LncRNA SNHG1 promotes liver cancer development through inhibiting p53 expression via binding to DNMT1.

Objective: This study aims to investigate whether long non-coding RNA (lncRNA) SNHG1 could regulate proliferative and invasive abilities of liver cancer (LC) cells via p53 and DNMT1, so as to regulate the occurrence and progression of LC.
Patients and Methods: SNHG1 expression in LC tissues and paracancerous tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between SNHG1 expression and tumor stage of LC patients was analyzed. The regulatory effects of SNHG1 and p53 on proliferative, invasive capacities and cell cycle were accessed by CCK-8 (cell counting kit-8), transwell assay and flow cytometry, respectively. The binding condition between SNHG1 and DNMT1 was determined by RNA binding protein immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP). Western blot was conducted to determine whether SNHG1 could regulate p53 in LC cells. Finally, rescue experiments were carried out to evaluate whether SNHG1 regulates proliferative and invasive abilities of LC cells through p53.
Results: SNHG1 expression was higher in LC tissues than that of paracancerous tissues. LC patients with stage III-IV presented higher expression level of SNHG1 than those with stage I-II. Similarly, SNHG1 was highly expressed in LC cells than that of normal liver cells. LC cell lines SMMC-7721 and SK-HEP-1 were selected for this study. SNHG1 knockdown inhibited the proliferative and invasive abilities, and arrested the cell cycle in the G0/G1 phase of SMMC-7721 and SK-HEP-1 cells. RIP and ChIP results demonstrated that SNHG1 could bind to DNMT1 and inhibit p53 expression. Overexpression of p53 partially reversed the inhibitory effects of SNHG1 on proliferative and invasive abilities of LC cells.
Conclusions: High expression of SNHG1 could promote proliferative and invasive abilities of LC cells through targeting inhibition of p53 expression by binding to DNMT1.