ArticleInternational journal of clinical and experimental pathology2025
MiR-183-5p inhibitor promotes mitoxantrone-induced immunogenic death of hepatoma cells by targeting STC1.
Article in International journal of clinical and experimental pathology, 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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6 authors.
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Abstract
This study aimed to unravel the regulatory mechanism of the microRNA (miR)-183-5p/STC1 axis in regulating mitoxantrone (MIT)-induced immunogenic cell death (ICD) within hepatocellular carcinoma (HCC) cells and assess its therapeutic potential. Dual-luciferase reporter assays were employed to validate that miR-183-5p directly interacts with the 3'-untranslated region (3'-UTR) of STC1 mRNA. HepG2 cells were subjected to treatment with MIT, either in the presence of miR-183-5p inhibitors or STC1 knockout. The expression levels of ICD markers, namely adenosine triphosphate (ATP), high mobility group box 1 (HMGB1), calreticulin (CALR), along with cellular proliferation and apoptosis, were subsequently evaluated. The dual-luciferase assays confirmed that miR-183-5p specifically binds to a defined sequence (5'-GUGCCAU-3') within the 3'-UTR of STC1 mRNA. In MIT-treated HepG2 cells, inhibition of miR-183-5p resulted in a significant upregulation of both STC1 mRNA (+0.78-fold) and protein levels (+0.21-fold). This was accompanied by an enhanced the expression of ICD markers, including a 0.26-fold increase in CALR membrane exposure, a 0.27-fold rise in ATP secretion, and a 0.44-fold elevation in HMGB1 release. Notably, the effects induced by miR-183-5p inhibition were partially mitigated by STC1 gene knockout. Further investigations demonstrated that combination of miR-183-5p inhibitors with MIT synergistically boosted STC1 expression by 5.08-fold. Conversely, STC1 knockout triggered a 184.1% surge in miR-183-5p expression, indicating a negative feedback loop between them. Functional cellular assays revealed that miR-183-5p inhibition significantly augmented MIT's anti-proliferative efficacy, increasing the inhibition rate from 41.9% to 68.0%, and enhanced its pro-apoptotic effects, elevating the apoptosis rate from 30.57% to 36.08%. However, STC1 knockout attenuated these effects. Collectively, our finding indicate that the miR-183-5p/STC1 axis modulates MIT's cytotoxicity through targeted regulation and a negative feedback mechanisms, thereby influencing HCC cell proliferation, apoptosis, and ICD. These insights offer noval strategies for synergistic therapy that integrate epigenetics and the immune microenvironment in HCC treatment.
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