LINC01232 promotes lung squamous cell carcinoma progression through modulating miR-181a-5p/SMAD2 axis

Background: LINC01232 has been implicated in the progression of multiple malignancies. Yet, the function of LINC01232 in the carcinogenesis of lung squamous cell carcinoma (LUSC) remains unclear. This study aims to examine the role LINC01232 plays in LUSC progression.Methods: mRNA and protein levels were assessed using qRT-PCR and western blot, respectively. Cell proliferation was assessed by CCK-8 and colony formation assays. Cell migration and invasion were evaluated by transwell assay. The interactions between LINC01232, miR-181a-5p, and SMAD2 were assessed using luciferase reporter, RNA pull-down, and RNA immuno-precipitation (RIP) assays. The subcellular distribution of LINC01232 was examined by cytosolic/nuclear fractionation assayResults: LINC01232 was upregulated in both LUSC tissues and cell lines. Knockdown of LINC01232 impaired cell prolifera-tion, migration and invasion capability in H1229 and A549 cells, a phenotype that could be reversed by miR-181a-5p silenc-ing. In addition, LINC01232 silencing reduced levels of N-cadherin, Vimentin, and Snail in H1229 and A549 cells, but increased the level of E-cadherin, which can be abrogated by miR-181a-5p inhibitors.Conclusions: In summary, our study demonstrates that LINC01232 expression increases in LUSC tissues and cell lines and promotes LUSC progression by modulating the miR-181a-5p/SMAD2 signaling, providing new potential drug targets for LUSC treatment.

Automated summary

This study found that LINC01232 is upregulated in lung squamous cell carcinoma (LUSC) and promotes LUSC progression by modulating the miR-181a-5p/SMAD2 signaling pathway. These findings provide potential new drug targets for the treatment of LUSC.