ArticleBMC cancer2025
The LncRNA RMST-miR-4295-ITPR1 axis: a key mechanism in regulating autophagy in triple-negative breast cancer cells.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- miRNA-lncRNA Cross-Regulation Landscape in Cancer: From Molecular Mechanisms to Therapeutic and Diagnostic Applications.Cancers · 2026Review
- Targeting Autophagy to Overcome Chemoresistance and Immune Resistance in Triple-Negative Breast Cancer.Cancers · 2026Review
- Global research status and frontiers on autophagy in triple negative breast cancer (TNBC): a comprehensive bibliometric and visualized analysis.Discover oncology · 2025Article
- Long non-coding RNAs and autophagy: dual drivers of Hepatocellular carcinoma progression.Cell death discovery · 2025Review
- Epi-nutrients for cancer prevention: Molecular mechanisms and emerging insights.Cell biology and toxicology · 2025Review
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Authors and funding
6 authors.
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Abstract
backgroundTriple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with poor prognosis and limited treatment options. Autophagy targeting plays a complex role in tumor resistance. The role of long noncoding RNA (LncRNA) RMST in TNBC progression and its potential involvement in autophagy regulation remain largely unexplored.
methodsWe performed a bioinformatics analysis using transcriptome sequencing data to identify differentially expressed genes related to autophagy and the LncRNA-miRNA-mRNA axis in TNBC. The effects of the LncRNA RMST-miR-4295-ITPR1 axis on TNBC cell proliferation and migration were investigated using CCK-8, EdU, Transwell, and wound healing assays. Additionally, a series of in vitro experiments, including flow cytometry, transmission electron microscopy, and western blotting, were performed to evaluate the role of the LncRNA RMST-miR-4295-ITPR1 axis in regulating autophagy.
resultsLncRNA RMST competes with ITPR1 mRNA for miR-4295 binding, thereby relieving the miR-4295-mediated suppression of ITPR1 and increasing ITPR1 expression. Overexpression of LncRNA RMST or ITPR1 significantly inhibited TNBC cell proliferation and migration, promoted apoptosis, and enhanced autophagy. Conversely, miR-4295 overexpression reversed these effects, confirming the regulatory role of the LncRNA RMST-miR-4295-ITPR1 axis in autophagy in TNBC.
conclusionsOur findings indicate that the LncRNA RMST-miR-4295-ITPR1 axis plays a crucial role in regulating autophagy in TNBC cells. The modulation of this axis may represent a novel therapeutic strategy for inhibiting TNBC progression and overcoming chemoresistance.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.