AI Article Synopsis
- The study focuses on the role of long non-coding RNA DDX11-AS1 in the progression of hepatocellular carcinoma (HCC), highlighting its significance as a potential therapeutic target.
- DDX11-AS1 expression is increased in HCC tissues, and silencing it leads to reduced cell proliferation, migration, invasion, and increased apoptosis, both in vitro and in animal models.
- The research also indicates that DDX11-AS1 interacts with miR-195-5p and MACC1, suggesting a regulatory network that influences HCC progression, emphasizing the importance of targeting this pathway for treatment strategies.
Article Abstract
Introduction And Aim: Long non-coding RNA (lncRNA) has been shown to be a vital regulator of cancer progression, including hepatocellular carcinoma (HCC). However, the role of DEAD/H box protein 11 antisense RNA 1 (DDX11-AS1) in HCC remains to be further studied.
Material And Methods: The expression levels of DDX11-AS1, miR-195-5p and metastasis-associated in colon cancer-1 (MACC1) were determined by quantitative real-time PCR (qRT-PCR). Cell counting kit-8 (CCK-8), transwell and apoptosis determination assays were used to evaluate cell proliferation, migration, invasion and apoptosis, respectively. Mice xenograft models were constructed to verify the effect of DDX11-AS1 on HCC tumor growth in vivo. Furthermore, lactate production, glucose consumption, ATP level and glucose uptake were detected to assess cell glucose metabolism. The interactions among DDX11-AS1, miR-195-5p and MACC1 were verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Moreover, western blot (WB) analysis was performed to evaluate the protein levels.
Results: DDX11-AS1 was upregulated in HCC tissues and cells, and its silencing could inhibit HCC cell proliferation, migration, invasion and glucose metabolism, and promote apoptosis in vitro. Also, DDX11-AS1 knockdown reduced HCC tumor growth in vivo. Besides, DDX11-AS1 could interact with miR-195-5p, and miR-195-5p inhibitor reversed the inhibitory effect of silenced DDX11-AS1 on HCC cell progression. In addition, MACC1 was a target of miR-195-5p, and its overexpression reversed the suppression effect of miR-195-5p on HCC cell progression.
Conclusion: Our data revealed that DDX11-AS1 could act as an oncogenic regulator in HCC, providing a potential therapeutic target for HCC treatment.
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| http://dx.doi.org/10.1016/j.aohep.2020.09.003 | DOI Listing |
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