ArticleScientific reports2025
The potential antitumor mechanism and clinical potential of Higd-1a in colorectal cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Colitis-Associated Colorectal Cancer-STAT3 Inhibition as a Preventive Strategy.International journal of molecular sciences · 2026Article
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4 authors.
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Abstract
Higd-1a is under expressed in colorectal cancer cells and its overexpression impaires the proliferation, migration, and invasiveness of colorectal cancer cells. However, the mechanism and clinical potential of Higd-1a in colorectal cancer remains to be further studied. This study investigated the potential of antitumor mechanism and clinical potential of Higd-1a in progression in colorectal cancer. We found that overexpression of Higd-1a in HCT-8 cancer cells suppressed tumor growth in nude mice. Higd-1a overexpression induced cle-caspase-3 and cle-caspase-9 and reduced Bcl-2 expressions, while p-AKT, p-JAK2 and p-STAT3 levels were significantly increased after downregulating Higd-1a in HCT-8 cancer cells. Ruxolitinib co-treatment completely enhanced the anticancer effect induced by inhibiting JAK2/AKT/STAT3 pathway in HCT-8 cells that downregulated Higd-1a. The expression rate in high Higd-1a expression group in stage I-II was considerably greater than that in stage III-IV, and Higd-1a expression and T stage were independent factors affecting the survival time of colorectal cancer. Higd-1a overexpression suppressed tumor growth in vivo and the molecular mechanisms may relate activation of apoptosis-related proteins and suppression JAK2/AKT/STAT3 pathway, and Higd-1a expression is helpful to evaluate the prognosis of colorectal cancer.
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