Long noncoding RNA (LncRNA) is closely associated with the development of colorectal cancer (CRC). The chip data and clinical information of GSE104364 and GSE151021 were downloaded by GEOquery. Limma and Kaplan-Meier analysis were performed. Lnc-S100B-2 was obtained, and high expression of Lnc-S100B-2 was predicted to be associated with a lower survival rate. Online software was adopted to predict downstream regulatory genes, and miR-331-3p and Mixed Lineage Leukemia Translocated to 10 (MLLT10) were screened and verified. After silencing Lnc-S100B-2 and MLLT10, the proliferative activity of CRC cells decreased, and the apoptosis rate increased. At the gene and protein levels, the expressions of PCNA, Ki67, and Bcl-2 were decreased in the sh-Lnc-S100B-2 group, sh-MLLT10 group, and sh-Lnc-S100B-2 + sh-MLLT10 group, while the expressions of cleaved caspase 3, caspase 9, and Bax were increased. In vivo, the volume and mass of the tumor decreased in the sh-Lnc-S100B-2 + sh-MLLT10 group. Proliferation and apoptosis-related index (PCNA, Ki67, cleaved caspase 3, caspase 9, Bax, and Bcl-2) expression level was also altered. Meanwhile, the infiltration of immune cells (CD3 (-), CD16 (+), and CD11b (+) cells) decreased. The expressions of epithelial-mesenchymal transformation (EMT) related indicators (E-cadherin, N-cadherin, Vimentin, β-catenin, Snail, and Slug) were changed. E-cadherin and β-catenin were increased in the sh-Lnc-S100B-2 + sh-MLLT10 group, while N-cadherin, vimentin, snail, and slug were decreased. In conclusion, our study found that the expression of Lnc-S100B-2 was dysregulated in CRC. Lnc-S100B-2 could affect cell apoptosis and the microenvironment of CRC through regulating MLLT10.
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