Rongjun Cui1,2, Chi Liu1, Ping Lin1, Hui Xie3, Wei Wang1, Jiabin Zhao4, Shan Jiang1, Jie Shi1, Xiaoguang Yu1. 1. Department of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150086, PR China. 2. Department of Biochemistry & Molecular Biology, Mudanjiang Medical University, Mudanjiang, Heilongjiang, 157011, PR China. 3. Teaching Experiment Center of Biotechnology, Harbin Medical University, Harbin, 150086, PR China. 4. Department of Emergency Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, PR China.
Abstract
Aim: To investigate the role and mechanisms of AC245100.4 in prostate cancer. Materials & methods: The expression and location of AC245100.4 were examined using real-time PCR and in situ hybridization. Cell Counting Kit-8, clone formation, flow cytometry and in vivo assays were conducted to determine the role of AC245100.4. RNA antisense purification with mass spectrometry and RNA immunoprecipitation were performed to identify proteins that bind to AC245100.4. Western blotting was performed to quantify the expression of protein. Results: AC245100.4 expression was upregulated in prostate cancer and mainly located in the cytoplasm. Knockdown of AC245100.4 inhibited proliferation of prostate cancer. Mechanistically, AC245100.4 bound to HSP90 and altered its chaperone function, increased the stability of IκB kinase and activated the NFκB signaling pathway. Conclusion: AC245100.4 promotes the proliferation of prostate cancer via binding of HSP90.
Aim: To investigate the role and mechanisms of AC245100.4 in prostate cancer. Materials & methods: The expression and location of AC245100.4 were examined using real-time PCR and in situ hybridization. Cell Counting Kit-8, clone formation, flow cytometry and in vivo assays were conducted to determine the role of AC245100.4. RNA antisense purification with mass spectrometry and RNA immunoprecipitation were performed to identify proteins that bind to AC245100.4. Western blotting was performed to quantify the expression of protein. Results:AC245100.4 expression was upregulated in prostate cancer and mainly located in the cytoplasm. Knockdown of AC245100.4 inhibited proliferation of prostate cancer. Mechanistically, AC245100.4 bound to HSP90 and altered its chaperone function, increased the stability of IκB kinase and activated the NFκB signaling pathway. Conclusion:AC245100.4 promotes the proliferation of prostate cancer via binding of HSP90.
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