LncRNA : A Promising Therapeutic Target for Colorectal Cancer by Regulating -Mediated Cell Proliferation, Invasion and Apoptosis.

BACKGROUND

Long non-coding RNA (lncRNA) zinc finger protein 667-antisense RNA 1 () is closely related to the advancement of a variety of cancers, but its functional role in colorectal cancer remains unclear. This study was designed to explore the function and molecular mechanisms of lncRNA in colorectal cancer.

METHODS

Reverse transcriptase real-time quantitative polymerase chain reaction (RT-qPCR) was used for the detection of and proline-rich nuclear receptor co-activator protein 2 () expression level. Cell counting kit-8 (CCK-8), 5-Ethynyl-2'- deoxyuridine (EdU), and colony formation assays were conducted to assess cell proliferation; flow cytometry and transwell invasion assay were performed separately to measure cell apoptosis and invasion. RNA immunoprecipitation (RIP) assay was utilized to analyze the relationship between and . Western blot was to test the PNRC2 protein expression. The role of in the advancement of colorectal cancer was evaluated by tumor xenograft assay.

RESULTS

LncRNA and were both decreased in colorectal cancer tissue samples and cells ( < 0.05). overexpression remarkably restrained proliferation and invasion in HCT-116 and LOVO cells, but enhanced cell apoptosis ( < 0.0001). Moreover, directly targeted , and positively regulated its expression. The influence of overexpression on invasion, apoptosis, and proliferation was suppressed by knockdown in HCT-116 and LOVO cells. Additionally, overexpression markedly inhibited tumor growth via upregulation of in mice ( < 0.05).

CONCLUSION

LncRNA expressed low in colorectal cancer. LncRNA repressed proliferation and invasion, and enhanced apoptosis of colorectal cancer cells by targeting .