Expression of miR-221 and miR-18a in patients with hepatocellular carcinoma and its clinical significance
- PMID: 36945332
- PMCID: PMC9942768
- DOI: 10.14216/kjco.22003
Expression of miR-221 and miR-18a in patients with hepatocellular carcinoma and its clinical significance
Abstract
Purpose: Recently, microRNA (miRNA) has been evaluated to provide a new diagnostic and therapeutic modality hepatocellular carcinoma (HCC) and other tumors. They are small non-coding RNA molecules that function as transcriptional and post-transcriptional regulators of gene expression by silencing target genes. The aim of this study was to evaluate the clinical significance of microRNA-18a, 221 (miR-18a, miR-221) expression in HCC formalin-fixed paraffin-embedded (FFPE) tissue.
Methods: miR-18a and miR-221 expressions were assessed by reverse transcription and real-time quantitative reverse transcription polymerase chain reaction in 50 pairs of FFPE HCC and the adjacent noncancerous liver tissues. And we evaluated the expression level in HCC tissues as compared with their adjacent noncancerous counterparts. And the relationship between miR-18a, miR-221 level and clinicopathological data and survival rates were analyzed.
Results: miR-221 and miR-18a were overexpressed in HCC tissue as compared with their adjacent noncancerous liver tissue (P<0.001). miR-221 expression was found to be correlated with larger tumor size (P=0.048). miR-18a expression was correlated with modified Union for International Cancer Control stage (P=0.05). The overall survival (P=0.02) of HCC patients with high miR-221 expression was significantly poorer compared to those patients with low expression. Multivariate analyses demonstrated that miR-221 may be a poor prognostic factor of HCC patients.
Conclusion: High expression of miR-221 in FFPE tissues could provide significance for prognosis of HCC patients. Although, miR-18a expression was significantly upregulated in HCC tissues, they are not correlated with prognosis. Further large prospective studies are needed to determine their clinical significance.
Keywords: Hepatocellular carcinoma; MicroRNA; miR-18a; miR-221.
Copyright © 2022 Korean Society of Surgical Oncology.
Conflict of interest statement
CONFLICT OF INTEREST Hae Il Jung is an editorial board members of the journal but was not involved in the peer reviewer selection, evaluation, or decision process of this article. No other potential conflicts of interest relevant to this article were reported.
Figures
Similar articles
-
Good or not good: Role of miR-18a in cancer biology.Rep Pract Oncol Radiother. 2020 Sep-Oct;25(5):808-819. doi: 10.1016/j.rpor.2020.07.006. Epub 2020 Aug 12. Rep Pract Oncol Radiother. 2020. PMID: 32884453 Free PMC article. Review.
-
Correlation between expression levels of lncRNA UCA1 and miR-18a with prognosis of hepatocellular cancer.Eur Rev Med Pharmacol Sci. 2020 Apr;24(7):3586-3591. doi: 10.26355/eurrev_202004_20820. Eur Rev Med Pharmacol Sci. 2020. PMID: 32329833
-
MicroRNA-18a promotes hepatocellular carcinoma proliferation, migration, and invasion by targeting Bcl2L10.Onco Targets Ther. 2018 Nov 9;11:7919-7934. doi: 10.2147/OTT.S180971. eCollection 2018. Onco Targets Ther. 2018. PMID: 30519035 Free PMC article.
-
Relevance of microRNA-18a and microRNA-199a-5p to hepatocellular carcinoma recurrence after living donor liver transplantation.Liver Transpl. 2016 May;22(5):665-76. doi: 10.1002/lt.24400. Liver Transpl. 2016. PMID: 26783726
-
MicroRNA-18a prevents estrogen receptor-alpha expression, promoting proliferation of hepatocellular carcinoma cells.Gastroenterology. 2009 Feb;136(2):683-93. doi: 10.1053/j.gastro.2008.10.029. Epub 2008 Nov 1. Gastroenterology. 2009. PMID: 19027010
References
-
- Karakatsanis A, Papaconstantinou I, Gazouli M, Lyberopoulou A, Polymeneas G, Voros D. Expression of microRNAs, miR-21, miR-31, miR-122, miR-145, miR-146a, miR-200c, miR-221, miR-222, and miR-223 in patients with hepatocellular carcinoma or intrahepatic cholangiocarcinoma and its prognostic significance. Mol Carcinog. 2013;52:297–303. - PubMed
LinkOut - more resources
Full Text Sources