, Ma, Chenyang, Liu, Kaitai, Chen, Xue, Cui, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279979/
https://www.ncbi.nlm.nih.gov/pubmed/35689549
http://dx.doi.org/10.1002/jcla.24539
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author Wang, Jianan
Li, Bo
Yang, Shaohui
Ma, Chenyang
Liu, Kaitai
Chen, Xue
Cui, Wei
author_facet Wang, Jianan
Li, Bo
Yang, Shaohui
Ma, Chenyang
Liu, Kaitai
Chen, Xue
Cui, Wei
author_sort Wang, Jianan
collection PubMed
description BACKGROUND: Colon cancer is highly prevalent, and cell proliferation and migration are major reasons for its progression to malignancy. The upregulation of INHBA, a glycoprotein hormone that regulates the secretion of pituitary hormones, is documented to be oncogenic in numerous cancers, consisting of breast, gastric, and ovarian cancer. Herein, we assessed the role of INHBA in the proliferation along with the migration of colon cancer cells. METHODS: TCGA datasets were used to assess INHBA expression and its correlation with prognosis in colon cancer patients. Analyses on JASPAR, PROMO, and ENCODE databases, uncovered high correlation between INHBA and BHLHE40. Western blot and RT‐qPCR analysis were used to determine protein and mRNA levels. Cell transfection inhibited the expression of INHBA and BHLHE40. Cell proliferation rates were determined using CCK8 analysis. Wound healing assays were adopted to explore cell migration. RESULTS: INHBA is markedly elevated in colon cancer tissues along with cells and is a predictive factor for patient's prognosis with colon cancer. INHBA silencing suppressed colon cancer cell proliferation and migration. Furthermore, we confirmed the association of INHBA with BHLHE40 in colon cancer cells. BHLHE40 could directly modulates INHBA expression. Here, we show that BHLHE40 modulates the expression of INHBA, which influences the proliferation, and migration of colon cancer cells. CONCLUSION: INHBA acts as an oncogene in colon cancer and it can be regulated by the transcription factor BHLHE40.
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spelling pubmed-92799792022-07-15 Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration Wang, Jianan Li, Bo Yang, Shaohui Ma, Chenyang Liu, Kaitai Chen, Xue Cui, Wei J Clin Lab Anal Research Articles BACKGROUND: Colon cancer is highly prevalent, and cell proliferation and migration are major reasons for its progression to malignancy. The upregulation of INHBA, a glycoprotein hormone that regulates the secretion of pituitary hormones, is documented to be oncogenic in numerous cancers, consisting of breast, gastric, and ovarian cancer. Herein, we assessed the role of INHBA in the proliferation along with the migration of colon cancer cells. METHODS: TCGA datasets were used to assess INHBA expression and its correlation with prognosis in colon cancer patients. Analyses on JASPAR, PROMO, and ENCODE databases, uncovered high correlation between INHBA and BHLHE40. Western blot and RT‐qPCR analysis were used to determine protein and mRNA levels. Cell transfection inhibited the expression of INHBA and BHLHE40. Cell proliferation rates were determined using CCK8 analysis. Wound healing assays were adopted to explore cell migration. RESULTS: INHBA is markedly elevated in colon cancer tissues along with cells and is a predictive factor for patient's prognosis with colon cancer. INHBA silencing suppressed colon cancer cell proliferation and migration. Furthermore, we confirmed the association of INHBA with BHLHE40 in colon cancer cells. BHLHE40 could directly modulates INHBA expression. Here, we show that BHLHE40 modulates the expression of INHBA, which influences the proliferation, and migration of colon cancer cells. CONCLUSION: INHBA acts as an oncogene in colon cancer and it can be regulated by the transcription factor BHLHE40. John Wiley and Sons Inc. 2022-06-11 /pmc/articles/PMC9279979/ /pubmed/35689549 http://dx.doi.org/10.1002/jcla.24539 Text en © 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Research Articles
Wang, Jianan
Li, Bo
Yang, Shaohui
Ma, Chenyang
Liu, Kaitai
Chen, Xue
Cui, Wei
Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration
title Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration
title_full Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration
title_fullStr Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration
title_full_unstemmed Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration
title_short Upregulation of INHBA mediated by the transcription factor BHLHE40 promotes colon cancer cell proliferation and migration
title_sort upregulation of inhba mediated by the transcription factor bhlhe40 promotes colon cancer cell proliferation and migration
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279979/
https://www.ncbi.nlm.nih.gov/pubmed/35689549
http://dx.doi.org/10.1002/jcla.24539
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