ArticleCell biology and toxicology2023
Linc-ROR drive adriamycin resistance by targeting AP-2α/Wnt/β-catenin axis in hepatocellular carcinoma.
Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 11 citations in OpenAlex.
- Icariside II sensitizes osteosarcoma to doxorubicin through the lincROR/Wnt/β-catenin signaling regulatory axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- LincRNA-miR interactions in hepatocellular carcinoma: comprehensive review and in silico analysis: a step toward ncRNA precision.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Long non-coding RNAs and autophagy: dual drivers of Hepatocellular carcinoma progression.Cell death discovery · 2025Review
- HOTTIP suppresses ferroptosis via mediating DGCR8/miR‑214‑3p/GPX4 regulatory axis in osteosarcoma.Oncology reports · 2025Article
- Chinese herbal medicines: the modifier of hepatocellular carcinoma targeting Wnt/β-catenin signaling pathway.Frontiers in pharmacology · 2025Review
- Wnt Signaling in Hepatocellular Carcinoma: Biological Mechanisms and Therapeutic Opportunities.Cells · 2024Review
- ZNF460-mediated upregulation of APCDD1L-DT promotes cholangiocarcinoma development by inhibiting the ubiquitin-mediated degradation of DVL2.Cancer gene therapy · 2024Article
- The interplay of miRNAs and ferroptosis in diseases related to iron overload.Apoptosis : an international journal on programmed cell death · 2024Review
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Authors and funding
6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Adriamycin is widely used as a chemotherapeutic strategy for advanced hepatocellular carcinoma (HCC). However, the clinical response was disappointing because of the acquired drug resistance with long-term usage. Revealing the underlying mechanism could provide promising therapeutics for the drug-resistant patients. The recently identified linc-ROR (long intergenic non-protein-coding RNA, regulator of reprogramming) has been found to be an oncogene in various cancers, and it also demonstrated to mediate drug resistance and metastasis. We thereby wonder whether this lincRNA could mediate adriamycin chemoresistance in HCC. In this study, linc-ROR was found to be upregulated in adriamycin-resistant HCC cells. And its overexpression accelerated epithelial-mesenchymal transition (EMT) program and adriamycin resistance. Conversely, its silence suppressed EMT and made HCC cells sensitize to adriamycin in vitro and in vivo. Further investigation revealed that linc-ROR physically interacted with AP-2α, mediated its stability by a post-translational modification manner, and sequentially activated Wnt/β-catenin pathway. Furthermore, linc-ROR expression was positively associated with β-catenin expression in human clinical specimens. Taken together, linc-ROR promoted tumorigenesis and adriamycin resistance in HCC via a linc-ROR/AP-2α/Wnt/β-catenin axis, which could be developed as a potential therapeutic target for the adriamycin-resistant patients.
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