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 inAnalytical cellular pathology (Amsterdam) Vol. 2021; pp. 6004821 - 10
Main Authors Tan, Lin, Qu, Weiming, Wu, Dajun, Liu, Minji, Wang, Qian, Ai, Qiongjia, Hu, Hongsai, Chen, Min, Chen, Weishun, Zhou, Hongbing
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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.
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
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Snippet GRHL3 is a factor associated with a tumor, of which the molecular mechanism remains a further investigation. We explored the underlying mechanism of...
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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
URI https://dx.doi.org/10.1155/2021/6004821
https://www.ncbi.nlm.nih.gov/pubmed/34888136
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Volume 2021
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