ArticleOncology letters2020
MALAT1 knockdown inhibits hypopharyngeal squamous cell carcinoma malignancy by targeting microRNA-194.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Current Advances of Treatments, Therapeutic Targets, Biomarkers, Novel Drugs, and Machine Learning for Hypopharyngeal Squamous Cell Carcinoma.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- LncRNA MALAT1 inhibits the proliferation and invasiveness of laryngeal squamous cell carcinoma Hep-2 cells by modulating miR-362-3p.American journal of translational research · 2022Article
- The Role and Mechanism of MALAT1 Long Non-Coding RNA in the Diagnosis and Treatment of Head and Neck Squamous Cell Carcinoma.OncoTargets and therapy · 2021Review
- Integrative analysis of lncRNA-miRNA-mRNA-associated competing endogenous RNA regulatory network involved in EV71 infection.American journal of translational research · 2021Article
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
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in the oncogenesis and progression of various types of cancer. However, the function of MALAT1 in hypopharyngeal squamous cell carcinoma (HSCC) is not completely understood. In the present study, MALAT1 expression levels were determined using reverse transcription-quantitative PCR, and Cell Counting Kit-8, Transwell and flow cytometry assays were performed to investigate the biological functions of HSCC cells. The results indicated that MALAT1 was upregulated in HSCC. MALAT1 knockdown suppressed HSCC cell proliferation, migration and invasion, and promoted apoptosis compared with the control group. Additionally, microRNA (miR)-194 was identified as a target of MALAT1 and was expressed at low levels in HSCC tissues compared with adjacent non-tumor tissues. A miR-194 agomir inhibited malignant cell behaviors, including cell proliferation, migration and invasion, whereas miR-194 antagomir promoted malignant behaviors compared with the corresponding control groups. In addition, the results suggested that MALAT1 knockdown inhibited the malignant behaviors of HSCC cells by binding miR-194. miR-194 inhibition partially reversed the MALAT1 knockdown-induced inhibitory effects on HSCC cells. Furthermore, MALAT1 knockdown combined with miR194 mimics resulted in the lowest tumor volume among all tested groups
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