Downregulation of RECQL4 inhibits gastric cancer cell proliferation and induces cell cycle arrest at G0/G1 phase

Background: The RECQ helicases are a family of DNA repair enzymes that unwind double-stranded nucleic acids and have a central role in maintaining genomic integrity. RECQL4 is a unique member of RecQ helicases family. Although it has been reported to participate in human cancer progression, the role of RECQL4 in gastric cancer (GC) remains unclear. Aims: In this study, we aimed to investigate the function of RECQL4 in GC. Methods: The expression of RECQL4 gene was analyzed by the Oncomine database and GC samples. Overall survival (OS) was performed using Kaplan-Meier plotter online analysis. qRT-PCR, Western blot, MTT assay, clonogenic assay, and flow cytometry were used to analyze the function of RECQL4 in GC. Results: In this study, we found that expression of RECQL4 gene was higher in GC tissues than in the normal tissues by Oncomine database mining and affected patients' OS as analyzed by the Kaplan-Meier plotter online database. RECQL4 was overexpressed in GC samples. Knockdown of RECQL4 significantly suppressed proliferation and colony formation abilities of AGS and SGC-7901 cells. Moreover, cell cycle analysis showed that inhibition of RECQL4 induced cell cycle arrested in G0/G1 phase in AGS and SGC-7901 cells. RECQL4 depletion impaired replication factor loading onto chromatin at the start of S phase. Conclusion: Our study indicates that downregulation of RECQL4 may inhibit GC cell proliferation and induce cell cycle arrest at G0/G1 phase. RECQL4 plays an important role in GC tumorigenesis and may serve as a potential therapeutic target for GC.