Journal
EPIGENOMICS
Volume 12, Issue 15, Pages -Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/epi-2020-0270
Keywords
AC245100.4; HSP90; IKK; LncRNA; LncRNA binding protein; NF kappa B; proliferation; prostate cancer; RAP-MS; signaling pathway
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Funding
- basic scientific research business fee project of Heilongjiang Provincial Department of Education [2019-KYYWF-0936]
- Postdoctoral Scientific Research Developmental Fund of Heilongjiang Province [LBH-Z18209]
- Postdoctoral Scientific Research Developmental Fund of China [212538]
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Aim: To investigate the role and mechanisms ofAC245100.4in prostate cancer. Materials & methods: The expression and location ofAC245100.4were examined using real-time PCR and in situhybridization. Cell Counting Kit-8, clone formation, flow cytometry andin vivoassays were conducted to determine the role ofAC245100.4. RNA antisense purification with mass spectrometry and RNA immunoprecipitation were performed to identify proteins that bind toAC245100.4. Western blotting was performed to quantify the expression of protein. Results: AC245100.4expression was upregulated in prostate cancer and mainly located in the cytoplasm. Knockdown ofAC245100.4inhibited proliferation of prostate cancer. Mechanistically,AC245100.4bound to HSP90 and altered its chaperone function, increased the stability of I kappa B kinase and activated the NF kappa B signaling pathway. Conclusion: AC245100.4promotes the proliferation of prostate cancer via binding of HSP90.
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