RNA binding protein PUM2 promotes hepatocellular carcinoma proliferation and apoptosis via binding to the 3'UTR of BTG3
Affiliations: Department of General Surgery, The First People's Hospital of Lin Ping District, Hangzhou, Zhejiang 311100, P.R. China, Department of General Surgery, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, Jiangsu 211100, P.R. China
- Published online on: August 17, 2022 https://doi.org/10.3892/ol.2022.13466
Copyright: © Liu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Pumilio homolog 2 (PUM2) is an RNA‑binding protein that functions as an oncogene in various types of cancer. However, its role in hepatocellular carcinoma (HCC) has remained to be fully elucidated. In the present study, the role of PUM2 was investigated in HCC and its regulation was assessed by examining its binding to the 3'‑untranslated region (UTR) of B‑cell translocation gene 3 (BTG3). The expression levels of PUM2 were determined in datasets from the UALCAN and Cancer Cell Line Encyclopedia databases. Furthermore, Gene Expression Profiling Interactive Analysis was used to analyze overall survival in patients with HCC. Reverse transcription‑quantitative PCR (RT‑qPCR) and western blot analyses were then performed to detect the expression levels of PUM2 and BTG3 in HCC cells. Cell proliferation was assessed using Cell Counting Kit‑8 and colony‑formation assays. The induction of cell apoptosis was evaluated using TUNEL and western blotting assays. StarBase and RNA‑Protein Interaction Prediction were used to determine the possible direct interaction between PUM2 and BTG3. The interaction between PUM2 and BTG3 was then verified by luciferase reporter and RNA‑binding protein immunoprecipitation assays. The results indicated that PUM2 expression was upregulated in HCC tissues and cells and that it was associated with the prognosis of patients with HCC. PUM2 silencing inhibited the proliferation and promoted the apoptosis of Huh‑7 cells. In addition, PUM2 was confirmed to directly bind to the 3'UTR of BTG3. Downregulation of BTG3 reversed the effects of PUM2 silencing on cell proliferation and apoptosis in Huh‑7 cells. Collectively, the results suggested that PUM2 regulated HCC cell proliferation and apoptosis via interacting with BTG3, which may provide a novel therapeutic strategy for the treatment of human HCC.