ArticleCancer management and research2019
Downregulated MCOLN1 Attenuates The Progression Of Non-Small-Cell Lung Cancer By Inhibiting Lysosome-Autophagy.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- Inhibition of lysosomal TRPML1 channel eliminates breast cancer stem cells by triggering ferroptosis.Cell death discovery · 2024Article
- Metabolomic Approach to Identify Potential Biomarkers in KRAS-Mutant Pancreatic Cancer Cells.Biomedicines · 2024Article
- Autophagy-related gene model as a novel risk factor for schizophrenia.Translational psychiatry · 2024Article
- Aza Analogs of the TRPML1 Inhibitor Estradiol Methyl Ether (EDME).Molecules (Basel, Switzerland) · 2023Article
- Modulation of Lysosomal ClCells · 2023Article
- Transient receptor potential channels as predictive marker and potential indicator of chemoresistance in colon cancer.Oncology research · 2023Article
- Coexpression of TRPML1 and TRPML2 Mucolipin Channels Affects the Survival of Glioblastoma Patients.International journal of molecular sciences · 2022Article
- Review
- p53 mitigates the effects of oncogenic HRAS in urothelial cells via the repression ofiScience · 2021Article
- Deciphering the Role of CaCancers · 2021Review
- Endolysosomal TRPMLs in Cancer.Biomolecules · 2021Review
- Knock-Down of Mucolipin 1 Channel Promotes Tumor Progression and Invasion in Human Glioblastoma Cell Lines.Frontiers in oncology · 2021Article
- TRPML1-Emerging Roles in Cancer.Cells · 2020Article
- Suppression of autophagy facilitates hydrogen gas-mediated lung cancer cell apoptosis.Oncology letters · 2020Article
- Prohibitin 2/PHB2 in Parkin-Mediated Mitophagy: A Potential Therapeutic Target for Non-Small Cell Lung Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Emerging Role of Mucolipins TRPML Channels in Cancer.Frontiers in oncology · 2020Article
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
objectivesAutophagy plays various roles in non-small-cell lung cancer (NSCLC). MCOLN1, a reactive oxygen species sensor, can regulate autophagy via lysosomal Ca(2+); however, the role of MCOLN1 in NSCLC is largely unknown. This study aimed to explore the effects of MCOLN1 on proliferation, invasion and migration in NSCLC and the underling mechanisms. MATERIALS AND
methodsThe tissues of NSCLC patients were collected, then MCOLN1 expression in tumor and adjacent tissues was measured and its relationship with pathological staging was analyzed. The Cell Counting Kit-8 (CCK-8) assay, wound healing assay and transwell migration assay were used to evaluate the proliferation, migration and invasion ability, respectively. Live-cell imaging and transmission electron microscopy (TEM) were used to observe autophagic flux and autolysosomes.
resultsIt was found that MCOLN1 expression was significantly decreased in human NSCLC tissues compared with normal lung tissues while more MCOLN1 in stage III-IV was shown than stage I-II, indicating that MCOLN1 increased along with the progression of NSCLC. Furthermore, CCK-8 assay, wound healing assay and transwell migration assay confirmed that the inhibition of MCOLN1 suppressed NSCLC cells proliferation migration and invasion. Overexpression of MCOLN1 promoted autophagy in A549 and H1299 cells with increased LC3-II/I, lamp1 expression and autolysosomes as well as autophagic flux shown by live-cell imaging and TEM.
conclusionOur study shows that downregulated MCOLN1 reduced lysosome-autophagy activity contributing to inhibited tumor progression, which reveals a novel role of MCOLN1 in NSCLC, and targeting MCOLN1 may be a therapeutic potential for NSCLC.
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