ArticleJournal of cellular and molecular medicine2021
lncRNA MALAT1 participates in metformin inhibiting the proliferation of breast cancer cell.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Antiproliferative Mechanisms of Metformin in Breast Cancer: A Systematic Review of the Literature.International journal of molecular sciences · 2024Pooled it
- Metformin as an Innate Immune Modulator: Metabolic and Epigenetic Reprogramming of Innate Immune Cells and Therapeutic Implications.Current issues in molecular biology · 2026Review
- Metformin triggers apoptosis via endoplasmic reticulum stress in HER2-positive breast cancer cell lines.Experimental and therapeutic medicine · 2026Article
- Metformin alleviates the progression of oral submucous fibrosis through downregulation of metastasis associated lung adenocarcinoma transcript 1 (MALAT1).Journal of dental sciences · 2026Article
- Genomic data mining reveals hub genes and lncRNAs as prognostic biomarkers in breast cancer.Scientific reports · 2025Article
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- The Role of Non-Coding Regions in Breast Cancer: From Gene Regulation to Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- RNA modifications in cancer.MedComm · 2025Review
- Non-coding RNAs as potential targets in metformin therapy for cancer.Cancer cell international · 2024Review
- Metformin and Breast Cancer: Current Findings and Future Perspectives from Preclinical and Clinical Studies.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Role of Harmaline in Inhibiting c-Myc, Altering Molecular Typing, and Promoting Apoptosis in Triple-Negative Breast Cancer.Breast cancer (Dove Medical Press) · 2024Article
- Autophagy-related lncRNAs in tumor progression and drug resistance: A double-edged sword.Genes & diseases · 2024Review
- Beyond the Genome: Deciphering the Role of MALAT1 in Breast Cancer Progression.Current genomics · 2024Review
- Mechanisms of Regulation of the Expression of miRNAs and lncRNAs by Metformin in Ovarian Cancer.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Integrative Analysis Revealed LINC00847 as a Potential Target of Tumor Immunotherapy.Applied biochemistry and biotechnology · 2023Article
- Melatonin regulates cancer migration and stemness and enhances the anti-tumour effect of cisplatin.Journal of cellular and molecular medicine · 2023Article
- Construction of a predictive model for breast cancer metastasis based on lncRNAs.Translational cancer research · 2023Article
- Metformin and long non-coding RNAs in breast cancer.Journal of translational medicine · 2023Review
- The anti-diabetic effects of metformin are mediated by regulating long non-coding RNA.Frontiers in pharmacology · 2023Review
- Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, the repurposing of conventional and chemotherapeutic drugs is recognized as an alternative strategy for health care. The main purpose of this study is to strengthen the application of non-oncological drug metformin on breast cancer treatment in the perspective of epigenetics. In the present study, metformin was found to inhibit cell proliferation, promote apoptosis and induce cell cycle arrest in breast cancer cells at a dose-dependent manner. In addition, metformin treatment elevated acH3K9 abundance and decreased acH3K18 level. The expression of lncRNA MALAT1, HOTAIR, DICER1-AS1, LINC01121 and TUG1 was up-regulated by metformin treatment. In metformin-treated cells, MALAT1 knock-down increased the Bax/Bcl2 ratio and enhanced p21 but decreased cyclin B1 expression. The expression of Beclin1, VDAC1, LC3-II, CHOP and Bip was promoted in the cells received combinatorial treatment of metformin and MALAT1 knock-down. The reduced phosphorylation of c-Myc was further decreased in the metformin-treated cells in combination with MALAT1 knock-down than metformin treatment alone. Taken together, these results provide a promising repurposed strategy for metformin on cancer treatment by modulating epigenetic modifiers.
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Registered trials
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.