ArticleInternational journal of biological sciences2023
The mitochondrial protein YME1 Like 1 is important for non-small cell lung cancer cell growth.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
- YME1L1 degradation by TRIM21 inhibits bladder cancer proliferation, metastasis, and mitochondrial function.Oncogene · 2026Article
- FSTL4 interaction with Gαi proteins activates the Akt-mTOR pathway to drive malignant phenotypes in non-small cell lung cancer.Cell communication and signaling : CCS · 2026Article
- YY1-mediated NDUFA9 upregulation promotes NSCLC cell growth through mitochondrial and Akt-mTOR pathway modulation.Cell death & disease · 2026Article
- Exploratory identification of lycorine as a potential inhibitor of the ACP2/YME1L1 prognostic axis in esophageal squamous cell carcinoma: a multi-omics and computational hypothesis.Molecular genetics and genomics : MGG · 2026Article
- Molecular mechanisms of mitochondrial AAA+ proteases.The Journal of biological chemistry · 2026Review
- Review
- MRPL17 is a critical regulator of mitochondrial function and a novel therapeutic target in non-small cell lung cancer.Cell death & disease · 2025Article
- Development of a Dual Gene-Targeted Multi-Sirna with Branched Structure and Its Role in the Therapy of Liver Cancer.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Exploring mitochondrial ribosomal protein S12 as a novel target for non-small cell lung cancer.NPJ precision oncology · 2025Article
- MZT2B promotes malignant phenotypes in NSCLC cells by enhancing mitochondrial function and COX5B expression.Cell death & disease · 2025Article
- Mechanical control of histone serotonylation initiates neural crest migrationbioRxiv : the preprint server for biology · 2025Article
- NADH:ubiquinone oxidoreductase core subunit S8 expression and functional significance in non-small cell lung cancer.Cell death & disease · 2025Article
- TIMM23 overexpression drives NSCLC cell growth and survival by enhancing mitochondrial function.Cell death & disease · 2025Article
- Mitochondrial carrier homolog 2 is important for mitochondrial functionality and non-small cell lung cancer cell growth.Cell death & disease · 2025Article
- The expression and functional role of proline-rich 15 in non-small cell lung cancer.Cell death & disease · 2025Article
- Elevated origin recognition complex subunit 6 expression promotes non-small cell lung cancer cell growth.Cell death & disease · 2024Article
- Targeting POLRMT by IMT1 inhibits colorectal cancer cell growth.Cell death & disease · 2024Article
- Expression and functional implications of YME1L in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Increased expression of REG3A promotes tumorigenic behavior in triple negative breast cancer cells.Breast cancer research : BCR · 2024Article
- Targeting the mitochondrial protein YME1L to inhibit osteosarcoma cell growth in vitro and in vivo.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
8 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression and biological function of the mitochondrial inner membrane protease YME1L (YME1 Like 1 ATPase) in NSCLC are tested here. Bioinformatical analyses and results from local human tissues show that YME1L expression is elevated in NSCLC tissues. YME1L upregulation was observed in primary and immortalized NSCLC cells. In NSCLC cells, shRNA-mediated silence of YME1L or dCas9/sgRNA-induced knockout (KO) of YME1L robustly suppressed cell growth and migration, and provoking apoptosis. YME1L shRNA/KO resulted in mitochondrial dysfunctions in NSCLC cells, leading to mitochondrial depolarization, ROS accumulation and ATP depletion. Conversely, ectopic YME1L overexpression augmented NSCLC cell proliferation and motility. Akt-S6K1 phosphorylation was reduced after YME1L shRNA/KO in primary NSCLC cells, but augmented after YME1L overexpression. Importantly, YME1L KO-caused anti-NSCLC cell activity was attenuated by a constitutively-activate Akt1 (S473D) construct.
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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.