ArticleScientific reports2018
MiR-29c reduces the cisplatin resistance of non-small cell lung cancer cells by negatively regulating the PI3K/Akt pathway.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Regulation of cisplatin resistance in lung cancer by epigenetic mechanisms.Clinical epigenetics · 2025Review
- MicroRNA Expression Analysis and Biological Pathways in Chemoresistant Non-Small Cell Lung Cancer.Cancers · 2025Article
- SJB2-043, a USP1 Inhibitor, Suppresses A549 Cell Proliferation, Migration, and EMT via Modulation of PI3K/AKT/mTOR, MAPK, and Wnt Signaling Pathways.Current issues in molecular biology · 2025Article
- A novel approach in the identification of microRNAs in malignant pleural effusion for lung cancer diagnosis.Oncology reviews · 2025Review
- A Novel Competing Endogenous RNA Network Reveals Potential Mechanisms and Biomarkers of Chemoresistance in Lung Adenocarcinoma.Journal of Cancer · 2025Article
- Article
- RP11-79H23.3 Inhibits the Proliferation and Metastasis of Non-small-cell Lung Cancer Through Promoting miR-29c.Biochemical genetics · 2023Article
- Advances in the role of microRNAs associated with the PI3K/AKT signaling pathway in lung cancer.Frontiers in oncology · 2023Review
- Ferroptosis as a Potential Cell Death Mechanism Against Cisplatin-Resistant Lung Cancer Cell Line.Advanced pharmaceutical bulletin · 2023Article
- Emerging role of non-coding RNAs in resistance to platinum-based anti-cancer agents in lung cancer.Frontiers in pharmacology · 2023Review
- MicroRNAs and Drug Resistance in Non-Small Cell Lung Cancer: Where Are We Now and Where Are We Going.Cancers · 2022Review
- Epigenetic underpinnings of inflammation: Connecting the dots between pulmonary diseases, lung cancer and COVID-19.Seminars in cancer biology · 2022Review
- MicroRNAs as Predictors of Lung-Cancer Resistance and Sensitivity to Cisplatin.International journal of molecular sciences · 2022Review
- CRISPR/Cas9 gene editing: a new approach for overcoming drug resistance in cancer.Cellular & molecular biology letters · 2022Review
- Integrative analyses of prognosis, tumor immunity, and ceRNA network of the ferroptosis-associated gene FANCD2 in hepatocellular carcinoma.Frontiers in genetics · 2022Article
- miR-130b suppresses the invasion and migration of prostate cancer via inhibiting DLL1 and regulating the PI3K/Akt pathways.Experimental and therapeutic medicine · 2022Article
- Exosomal microRNA panel as a diagnostic biomarker in patients with hepatocellular carcinoma.Frontiers in cell and developmental biology · 2022Article
- Downregulation of miR-29c promotes muscle wasting by modulating the activity of leukemia inhibitory factor in lung cancer cachexia.Cancer cell international · 2021Article
- Cyanidin-3-glucoside suppresses the progression of lung adenocarcinoma by downregulating TP53I3 and inhibiting PI3K/AKT/mTOR pathway.World journal of surgical oncology · 2021Article
- Targeting Akt-associated microRNAs for cancer therapeutics.Biochemical pharmacology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In previous studies, miR-29s showed tumor suppressor properties against lung cancer, which improved the survival of patients upon the administration of chemotherapy via an unknown mechanism. Here, we investigated the regulatory effects of miR-29s on the cisplatin resistance of NSCLC cells. The expression of miR-29s was assessed in 130 clinical patients and in cisplatin-treated NSCLS cell lines. MiR-29c expression was decreased in 77% of NSCLC patients. Cisplatin treatment increased the expression of miR-29c and decreased the expression of its oncogenic target AKT2 in NSCLC cell lines. A Kaplan-Meier survival analysis indicated that higher miR-29c levels led to a longer disease-free survival. In particular, patients who experienced cancer recurrences after cisplatin chemotherapy exhibited a lower level of miR-29c expression, suggesting that miR-29c activation may contribute to the chemotherapeutic efficiency of cisplatin. The enforced expression of miR-29c enhanced the cisplatin sensitivity of NSCLC cells, while the knocking down of miR-29c led to cisplatin resistance. MiR-29c amplified the therapeutic effects of cisplatin in vivo. Rescue experiments suggested that miR-29c regulates the cisplatin resistance of NSCLS cells by negatively regulating the PI3K/Akt pathway. Overall, our results demonstrated that miR-29c enhances the sensitivity of NSCLC cells to cisplatin by targeting the PI3K/Akt pathway.
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