ArticleOncology letters2016
miR-96 induces cisplatin chemoresistance in non-small cell lung cancer cells by downregulating SAMD9.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Effects of AntagomiRs on Different Lung Diseases in Human, Cellular, and Animal Models.International journal of molecular sciences · 2019Pooled it
- Article
- MicroRNAs in lung cancer: their role in tumor progression, biomarkers, diagnostic, prognostic, and therapeutic relevance.Discover oncology · 2025Review
- Transcriptomics driven identification of hub gene miRNA interactions for biomarker and therapeutic target discovery in gynecological cancers.Frontiers in oncology · 2025Article
- Article
- PARP14 correlates with GBM proliferation and poor prognosis by elevating expression of SAMD/SAMD9L.Irish journal of medical science · 2024Article
- The miR-183 Cluster: Biogenesis, Functions, and Cell Communication via Exosomes in Cancer.Cells · 2023Review
- The Small RNA Landscape in NSCLC: Current Therapeutic Applications and Progresses.International journal of molecular sciences · 2023Review
- A perspective to weaponize microRNAs against lung cancer.Non-coding RNA research · 2023Review
- MicroRNA-96-5p is negatively regulating GPC3 in the metastasis of papillary thyroid cancer.SAGE open medicine · 2023Article
- Emerging role of non-coding RNAs in resistance to platinum-based anti-cancer agents in lung cancer.Frontiers in pharmacology · 2023Review
- LIM-domain binding protein 2 was down-regulated by miRNA-96-5p inhibited the proliferation, invasion and metastasis of lung cancer H1299 cells.Clinics (Sao Paulo, Brazil) · 2023Article
- Extracellular Vesicle (EVs) Associated Non-Coding RNAs in Lung Cancer and Therapeutics.International journal of molecular sciences · 2022Review
- Article
- MicroRNA-96: A therapeutic and diagnostic tumor marker.Iranian journal of basic medical sciences · 2022Review
- FOXO3a and Its Regulators in Prostate Cancer.International journal of molecular sciences · 2021Review
- Clinical evolution, genetic landscape and trajectories of clonal hematopoiesis in SAMD9/SAMD9L syndromes.Nature medicine · 2021Article
- AIMP3 inhibits cell growth and metastasis of lung adenocarcinoma through activating a miR-96-5p-AIMP3-p53 axis.Journal of cellular and molecular medicine · 2021Article
- Crosstalk between autophagy and DNA repair systems.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- miR-146b-5p Enhances the Sensitivity of NSCLC to EGFR Tyrosine Kinase Inhibitors by Regulating the IRAK1/NF-κB Pathway.Molecular therapy. Nucleic acids · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin is effective as a single agent or in combination with other drugs for the treatment of non-small cell lung cancer (NSCLC). A concerning clinical challenge with cisplatin-based NSCLC chemotherapy is the intrinsic and acquired chemoresistance to cisplatin. The sterile α motif domain-containing (SAMD9) gene has been reported as a potent tumor suppressor gene that inhibits tumorigenesis and progression of NSCLC. microRNAs (miRNA) have been revealed to play important roles in the regulation of cancer chemoresistance. To the best of our knowledge the present study explored the role of miRNA/SAMD9 signaling in regulating cisplatin chemoresistance in NSCLC for the first time. Out of the several candidate miRNAs predicted to bind the 3'-untranslated region (UTR) of the SAMD9 gene, miRNA-96 (miR-96) demonstrated significant target-sequence-specific inhibition of the SAMD9 3'-UTR luciferase reporter activity in NSCLC cells. In addition, while NSCLC tumor samples exhibited significantly higher expression levels of miR-96 compared with adjacent normal tissues, the expression levels of SAMD9 were significantly lower than those in adjacent normal tissues. miR-96 and SAMD9 were overexpressed and knocked down in the human NSCLC H358 and H23 cell lines and the half maximal inhibitory concentration (IC
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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.