Qi SX, Sun H, Liu H, Yu J, Jiang ZY, Yan P. Role and mechanism of circ-PRKCI in hepatocellular carcinoma. World J Gastroenterol 2019; 25(16): 1964-1974 [PMID: 31086464 DOI: 10.3748/wjg.v25.i16.1964]
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Su-Xia Qi, Jing Yu, Ping Yan, Emergency Department, Qingdao Municipal Hospital (Group), Qingdao 266000, Shandong Province, China
Hui Sun, Department of Clinical Laboratory, Qingdao Municipal Hospital (Group), Qingdao 266000, Shandong Province, China
Hui Liu, Department of Clinical Laboratory, Qingdao Women's and Children's Hospital, Qingdao 266034, Shandong Province, China
Zhi-Yong Jiang, Department of Clinical Laboratory, Qingdao Haici Medical Group, Qingdao 266034, Shandong Province, China
Author contributions: Yan P designed the research; Qi SX wrote the article; Sun H and Liu H performed the research and acquired and analyzed the data; Yu J and Jiang ZY performed the majority of experiments; Qi SX, Sun H and Liu H contributed equally to this work.
Institutional review board statement: This study was reviewed and approved by the Qingdao Municipal Hospital (Group) Ethics Committee.
Conflict-of-interest statement: The authors declare no conflict of interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Received: February 20, 2019 Peer-review started: February 20, 2019 First decision: March 13, 2019 Revised: March 21, 2019 Accepted: March 24, 2019 Article in press: March 25, 2019 Published online: April 28, 2019 Processing time: 64 Days and 16.9 Hours
ARTICLE HIGHLIGHTS
Research background
Digestive system tumors have high morbidity and mortality and account for a large proportion of all tumors. It has been confirmed that circRNAs are important in the occurrence and development of some digestive system tumors, such as gastric cancer, liver cancer, and colon cancer.
Research motivation
Does circ-PRKCI affect the occurrence and development of digestive tract tumors, especially hepatocellular carcinoma?
Research objectives
To investigate the role and molecular mechanism of circ-PRKCI in the progression of hepatocellular carcinoma.
Research methods
This study used quantitative real-time PCR, Western blot, knockdown and overexpression experiments, fluorescence in situ hybridization, survival analysis, and statistical analyses.
Research results
The level of circ-PRKCI was significantly higher in HCC tissues than in adjacent tissues. Circ-PRKCI substantially inhibited cell apoptosis and promoted cell invasion. It was found that circ-PRKCI can act as the sponge of miRNA-545 to reduce the expression of AKT3 protein. Circ-PRKCI target gene E2F7 can reduce liver cancer patients’ survival rate. Circ-PRKCI was positively correlated with the depth of invasion, lymph node metastasis, distant metastasis, and TNM stage.
Research conclusions
Circ-PRKCI is significantly involved in the development of hepatocellular carcinoma.
Research perspectives
This study provides a new research direction and theoretical basis for the treatment of hepatocellular carcinoma.
