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 .