Published online Sep 21, 2019. doi: 10.3748/wjg.v25.i35.5283
Peer-review started: April 26, 2019
First decision: May 24, 2019
Revised: June 7, 2019
Accepted: July 19, 2019
Article in press: May 24, 2019
Published online: September 21, 2019
Processing time: 148 Days and 22.5 Hours
Long non-coding RNA highly up-regulated in liver cancer (lncRNA HULC) is highly expressed in hepatocellular carcinoma (HCC), and involved in the development and regulation of tumorigenesis. The relationship between HULC and exosomes has not yet been reported. Studying the mechanism of exosome secretion is helpful to reveal the pathogenesis of HCC.
Although HULC has long been known to play important roles in HCC, its function and regulatory mechanism are unclear. Since exosomes participate in the progression of HCC, they have been actively studied. We are interested in exploring whether HULC regulates exosome secretion and is involved in the occurrence and development of hepatocellular carcinoma. This study will provide novel insights into the mechanism of action of HULC in HCC.
The main objective of the study was to explore the molecular mechanism of HULC to regulate exosome secretion and and provide novel insights into the mechanism of action of HULC in HCC.
We collected samples from serum and tissues of 30 patients with HCC. We measured HULC expression in the serum exosomes and liver cancer tissues of patients, and compared the data to those obtained from controls. We further explored the effect of HULC upregulation in HCC cell lines and studied the relationship between HULC and other RNAs using qPCR and dual-luciferase reporter assays. NTA was used to detect the quantity of exosomes.
HULC expression in serum exosomes of patients with HCC was higher than that in serum exosomes of healthy controls, and HULC levels were higher in liver cancer tissues than in adjacent tissues. The expression of HULC in serum exosomes and liver cancer tissues correlated with the tumor-node-metastasis (TNM) classification and HULC expression in tissues correlated with that in serum exosomes. HULC promoted HCC cell growth and invasion and repressed apoptosis. Additionly, it also facilitated the secretion of exosomes from HCC cells. Moreover, qPCR assays show that HULC repressed microRNA-372-3p (miR-372-3p) expression. We also identified Rab11a as a downstream target of miR-372-3p. Dual-luciferase reporter assays suggest that miR-372-3p could directly bind both HULC and Rab11a.
HULC regulates Rab11a to promote secretion of exosomes by competitive miR-372-3p sharing, and this finding provides new insights into the molecular mechanism to regulate the secretion of exosomes from HCC cells.
We aim to further explore the potential of serum exosome HULC as a sensitive preoperative marker for HCC and the role of HULC in the staging and prognosis evaluation of HCC.