HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27

Du, Wei; Guo, Kai; Wang, Peng; Zhong, Jianye; Jiang, Ning

doi:10.7150/jca.89994

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International Journal of Medical Sciences

Theranostics

Journal of Genomics

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J Cancer 2024; 15(3):645-658. doi:10.7150/jca.89994 This issue Cite

Research Paper

HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27

Wei Du^#, Kai Guo^#, Peng Wang, Jianye Zhong, Ning Jiang^✉

Department of Urological Surgery, Zhujiang Hospital of Southern Medical University, Guangdong, Guangzhou, 510280, China.
^#These authors contributed equally to this study.

Citation:

Du W, Guo K, Wang P, Zhong J, Jiang N. HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27. J Cancer 2024; 15(3):645-658. doi:10.7150/jca.89994. https://www.jcancer.org/v15p0645.htm

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Abstract

Bladder cancer (BCa) stands as a significant malignancy within the genitourinary system. Notably, heat shock proteins (HSPs) exhibit elevated expression in cells subjected to environmental stresses and have been linked to the progression of many human malignancies. Among these, the functional implications and specific mechanism of HSPB8 in BCa have yet to be fully explored. In this study, we measured HSPB8 expression in both BCa tissues and various cell lines, further delving into its influence on cellular behaviors. Our observations pinpoint an upregulation of HSPB8 in BCa, a trend strongly associated with more advanced clinical manifestations. Suppressing HSPB8 exhibited marked reductions in cell proliferation and migration capabilities, while simultaneously amplifying apoptosis and inducing cell cycle arrest. Reinforcing these findings, our in vivo analyses using mouse models showed similar trends. Notably, upon HSPB8 knockdown, levels of specific proteins including eNOS (S1177), Hsp27 (S78/S82), PRAS40(T246), RSK1/2(S221/S227), and STAT3 (S727) decreased, with Hsp27 (S78/S82) and PRAS40(T246) experiencing the most profound drops. Furthermore, the application of an HSP27 inhibitor effectively reversed the phenotypes caused by increased HSPB8 expression. Collectively, our results suggest that elevated HSPB8 expression could act as a potential prognostic marker for BCa, and targeting HSPB8 might open new therapeutic avenues for treating this malignancy.

Keywords: HSPB8, HSP22, HSP27, HSPB1, Bladder cancer

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APA

Du, W., Guo, K., Wang, P., Zhong, J., Jiang, N. (2024). HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27. Journal of Cancer, 15(3), 645-658. https://doi.org/10.7150/jca.89994.

ACS

Du, W.; Guo, K.; Wang, P.; Zhong, J.; Jiang, N. HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27. J. Cancer 2024, 15 (3), 645-658. DOI: 10.7150/jca.89994.

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CSE

Du W, Guo K, Wang P, Zhong J, Jiang N. 2024. HSPB8 Facilitates the Oncogenesis and Advancement of Bladder Cancer via Activation of HSP27. J Cancer. 15(3):645-658.

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