UBE2K regulated by IGF2BP3 promotes cell proliferation and stemness in pancreatic ductal adenocarcinoma
Affiliations: Qingdao Medical College, Qingdao University, Qingdao, Shandong 266071, P.R. China, The Key Laboratory of Tumor Molecular Diagnosis and Individualized Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, Zhejiang 310014, P.R. China, Zhejiang University of Technology, Hangzhou, Zhejiang 310014, P.R. China
- Published online on: March 9, 2023 https://doi.org/10.3892/ijo.2023.5500
- Article Number: 52
Copyright: © Fu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Pancreatic ductal adenocarcinoma (PDAC) is a noteworthy malignant carcinoma with an unsatisfactory prognosis attributed to late diagnosis. Ubiquitin‑conjugating enzyme E2K (UBE2K) has been found to serve important roles in a number of diseases. However, its function and the exact molecular mechanism of UBE2K in PDAC remain to be elucidated. The present study discovered that UBE2K was expressed at high levels and indicated the poor prognosis of patients with PDAC. Following this, the CCK‑8, colony formation, and sphere formation assays showed that UBE2K promoted proliferation and the stemness phenotype of PDAC cells in vitro. Evidence from subcutaneous tumor‑bearing nude mice experiments further confirmed that UBE2K enhanced PDAC cell tumorigenesis in vivo. Additionally, the present study demonstrated that insulin‑like growth factor 2 RNA binding protein 3 (IGF2BP3) functioned as an RNA‑binding protein to increase UBE2K expression by enhancing the RNA stability of UBE2K. The knockdown or overexpression of IGF2BP3 could attenuate the change in cells growth induced by the overexpression or knockdown of UBE2K. In summary, the findings indicated the oncogenic roles of UBE2K in PDAC. In addition, IGF2BP3 and UBE2K constitute a functional axis to regulate the malignant progression of PDAC.