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.
Supplementary data
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Financial & competing interests disclosure
This research was funded by the basic scientific research business fee project of Heilongjiang Provincial Department of Education (2019-KYYWF-0936), the Postdoctoral Scientific Research Developmental Fund of Heilongjiang Province (LBH-Z18209) and the Postdoctoral Scientific Research Developmental Fund of China (no. 212538). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.
Ethical conduct of research
The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations.