Roles of lncRNAs Mediating Wnt/β-Catenin Signaling in HCC.

Yating Xu,Zongzong Sun,Yuting He,Wenzhi Guo,Xiao Yu

doi:10.3389/fonc.2022.831366

Abstract

Hepatocellular carcinoma (HCC) is considered the second most deadly cancer worldwide. Due to the absence of early diagnostic markers and effective therapeutic approaches, distant metastasis and increasing recurrence rates are major difficulties in the clinical treatment of HCC. Further understanding of its pathogenesis has become an urgent goal in HCC research. Recently, abnormal expression of long noncoding RNAs (lncRNAs) was identified as a vital regulator involved in the initiation and development of HCC. Activation of the Wnt/β-catenin pathway has been reported to obviously impact cell proliferation, invasion, and migration of HCC. This article reviews specific interactions, significant mechanisms and molecules related to HCC initiation and progression to provide promising strategies for treatment.

Highlights

Liver cancer has become one of most prevalent malignant diseases worldwide, and hepatocellular carcinoma (HCC) accounts for most liver cancer cases [1–3]
On the basis of these findings that LncTCF7 impacts the biological processes of HCC via the TCF7/Wnt/b-catenin axis, it could be a promising therapeutic target to effectively improve the prognosis of HCC patients
The poor prognosis and rapid recurrence of HCC indicate the urgency of these studies and explorations on emerging methods for effective treatment

Summary

Introduction

Liver cancer has become one of most prevalent malignant diseases worldwide, and hepatocellular carcinoma (HCC) accounts for most liver cancer cases [1–3]. Overexpression of lncRNAs positively related to the Wnt/bcatenin signaling pathway plays an indispensable role in the progression of bladder cancer [31–33]. These results indicated that high expression of CRNDE promotes the invasion of HCC cells by inducing upregulation of the Wnt/b‐catenin cascades. LncRNA ASB16-AS1 might sponge miR-1827 to decrease its expression level, resulting in upregulating FZD and triggering Wnt/b-catenin pathway to involve in tumorigenesis of HCC.

Results

Conclusion