GRHL3 Promotes Tumor Growth and Metastasis via the MEK Pathway in Colorectal Cancer
GRHL3 is a factor associated with a tumor, of which the molecular mechanism remains a further investigation. We explored the underlying mechanism of tumor-promoting effect of GRHL3 in colorectal cancer (CRC), which is involved in the MEK1/2 pathway. The expression of GRHL3 was measured in CRC and ad...
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Published in | Analytical cellular pathology (Amsterdam) Vol. 2021; pp. 6004821 - 10 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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2021
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Abstract | GRHL3 is a factor associated with a tumor, of which the molecular mechanism remains a further investigation. We explored the underlying mechanism of tumor-promoting effect of GRHL3 in colorectal cancer (CRC), which is involved in the MEK1/2 pathway. The expression of GRHL3 was measured in CRC and adjacent normal tissue using qPCR and immunohistochemical staining. Lentivirus-mediated knockdown expression of GRHL3 was performed in the CRC cell line HT29. Cell proliferation and metastasis were assayed in vitro, and tumorigenicity was investigated in vivo. We found higher GRHL3 expression in colorectal cancer, which was negatively correlated with patients’ prognosis. Results from studies in vitro and in vivo indicated that downregulation of GRHL3 expression inhibited tumor growth and metastasis and inhibited the activation of the MEK1/2 pathway. The effect of GRHL3 downexpression was the same as that of MEK1/2 antagonists on suppression of tumor growth and metastasis. Our results suggested that GRHL3 may act as an oncogene to promote tumor growth and metastasis via the MEK pathway in colorectal cancer. |
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AbstractList | GRHL3 is a factor associated with a tumor, of which the molecular mechanism remains a further investigation. We explored the underlying mechanism of tumor-promoting effect of GRHL3 in colorectal cancer (CRC), which is involved in the MEK1/2 pathway. The expression of GRHL3 was measured in CRC and adjacent normal tissue using qPCR and immunohistochemical staining. Lentivirus-mediated knockdown expression of GRHL3 was performed in the CRC cell line HT29. Cell proliferation and metastasis were assayed in vitro, and tumorigenicity was investigated in vivo. We found higher GRHL3 expression in colorectal cancer, which was negatively correlated with patients' prognosis. Results from studies in vitro and in vivo indicated that downregulation of GRHL3 expression inhibited tumor growth and metastasis and inhibited the activation of the MEK1/2 pathway. The effect of GRHL3 downexpression was the same as that of MEK1/2 antagonists on suppression of tumor growth and metastasis. Our results suggested that GRHL3 may act as an oncogene to promote tumor growth and metastasis via the MEK pathway in colorectal cancer. |
Author | Qu, Weiming Wu, Dajun Liu, Minji Ai, Qiongjia Wang, Qian Chen, Min Chen, Weishun Tan, Lin Zhou, Hongbing Hu, Hongsai |
AuthorAffiliation | Department of Gastroenterology, The Affiliated Zhuzhou Hospital Xiangya Medical College CSU, Zhuzhou, China 412007 |
AuthorAffiliation_xml | – name: Department of Gastroenterology, The Affiliated Zhuzhou Hospital Xiangya Medical College CSU, Zhuzhou, China 412007 |
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SubjectTerms | Animals Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Colorectal Neoplasms - genetics Colorectal Neoplasms - metabolism Colorectal Neoplasms - pathology DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Female Gene Expression Regulation, Neoplastic HCT116 Cells HT29 Cells Humans Male MAP Kinase Signaling System - genetics Mice Mice, Inbred BALB C Mice, Nude Middle Aged Neoplasm Metastasis RNAi Therapeutics - methods Transcription Factors - genetics Transcription Factors - metabolism Tumor Burden - genetics Xenograft Model Antitumor Assays - methods |
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Title | GRHL3 Promotes Tumor Growth and Metastasis via the MEK Pathway in Colorectal Cancer |
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