[LINC01285 promotes proliferation and metastasis of colorectal cancer cells by regulating epithelial-mesenchymal transition].

OBJECTIVE

To clarify the mechanism by which LINC01285 regulates proliferation and migration of colorectal cancer (CRC) cells and the clinical implications.

METHODS

We analyzed the expression of LINC01285 in CRC tissues and normal tissues using data from Starbase public database. We also examined the expression levels of LINC01285 in 70 pairs of CRC and adjacent tissue samples collected from our center and in different CRC cell lines using RT-qPCR, and analyzed the correlation of LINC01285 expression with the clinicopathological parameters and tumor-free survival time of the patients. In CRC cell lines (SW620 and HT-29), the changes in cell proliferation, apoptosis, metastasis and epithelial-mesenchymal transition (EMT) phenotype following LINC01285 knockdown were analyzed using CCK-8 assay, flow cytometry, Transwell assay and Western blotting.

RESULTS

The TCGA-COAD transcriptome sequencing data obtained from the Starbasev3.0 public database revealed a significantly higher expression level of LINC01285 in CRC tissues than in adjacent tissues (=0.00016), which was verified by RT-qPCR results of the clinical samples (=0.0002). In CRC patients, the expression level of LINC01285 was closely correlated with histological differentiation of the tumor (=0.036), T classification (=0.000), lymph node metastasis (=0.001), TNM stage (=0.000), Duke stage (=0.009) and relapse-free survival (=0.0102). In SW620 and HT-29 cells, which expressed significantly higher levels of LINC01285 than normal colorectal mucosal cells ( < 0.001), LINC01285 knockdown significantly inhibited cell proliferation ( < 0.001), increased early apoptosis, late apoptosis and total apoptosis rates ( < 0.05), suppressed cell migration and invasion ( < 0.001), upregulated the expression of E-cadherin ( < 0.001), and downregulated the expression of N-cadherin ( < 0.001).

CONCLUSION

The expression level of LINC01285, which modulates the EMT pathway to regulate the proliferation, apoptosis and metastasis of CRC cells, is closely correlated with the prognosis of CRC patients.