Title:Linc01559 Served as a Potential Oncogene and Promoted Resistance of Hepatocellular Carcinoma to Oxaliplatin by Directly Sponging miR-6783-3p
VOLUME: 21 ISSUE: 2
Author(s):Shunbin Dong, Ying Fu, Kaibo Yang, Xing Zhang, Runchen Miao, Yunxiang Long and Chang Liu*
Affiliation:Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi, Department of Oncology, Liaocheng People's Hospital, Liaocheng, 252000, Shandong Province, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi, Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shaanxi
Keywords:Linc01559, miR-6783-3p, miR-1343-3p, oxaliplatin resistance, nomogram, hepatocellular carcinoma.
Abstract:Background: Oxaliplatin (L-OHP)-based chemotherapy, such as FOLFOX4 (5-fluorouracil, leucovorin,
and L-OHP), improves the prognosis of patients with late-stage Hepatocellular Carcinoma (HCC). However,
the development of resistance to L-OHP leads to the failure of chemotherapy. The aim of this study was to
investigate the role of linc01559 and miR-6783-3p in regulating resistance to L-OHP.
Methods: Quantitative reverse transcription-polymerase chain reaction was used to determine the expression
profile. The Cell Counting Kit-8 test and wound healing assay were also used. Dual-luciferase reporter gene
assay, RNA pull-down assay, and RNA immunoprecipitation were used to evaluate the interaction between
linc01559 and miR-6783-3p.
Result: linc01559 expression was associated with response to FOLFOX4, as well as miR-1343-3p and miR-
6783-3p expression in vivo. A nomogram, including linc01559 and miR-1343-3p, precisely and accurately predicted
the overall survival of patients with HCC. Regarding the in vitro tests, linc01559 showed higher expression
in L-OHP-resistant cell lines, whereas miR-6783-3p was downregulated. Knockdown of linc01559 led to
decreased proliferation and migration ability, and increased expression of miR-6783-3p; however, it did not
influence the expression of miR-1343-3p. We also found that linc01559 directly interacted with miR-6783-3p.
Furthermore, linc01559 and miR-6783-3p regulated the viability of L-OHP-resistant cells following treatment
with L-OHP.
Conclusion: linc01559 promoted the proliferation of HCC by sponging miR-6783-3p. This suggests that
linc01559/miR-6783-3p may be key factors in regulating resistance and response to L-OHP. Moreover, they
may be potential therapeutic targets for improving sensitivity to L-OHP in patients with HCC.
