ArticleAnalytical cellular pathology (Amsterdam)2021
GRHL3 Promotes Tumor Growth and Metastasis via the MEK Pathway in Colorectal Cancer.
Article in Analytical cellular pathology (Amsterdam), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 12 citations in OpenAlex.
- The immunoregulatory role of lncRNA UCA1: a pan-cancer perspective with a focus on colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- ZNF217 Mediates Transcriptional Activation of GRHL3 to Regulate SLC22A31 and Promote Malignant Progression in Thyroid Cancer.Molecular biotechnology · 2025Article
- Transcription factor-target gene regulatory network analysis in human lung adenocarcinoma.Journal of thoracic disease · 2023Article
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Authors and funding
10 authors at 1 institution in 1 country.
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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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