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Published on: April 25, 2018
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Long noncoding RNA RHPN1-AS1 promotes hepatocellular carcinoma progression under hypoxia through interaction with
Qin Peng1,2, Yu-Ting Cai1,2, Qi Ding1,2
1Ward II, Department of Gastrointestinal Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, No.107 Huanhu East Road, Shushan District, Hefei, 230031, China.
Medical Oncology (Northwood, London, England)
|September 30, 2025
Summary
Hypoxia increases RHPN1-AS1 long noncoding RNA in liver cancer cells, promoting tumor growth by stabilizing RPS15A protein and activating the beta-catenin pathway. This highlights RHPN1-AS1 as a therapeutic target in hypoxic hepatocellular carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Hypoxia is a key feature of hepatocellular carcinoma (HCC), driving cancer progression.
- Long noncoding RNAs (lncRNAs) like RHPN1-AS1 are implicated in various cancers, but their role in hypoxic HCC is unclear.
Purpose of the Study:
- To investigate RHPN1-AS1 expression and function in HCC under hypoxic conditions.
- To identify the protein partner and molecular mechanism of RHPN1-AS1 in hypoxic HCC.
Main Methods:
- Investigated RHPN1-AS1 expression changes in HCC cells exposed to hypoxia.
- Performed knockdown and overexpression studies of RHPN1-AS1.
- Utilized chromatin immunoprecipitation and protein interaction assays.
- Conducted in vivo tumorigenic studies in xenograft models.
Main Results:
- Hypoxia increased RHPN1-AS1 levels, regulated by HIF-1α.
- RHPN1-AS1 knockdown inhibited, while overexpression promoted, HCC cell proliferation and invasion under hypoxia.
- RHPN1-AS1 stabilized RPS15A protein, enhancing HCC cell aggressiveness via β-catenin signaling.
- RPS15A depletion reduced tumor growth in vivo.
Conclusions:
- RHPN1-AS1 is a hypoxia-responsive lncRNA in HCC.
- RHPN1-AS1 promotes HCC progression by interacting with RPS15A and activating the β-catenin pathway.
- RHPN1-AS1 and RPS15A represent potential therapeutic targets for hypoxic HCC.
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