E2F1-Induced lncRNA BAIAP2-AS1 Overexpression Contributes to the Malignant Progression of Hepatocellular Carcinoma via miR-361-3p/SOX4 Axis | Zendy

Yan Yang | Zendy; Hong Ge | Zendy; Deqing Li | Zendy; Aixia Xu | Zendy

Open Access

E2F1-Induced lncRNA BAIAP2-AS1 Overexpression Contributes to the Malignant Progression of Hepatocellular Carcinoma via miR-361-3p/SOX4 Axis

Author(s) -

Yan Yang,

Hong Ge,

Deqing Li,

Aixia Xu

Publication year - 2021

Publication title -

disease markers

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.912

H-Index - 66

eISSN - 1875-8630

pISSN - 0278-0240

DOI - 10.1155/2021/6256369

Subject(s) - sox4 , hepatocellular carcinoma , cancer research , long non coding rna , downregulation and upregulation , competing endogenous rna , metastasis , biology , gene knockdown , biomarker , cell culture , cancer , gene expression , gene , promoter , genetics , biochemistry

Currently, plenty of researches have revealed that long noncoding RNAs (lncRNAs) can act as crucial roles during the progression of various tumors, including hepatocellular carcinoma (HCC). Here, we measured the expression of lncRNA BAIAP2 antisense RNA 1(BAIAP2-AS1) as well as its contribution to the developments of HCC. In this study, the expressions of BAIAP2-AS1 and SOX4 were distinctly upregulated in HCC cells and tissues, and high BAIAP2-AS1 may be a novel biomarker for HCC. E2F1 activated BAIAP2-AS1 expression. The silence of BAIAP2-AS1 inhibited the proliferation and metastasis of HepG2 and PLC5 cells. Assays for relationship verification showed that BAIAP2-AS1 regulated the expression of SOX4 and miR-361-3p. Rescue experiments further confirmed the positive interaction between miR-361-3p and BAIAP2-AS1 as well as between miR-361-3p and SOX4. Overall, BAIAP2-AS1 modulated the miR-361-3p/SOX4 axis to promote the development of HCC. Thus, our study offers a potential therapeutic target for treating HCC.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research