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• W2989656503 endingPage "111739" @default.
• W2989656503 startingPage "111739" @default.
• W2989656503 abstract "Chemo-resistance to conventional therapy is a major barrier requiring further investigation in hepatocellular carcinoma (HCC). Cancer stem like cells (CSCs) contribute to the tumorigenicity, progression, and chemo-resistance of malignancies. Studies have implicated the anti-cancer effects of arsenic trioxide (ATO) and have explored the underlying mechanisms. However, whether ATO might reverse chemo-resistance by inhibiting the CSC like properties remains under investigation. Here, we explored the potential of ATO in chemotherapy in constructed multiple drug resistant (MDR) liver cancer cells. ATO re-sensitized the MDR Bel-7402 cells (BelMDR) cells to chemotherapeutic drugs, an effect mediated by the inhibition of NF-κB pathway and CSCs properties. For the molecular mechanisms, via inducing the DNA de-methylation, ATO activated the microRNA-148a (miR-148a), leading to the repression of NF-κB pathway by targeting the 3'-UTR of p65. In summary, epigenetic regulation of miR-148a by ATO is an important mechanism in drug resistance that decreases the expression of NF-κB and hence represses CSC like phenotype. These findings may suggest a novel mechanism for HCC treatment." @default.
• W2989656503 created "2019-12-05" @default.
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• W2989656503 date "2020-01-01" @default.
• W2989656503 modified "2023-09-26" @default.
• W2989656503 title "De-methylation of miR-148a by arsenic trioxide enhances sensitivity to chemotherapy via inhibiting the NF-κB pathway and CSC like properties" @default.
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• W2989656503 doi "https://doi.org/10.1016/j.yexcr.2019.111739" @default.
• W2989656503 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31759055" @default.
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