ArticleOncology letters2018
Increased MALAT1 expression contributes to cisplatin resistance in non-small cell lung cancer.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- Functional role of long non-coding RNA MALAT1 and HOTAIR in lung cancer.Non-coding RNA research · 2026Review
- Critical Assessment of a Structure-Based Pipeline for Targeting the Long Noncoding RNA MALAT1.Journal of chemical information and modeling · 2026Article
- Boolean-network simplification and rule fitting to unravel chemotherapy resistance in non-small cell lung cancer.PloS one · 2026Article
- Harnessing miR-145 in NSCLC: mechanistic roles, diagnostic-prognostic utility, and therapeutic potential.Cancer cell international · 2025Review
- LncRNA-Mediated miR-145 Sponging Drives FN1 and CCND1 Expression: Prognostic and Therapeutic Targets in NSCLC.Biomolecules · 2025Article
- Targeting NSCLC drug resistance: Systems biology insights into the MALAT1/miR-145-5p axis and Wip1 in regulating ferroptosis and apoptosis.Journal of the Royal Society, Interface · 2025Article
- Non-Viral RNA Therapies for Non-Small Cell Lung Cancer and Their Corresponding Clinical Trials.Molecular pharmaceutics · 2025Review
- A dynamic Boolean network reveals that the BMI1 and MALAT1 axis is associated with drug resistance by limiting miR-145-5p in non-small cell lung cancer.Non-coding RNA research · 2024Article
- Article
- Let-7c-5p Represses Cisplatin Resistance of Lung Adenocarcinoma Cells by Targeting CDC25A.Applied biochemistry and biotechnology · 2023Article
- Article
- Contribution of MicroRNAs in Chemoresistance to Cisplatin in the Top Five Deadliest Cancer: An Updated Review.Frontiers in pharmacology · 2022Review
- Focus on long non-coding RNA MALAT1: Insights into acute and chronic lung diseases.Frontiers in genetics · 2022Review
- Current research advances in microRNA-mediated regulation of Krüppel-like factor 4 in cancer: a narrative review.Annals of translational medicine · 2021Review
- Jorunnamycin A Suppresses Stem-Like Phenotypes and Sensitizes Cisplatin-Induced Apoptosis in Cancer Stem-Like Cell-Enriched Spheroids of Human Lung Cancer Cells.Marine drugs · 2021Article
- Novel Insights IntoFrontiers in oncology · 2021Review
- The Emerging Roles of Long Noncoding RNAs as Hallmarks of Lung Cancer.Frontiers in oncology · 2021Review
- Circular RNA hsa_circ_0096157 contributes to cisplatin resistance by proliferation, cell cycle progression, and suppressing apoptosis of non-small-cell lung carcinoma cells.Molecular and cellular biochemistry · 2020Article
- The physiological function of long-noncoding RNAs.Non-coding RNA research · 2020Review
- Recent Discoveries on the Involvement of Krüppel-Like Factor 4 in the Most Common Cancer Types.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cisplatin-based chemotherapy is commonly used for the clinical treatment of patients with non-small cell lung cancer (NSCLC). However, the anti-tumor efficacy of cisplatin is limited by poor clinical response and the development of chemoresistance. At present, the underlying mechanism for cisplatin resistance remains unclear. In the present study, it was identified that metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA that has been demonstrated to function as an oncogene, was increased in tumor tissues from patients with cisplatin-resistant NSCLC. In addition, the MALAT1 level was increased in A549rCDDP cells compared with the parental A549 cells. Silencing of MALAT1 sensitized A549rCDDP cells to cisplatin treatment, while overexpression of MALAT1 in A549 cells decreased their sensitivity towards cisplatin. Through analysis of the gene expression in patient samples, a decrease in miR-145 and an increase in Kruppel-like factor 4 (KLF4) in tumor tissues compared with adjacent normal tissues was observed. A negative association between MALAT1 and miR-145 was also identified in A549 cells and A549rCDDP cells. Furthermore, reverse transcription quantitative polymerase chain reaction and western blotting identified that KLF4 was positively and negatively regulated by MALAT1 and miR-145, respectively. The direct regulatory association between MALAT1 and miR-145 and the target gene KLF4 was additionally confirmed using a luciferase reporter assay. Knockdown of MALAT1 reversed cisplatin resistance in A549rCDDP cells. Taken together, these data indicated that MALAT1 decreased the sensitivity of NSCLC to cisplatin via the regulation of miR-145 and KLF4.
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Registered trials
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