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ACTG1 facilitates proliferation and epithelial-mesenchymal transition-mediated metastasis via COL21A1 in gastric cancer.

iScience 2026 Vol.29(2) p. 114666

Li S, Lan B, Pan L, Sun M, Cui M, Huang Y, Wei S, Huang H

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Gastric cancer (GC) remains a lethal malignancy with limited therapeutic options.

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APA Li S, Lan B, et al. (2026). ACTG1 facilitates proliferation and epithelial-mesenchymal transition-mediated metastasis via COL21A1 in gastric cancer.. iScience, 29(2), 114666. https://doi.org/10.1016/j.isci.2026.114666
MLA Li S, et al.. "ACTG1 facilitates proliferation and epithelial-mesenchymal transition-mediated metastasis via COL21A1 in gastric cancer.." iScience, vol. 29, no. 2, 2026, pp. 114666.
PMID 41704754
DOI 10.1016/j.isci.2026.114666

Abstract

Gastric cancer (GC) remains a lethal malignancy with limited therapeutic options. We investigated the role of γ-actin (ACTG1) in GC progression. Bioinformatics analyses revealed that ACTG1 is upregulated in GC tissues and correlates with poor patient prognosis. Functionally, the knockdown of ACTG1 suppressed GC cell proliferation and metastasis in both and models. Transcriptomic sequencing identified COL21A1 as a key downstream effector, and KEGG analysis indicated involvement in epithelial-mesenchymal transition (EMT). Critically, overexpression of COL21A1 rescued the inhibitory effects of ACTG1 knockdown on proliferation, migration, and EMT. These findings demonstrate that the ACTG1/COL21A1 axis promotes GC progression by regulating EMT, highlighting its potential as a therapeutic target for patients with GC.

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