ArticleAmerican journal of translational research2022
LncRNA MALAT1 inhibits the proliferation and invasiveness of laryngeal squamous cell carcinoma Hep-2 cells by modulating miR-362-3p.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- The emerging role of miR-362 in cancer: expression and function across different cancer types.Medical oncology (Northwood, London, England) · 2025Review
- The Role and Function of Non-Coding RNAs in Cholangiocarcinoma Invasiveness.Biomedicines · 2025Review
- The regulation of LRPs by miRNAs in cancer: influencing cancer characteristics and responses to treatment.Cancer cell international · 2025Review
- Inhibition of the long non-coding RNA MALAT1 downregulates MAP2K1, suppressing the progression of hypopharyngeal squamous cell carcinoma.Biomolecules & biomedicine · 2025Article
- Long noncoding RNA MALAT-1: A versatile regulator in cancer progression, metastasis, immunity, and therapeutic resistance.Non-coding RNA research · 2024Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the mechanism of lncRNA MALAT1 (MALAT1) inhibiting the proliferation and invasiveness of laryngeal squamous cell carcinoma (LSCC) Hep-2 cells by modulating miR-362-3p.
methodsWe collected the expression profile of lncRNAs and miRNAs in LSCC downloaded from The Cancer Genome Atlas (TCGA) database as well as LSCC tissue samples and adjacent normal counterparts resected from LSCC patients in Lvliang People's Hospital and First Hospital of Shanxi Medical University between January 2018 and June 2020 for analysis. Human LSCC Hep-2 cells were selected for experiments. The expression of miR-362-3p and MALAT1 was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cells were subsequently transfected to knock out MALAT1, and the growth, metastasis and invasiveness of cells were evaluated by CCK-8 assay, plate clone formation, wound healing, and Transwell invasion assays respectively. The binding of MALAT1 to miR-362-3p was verified by RNA pull-down, RNA binding protein immunoprecipitation (RIP), and dual-luciferase reporter assays.
resultsMALAT1 was highly expressed while miR-362-3p was lowly expressed in both LSCC tissues and cells compared with normal counterparts. MALAT1 knockdown inhibited the viability of Hep-2 cells, reducing the number of plate clone-forming cells as well as the number of migrated and invaded cells. Transfection of miR-362-3p inhibitor into Hep-2 cells treated by si-MALAT1 reversed the inhibition of si-MALAT1 on the proliferation of Hep-2 cells, and promoted cell invasiveness and migration. MALAT1 can sponge miR-362-3p and inhibit its expression.
conclusionsKnockdown of MALAT can inhibit Hep-2 cell proliferation and reduce its invasiveness and migration by modulating miR-362-3p.
Indexed as
Identifiers
35836842PMC9274578W4285613284What OpenQuestion holds
Registered trials
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