Wang, Qianrong, Han, Anna, Chen, Liyan, Sun, Jie, Lin, Zhenhua, Zhang, Xianglan, and Ren, Xiangshan
Qianrong Wang,1,* Anna Han,1,* Liyan Chen,1,2 Jie Sun,1 Zhenhua Lin,1,2 Xianglan Zhang,3,4 Xiangshan Ren1,21Department of Pathology and Cancer Research Center, Yanbian University Medical College, Yanji 133002, People’s Republic of China; 2Key Laboratory of the Science and Technology Department of Jilin Province, Yanji 133002, People’s Republic of China; 3Department of Pathology, Yanbian University Hospital, Yanji City, Jilin Province, People’s Republic of China; 4Oral Cancer Research Institute, Yonsei University College of Dentistry, Seoul, KoreaCorrespondence: Xiangshan RenDepartment of Pathology & Cancer Research Center, Yanbian University Medical College, No. 977, Gongyuan Road, Yanji City 133002, People’s Republic of ChinaEmail renxsh@ybu.edu.cn*These authors contributed equally to this workBackground: Gastric cancer (GC) is a major leading cause of cancer mortality worldwide. Polyadenylate (poly(A))-binding protein (PABP)-interacting protein 1 (Paip1) is a key regulator in the initiation of translation; however, its role in GC remains to be investigated.Purpose: The purpose of this study is to determine Paip1 expression levels and investigate its underlying molecular mechanism in GC.Patients and methods: In the present study, a total of 90 GC samples and 90 adjacent noncancerous tissues were used to examine the expression of Paip1. In order to gain a deep insight into the molecular mechanism of Paip1 in GC, the Paip1 siRNA sequences were transfected into GC cell lines (MGC-803 and SGC-7901), respectively. Meanwhile, Paip1 plasmid was used to mediate overexpression of Paip1. Cell proliferation were examined via colony formation assay, EdU assay and flow cytometry assay. Cell metastasis were discovered via wound healing assay and Transwell assays. In addition, key EMT makers were detected by Western blotting assay.Results: In this study, Paip1 expression was observed to be upregulated in GC and was associated with shorter overall survival. Knockdown of Paip1 inhibited cell proliferation, migration and caused cell cycle arrest in GC cells, whereas its overexpression reversed these effects. Another mechanistic study showed that Paip1 overexpression promoted EMT progression and regulated its targets expression.Conclusion: High expression of Paip1 plays a significant role in the progression of GC and may be a potential biomarker of poor prognosis as well as a therapeutic target.Keywords: Paip1, metastasis, proliferation, gastric cancer, prognostic marker