ArticleOncology letters2026
Transcriptional activation of GSTP1 by ANXA3 is associated with cisplatin sensitivity in colorectal cancer cells.
Article in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Although platinum-based chemotherapeutic agents demonstrate efficacy against colorectal cancer (CRC), the development of resistance to these agents remains a notable clinical challenge, with the underlying mechanisms still incompletely understood. In the present study, public tumor databases revealed that annexin A3 (ANXA3) was significantly upregulated in CRC primary tumors. This upregulation was then validated at the protein level using a tissue microarray, which confirmed elevated ANXA3 expression in CRC tumor tissues. The Kaplan-Meier curve analysis further demonstrated that patients with CRC with high ANXA3 expression exhibited shorter overall survival compared with those with low expression. Notably, CRC cell lines with high ANXA3 expression showed reduced sensitivity to cisplatin. Moreover, overexpression of ANXA3 significantly diminished cisplatin sensitivity in CRC cells, whereas silencing ANXA3 enhanced this sensitivity. These results collectively indicated that ANXA3 modulated cisplatin sensitivity in CRC cells. Subsequent investigations revealed that ANXA3 upregulated glutathione S-transferase P1 (GSTP1) expression in CRC cells in an NF-κB-dependent manner, a pathway mechanistically implicated in clinically observed chemotherapy resistance. In addition, ANXA3-overexpressing exosomes were found to upregulate GSTP1 transcriptional expression and decrease cisplatin sensitivity in CRC cells. Finally,
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