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Updated: Jan 21, 2026

Orthotopic Mouse Model of Colorectal Cancer
Published on: December 4, 2007
Targeting p38γ to inhibit human colorectal cancer cell progression
Chang Su1, Qi Sun1, Shaoqun Liu1
1Department of Surgery, Minhang Hospital, Fudan University, Shanghai, China.
Abstract:
Colorectal cancer (CRC) is a common malignancy globally causing significant cancer-related mortality. Recent studies have proposed p38gamma (p38γ) as a novel cyclin-dependent kinase (CDK)-like kinase, promoting tumorigenesis and cancer progression. The current study evaluates p38γ expression and potential role in CRC. In HT-29 cells and primary human colon cancer cells, shRNA-induced p38γ silencing or CRISPR/Cas9-mediated p38γ knockout inhibited cell growth, proliferation, and migration, and induced significant apoptosis. Conversely, ectopic overexpression of p38γ further promoted the growth, proliferation, and migration of HT-29 cells and primary colon cancer cells. Retinoblastoma (Rb) phosphorylation and cyclins (E1/A) expression were decreased by p38γ silencing or KO, but increased with p38γ overexpression. p38γ mRNA and protein levels are significantly upregulated in human colon cancer tissues, when compared to levels in surrounding colon epithelial tissues. These results demonstrate that overexpression of p38γ can promote human CRC cell progression, and identify p38γ as a novel therapeutic target.
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