ArticleDrug design, development and therapy2015
Autophagy facilitates lung adenocarcinoma resistance to cisplatin treatment by activation of AMPK/mTOR signaling pathway.
Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 81 citations in OpenAlex.
- Radiotherapy resistance in glioblastoma: Mechanistic insights and novel therapeutic approaches (Review).International journal of oncology · 2026Review
- ATG4B is required for mTORC1-mediated anabolic activity and is associated with clinical outcomes in non-small cell lung cancer.FEBS open bio · 2026Article
- Review
- Review
- Natural Compounds and their Nano-formulations in Combating Autophagy-mediated Drug Resistance in Human Cancers.Current topics in medicinal chemistry · 2025Review
- Resistance to the platinum‑based chemotherapeutic drugs in oral cancer: Focus on the role of p22phox (Review).Biomedical reports · 2024Review
- O-GlcNAcylation promotes malignancy and cisplatin resistance of lung cancer by stabilising NRF2.Clinical and translational medicine · 2024Article
- Sesamol-mediated targeting of EPHA2 sensitises cervical cancer for cisplatin treatment by regulating mitochondrial dynamics, autophagy, and mitophagy.Molecular biology reports · 2024Article
- Chromatin remodeling-driven autophagy activation induces cisplatin resistance in oral squamous cell carcinoma.Cell death & disease · 2024Article
- CACNA1H restrains chemotherapy resistance in ovarian clear cell carcinoma cells by repressing autophagy.Molecular genetics and genomics : MGG · 2024Article
- CUR5g, a novel autophagy inhibitor, exhibits potent synergistic anticancer effects with cisplatin against non-small-cell lung cancer.Cell death discovery · 2022Article
- Modulating p-AMPK/mTOR Pathway of Mitochondrial Dysfunction Caused by MTERF1 Abnormal Expression in Colorectal Cancer Cells.International journal of molecular sciences · 2022Article
- Ad-VT enhances the sensitivity of chemotherapy-resistant lung adenocarcinoma cells to gemcitabine and paclitaxel in vitro and in vivo.Investigational new drugs · 2022Article
- Autophagy-related signaling pathways in non-small cell lung cancer.Molecular and cellular biochemistry · 2022Review
- Recent advances of tanshinone in regulating autophagy for medicinal research.Frontiers in pharmacology · 2022Review
- Autophagy Inhibition Enhances the Anti-Tumor Activity of Methylseleninic Acid in Cisplatin-Resistance Human Lung Adenocarcinoma Cells.Frontiers in pharmacology · 2022Article
- LOC100996425 acts as a promoter in prostate cancer by mediating hepatocyte nuclear factor 4A and the AMPK/mTOR pathway.Journal of cellular and molecular medicine · 2021Article
- Cisplatin-induced hydroxyl radicals mediate pro-survival autophagy in human lung cancer H460 cells.Biological research · 2021Article
- Mammalian/mechanistic target of rapamycin (mTOR) complexes in neurodegeneration.Molecular neurodegeneration · 2021Review
- The miR-136-5p/ROCK1 axis suppresses invasion and migration, and enhances cisplatin sensitivity in head and neck cancer cells.Experimental and therapeutic medicine · 2021Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to cisplatin-based therapy is a major challenge in the control of lung cancer progression. However, the underlying mechanisms remain largely unclear. Autophagy is closely associated with resistance to lung cancer therapy, but the function of autophagy in cisplatin treatment is still controversial. Here, we investigated whether autophagy was involved in lung adenocarcinoma resistance to cisplatin and further elucidated the underlying molecular mechanisms. Cisplatin-refractory lung adenocarcinoma cells increased autophagic vacuole formation detected by monodansylcadaverine staining. When exposed to cisplatin, lung adeno-carcinoma cells demonstrated increased levels of autophagy detected by MAP1A/1B LC3B and mammalian homologue of yeast Atg6 (Beclin-1) expression using Western blot analysis. Activation of cisplatin-induced autophagic flux was increased by using chloroquine (CQ), which can accumulate LC3B-II protein and increase punctate distribution of LC3B localization. The combination of cisplatin with CQ was more potent than cisplatin alone in inhibiting lung adenocarcinoma cell growth, which also increased cisplatin-induced apoptosis. Compared to cisplatin treatment alone, the combination of cisplatin and CQ decreased p-AMPK and increased p-mTOR protein expressions, in addition, the AMPK inhibitor Compound C plus cisplatin downregulated p-AMPK and upregulated p-mTOR as well as depressed LC3B cleavage. These findings demonstrate that activation of autophagy is a hallmark of cisplatin exposure in human lung adenocarcinoma cells, and that there is a cisplatin-induced autophagic response via activation of the AMPK/mTOR signaling pathway. We speculate that autophagy can be used as a novel therapeutic target to overcome cisplatin-resistant lung adenocarcinoma.
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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.