Long non-coding RNA MIR4435-2HG modulates pancreatic cancer stem cells and chemosensitivity to gemcitabine by targeting the miR-1252-5p/STAT1 DOI Creative Commons
Baocheng Xie, Pei‐Shan Wu, Hongyu Liu

et al.

Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 7, 2025

Cancer stem cells (CSCs) are key drivers of cancer progression and therapeutic resistance. Long non-coding RNAs (lncRNAs) have emerged as critical regulators CSC properties. The aim this study was to investigate the role MIR4435-2HG in regulating characteristics, tumorigenesis, chemoresistance pancreatic cancer. Functional assays were conducted evaluate self-renewal, tumorigenic potential, with altered expression MIR4435-2HG. RNA interference (RNAi) employed knock down MIR4435-2HG, a STAT1 reintroduction model established examine downstream signaling pathways. miR-1252-5p competing endogenous also explored. Overexpression significantly enhanced self-renewal whereas silencing notably diminished these Mechanistically, promoted by sponging miR-1252-5p, thereby enhancing stemness tumorigenesis. Moreover, depletion sensitized gemcitabine-induced growth inhibition ferroptosis. Reintroduction restored gemcitabine resistance MIR4435-2HG-deficient cells. Our findings demonstrate that plays modulating properties through MIR4435-2HG/miR-1252-5p/STAT1 axis. Targeting presents promising approach regulate CSCs improve efficacy chemotherapy

Language: Английский

Long non-coding RNA MIR4435-2HG modulates pancreatic cancer stem cells and chemosensitivity to gemcitabine by targeting the miR-1252-5p/STAT1 DOI Creative Commons
Baocheng Xie, Pei‐Shan Wu, Hongyu Liu

et al.

Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)

Published: Feb. 7, 2025

Cancer stem cells (CSCs) are key drivers of cancer progression and therapeutic resistance. Long non-coding RNAs (lncRNAs) have emerged as critical regulators CSC properties. The aim this study was to investigate the role MIR4435-2HG in regulating characteristics, tumorigenesis, chemoresistance pancreatic cancer. Functional assays were conducted evaluate self-renewal, tumorigenic potential, with altered expression MIR4435-2HG. RNA interference (RNAi) employed knock down MIR4435-2HG, a STAT1 reintroduction model established examine downstream signaling pathways. miR-1252-5p competing endogenous also explored. Overexpression significantly enhanced self-renewal whereas silencing notably diminished these Mechanistically, promoted by sponging miR-1252-5p, thereby enhancing stemness tumorigenesis. Moreover, depletion sensitized gemcitabine-induced growth inhibition ferroptosis. Reintroduction restored gemcitabine resistance MIR4435-2HG-deficient cells. Our findings demonstrate that plays modulating properties through MIR4435-2HG/miR-1252-5p/STAT1 axis. Targeting presents promising approach regulate CSCs improve efficacy chemotherapy

Language: Английский

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