ArticleOncoTargets and therapy2020
lncRNA MALAT1 Promotes EMT Process and Cisplatin Resistance of Oral Squamous Cell Carcinoma via PI3K/AKT/m-TOR Signal Pathway.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 53 citations in OpenAlex.
- Non-Coding RNAs in Oral Diseases: From Pathogenesis to Clinical Translation.International journal of molecular sciences · 2026Review
- Experimental Models and Nanotechnology-Based Platforms in Oral Squamous Cell Carcinoma: From Tumor Biology to Translational Applications.Pharmaceutics · 2026Review
- Molecular Mechanisms in Oral Squamous Cell Carcinoma: Integrative Roles of Cancer-Associated Fibroblasts, Immune Microenvironment, and Precision Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Fibronectin Is a Likely Therapeutic Target Shared by Oral and Breast Carcinomas.International journal of molecular sciences · 2026Article
- MALAT1 as a molecular driver of tumor progression, immune evasion, and resistance to therapy.Molecular cancer · 2025Review
- Long non-coding RNAs as therapeutic targets in head and neck squamous cell carcinoma and clinical application.FEBS open bio · 2025Review
- Article
- Identifying ATP-Binding Cassette Member B5 as a New Biomarker for Oral Squamous Cell Carcinoma.Oncology research · 2025Article
- Oral squamous cell carcinoma pharmacological treatment; A long non-coding RNAs (long ncRNAs) story.International journal of molecular and cellular medicine · 2025Review
- Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers.Oncology research · 2025Review
- Review
- Review
- MALAT-1 Is a Key Regulator of Epithelial-Mesenchymal Transition in Cancer: A Potential Therapeutic Target for Metastasis.Cancers · 2024Review
- Novel insights on oral squamous cell carcinoma management using long non-coding RNAs.Oncology research · 2024Review
- Investigating the potential of oncolytic viruses for cancer treatment via MSC delivery.Cell communication and signaling : CCS · 2023Review
- Long Non-Coding RNAs as Emerging Targets in Lung Cancer.Cancers · 2023Review
- Functions and mechanisms of lncRNA MALAT1 in cancer chemotherapy resistance.Biomarker research · 2023Review
- Nutlin-3 suppresses tumorigenesis and progression of oral squamous cell carcinoma and enhances chemosensitivity to cisplatin.Cytotechnology · 2023Article
- Absence of Scaffold Protein Tks4 Disrupts Several Signaling Pathways in Colon Cancer Cells.International journal of molecular sciences · 2023Article
- Long non-coding RNA HCG22 inhibits the proliferation, invasion and migration of oral squamous cell carcinoma cells by downregulating miR-425-5p expression.Experimental and therapeutic medicine · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCisplatin (DDP) is the first-line chemotherapy agent for the treatment of oral squamous cell carcinoma (OSCC). The emergence of DDP resistance leads to diminished drug efficacy and survival benefit. lncRNA MALAT1 has been considered as one of the most important factors in OSCC. It has also been reported to enhance chemo-resistance in other kinds of carcinomas. However, little is known about the role of lncRNA MALAT1 in DDP resistance of OSCC. MATERIALS AND
methodsTwo kinds of human DDP-resistant cell lines (CAL-27R and SCC-9R) were developed from cisplatin-naïve cell lines (CAL-27 and SCC-9, respectively) as in vitro cell models. Cell transfection was performed to overexpress or knockdown MALAT1 in these cells. Mouse xenograft models were also established. The following measurements were performed: cell proliferation, colony formation, wound healing, transwell, and TUNEL assays, as well as Western blot and immunofluorescence staining.
resultsDDP-resistant cells showed higher expression level of MALAT1 compared to cisplatin-naïve cells. The overexpression of MALAT1 in cisplatin-naïve cells enhanced DDP resistance and suppressed apoptosis in OSCC cells. However, the knockdown of MALAT1 in DDP-resistance cells induced apoptotic cell death and restored the sensitivity to DDP. Further analyses suggested that MALAT1 might promote DDP resistance via regulating P-glycoprotein expression, epithelial-mesenchymal transition process, and the activation of PI3K/AKT/m-TOR signaling pathway.
conclusionMALAT1 might be a potential therapeutic target for the treatment of DDP-resistant OSCC.
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