Downregulated LINC00628 aggravates the progression of colorectal cancer via inhibiting p57 level.

OBJECTIVE

To uncover the potential function of LINC00628 in influencing the progression of colorectal cancer (CRC) and its underlying mechanism.

PATIENTS AND METHODS

Relative levels of LINC00628 and p57 in CRC tissues and cell lines were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Regulatory effects of LINC00628 and p57 on proliferation, cell cycle, and apoptosis of SW480 and SW620 cells were assessed. Subcellular distribution of LINC00628 in CRC cells was analyzed. Moreover, the interaction between LINC00628 and enhancer of zeste homolog 2 (EZH2) was evaluated by the RNA Binding Protein Immunoprecipitation (RIP) assay.

RESULTS

LINC00628 was downregulated in CRC tissues and cell lines. CRC patients expressing a low level of LINC00628 suffered worse prognosis. The. knockdown of LINC00628 enhanced proliferative ability, prolonged S phase in cell cycle progression, and inhibited apoptosis in SW480 and SW620 cells. LINC00628 was mainly distributed in the nucleus. The RIP assay demonstrated that LINC00628 could bind to EZH2 to upregulate the p57 level. Rescue experiments verified that the overexpression of p57 could reverse regulatory effects of downregulated LINC00628 on proliferative and apoptotic abilities of CRC.

CONCLUSIONS

LINC00628 is downregulated in CRC. It aggravates the progression of CRC by binding to EZH2 to further inhibit the p57 level.