Abstract
BackgroundTongue squamous cell carcinoma (TSCC) is the second most common malignancy in oral carcinoma. lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was regarded as an oncogenic factor in various carcinomas. However, its underlying molecular mechanisms in the development and progression of TSCC have not been well featured till now.MethodsThe expressions of MALAT1, miR-140-5p and p21 (RAC1)-activated kinase 1 (PAK1) mRNA were measured by RT-qPCR assay. The protein level of PAK1 was determined by western blot analysis. Cell viability was detected by Cell Counting Kit-8 assay. Transwell chamber was used to detect cell migratory and invasive capability. Luciferase reporter assay, RNA-binding protein immunoprecipitation (RIP) assay and biotin pull-down assay were applied to evaluate the relationship between MALAT1, miR-140-5p and PAK1. Xenograft experiments were performed to assess the effect and mechanism of MALAT1 in TSCC tumor growth.ResultsThe expression of MALAT1 and p21 (RAC1)-activated kinase 1 (PAK1) was upregulated and microRNA-140-5p (miR-140-5p) expression was downregulated in TSCC tissues and cells. MALAT1 knockdown induced miR-140-5p expression by direct interaction. Moreover, MALAT1 knockdown inhibited proliferation, migration, and invasion by upregulating miR-140-5p expression in TSCC cells. Additionally, PAK1 was identified as a direct target of miR-140-5p. Also, MALAT1 knockdown inhibited PAK1 expression by upregulating miR-140-5p in TSCC cells. Furthermore, miR-140-5p overexpression curbed the proliferation, migration, and invasion of TSCC cells by targeting PAK1. Finally, MALAT1 knockdown inhibited tumor growth by upregulating miR-140-5p and downregulating PAK1 in mouse xenograft models of TSCC.ConclusionMALAT1 contributed to TSCC progression via miR-140-5p-PAK1 regulatory axis, highlighting a potential target for TSCC management.
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