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Copyright (c) 2023 Yingmin Mao, Zhe Hu, Yunjian Zeng, Yuqi Zhou, Zili Shi
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.LINC01094 accelerates the metastasis of hepatocellular carcinoma via the miR-26b-3p/MDM4 axis
Corresponding Author(s) : Zili Shi
Cellular and Molecular Biology,
Vol. 69 No. 6: Issue 6
Abstract
To elucidate the role of LINC01094 in accelerating the metastatic potential of hepatocellular carcinoma (HCC) via the miR-26b-3p/MDM4 axis. Differential levels of LINC01094 in clinical samples of HCC and their influence on pathological indicators of recruited HCC patients were detected. Hep3B and SK-HEP-1 cell lines with stable knockdown of LINC01094 were generated by shRNA transfection, followed by detection of migration and invasion by Transwell and wound healing assay. Bioinformatic analysis, dual-luciferase reporter assay and rescue experiments were conducted to assess the interaction between LINC01094 and the miR-26b-3p/MDM4 axis. LINC01094 was upregulated in clinical samples of HCC and its level was linked to the incidences of lymphatic and distant metastasis of HCC patients. Knockdown of LINC01094 weakened migratory and invasive abilities in Hep3B and SK-HEP-1 cells. MiR-26b-3p was the downstream target of LINC01094, which was lowly expressed in HCC tissues and negatively correlated to the LINC01094 level. Moreover, MDM4 was the target gene of miR-26b-3p, which was highly expressed in HCC tissues and negatively correlated to the miR-26b-3p level. Rescue experiments showed that the knockdown of miR-26b-3p could reverse the inhibited metastasis in Hep3B and SK-HEP-1 cells with a stable knockdown of LINC01094. LINC01094 accelerates the metastasis of HCC via the miR-26b-3p/MDM4 axis, which is a potential biomarker and therapeutic target to be utilized in clinical practice.
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