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Hypoxia upregulates Hsp90α expression via STAT5b in cancer cells. | LitMetric

AI Article Synopsis

  • Hsp90α is a chaperone protein crucial for the development of cancer-related signaling proteins and is being targeted for cancer therapy, despite potential side effects.
  • The study explores the link between the Jak2/STAT5b signaling pathway and Hsp90α expression under hypoxic conditions commonly found in solid tumors, indicating that treatment resistance and poor prognosis in cancers like breast cancer are linked to this pathway.
  • Findings demonstrate that STAT5b directly regulates Hsp90α expression during hypoxia, suggesting that targeting the Jak2/STAT5b pathway could be an effective strategy for treating solid tumors.

Article Abstract

Hsp90α is a molecular chaperone protein involved in the structural maturation of oncogenic signaling proteins. Hsp90 was recently identified as an anticancer target; various studies are ongoing to find ways for managing cancer through Hsp90α. However, this approach is limited by reported side-effects. Hypoxia is a hallmark of solid tumors, including those of breast cancer and the extent of tumor hypoxia is associated with resistance to treatment and poor prognosis. One of the major signaling pathways in cancer cells, the Jak2/STAT5b pathway, has been found to be closely correlated with hypoxia. The objective of this study was to investigate the role of Jak2/STAT5b in the regulation of Hsp90α expression so that Hsp90α targeting can be achieved indirectly by modulating the Jak2/STAT5b pathway. We examined the role of the Jak2/STAT5b pathway in the expression of Hsp90α under hypoxic conditions by immunoblotting, reporter gene assays, EMSA and RNA interference analysis. With the help of in vivo models, we also analyzed the expression of Hsp90α in different parts of solid tumor tissues. We found a close association between hypoxic stress and Hsp90α expression. We also determined that STAT5b regulates the expression of Hsp90α during hypoxic stimulation. Under hypoxic conditions the expression of Hsp90α and STAT5b were proportional. siRNA analysis and nucleotide analysis showed that the promoter of Hsp90α has a STAT5b binding domain. Our work confirmed that STAT5b is one of the transcription factors that regulate Hsp90α. We, therefore, concluded that under hypoxic conditions, the Jak2/STAT5b pathway regulates Hsp90α expression and it could serve as a promising target for the treatment of solid tumors.

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Source
http://dx.doi.org/10.3892/ijo.2012.1450DOI Listing

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