HSPB8 facilitates prostate cancer progression via activating the JAK/STAT3 signaling pathway

被引:3
|
作者
Zhang, Kan [1 ]
Yin, Weiqi [1 ]
Ma, Luping [2 ]
Liu, Zhili [2 ]
Li, Qiang [2 ]
机构
[1] Ningbo First Hosp, Dept Urinary Surg, 59,Liuting St, Ningbo 315000, Zhejiang Provin, Peoples R China
[2] Shihezi Univ, Affiliated Hosp 1, Dept Urinary Surg, Sch Med, 107,North 2nd Rd, Shihezi 832008, Xinjiang Provin, Peoples R China
关键词
PC; HSPB8; malignant phenotype; JAK; STAT3 signaling pathway; HEAT-SHOCK-PROTEIN; B8; HSPB8; MISFOLDED PROTEINS; AUTOPHAGIC REMOVAL; PD-L1; EXPRESSION; PROLIFERATION; CONSTRUCTION; CHALLENGES; RESISTANCE; PROGNOSIS;
D O I
10.1139/bcb-2022-0205
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Prostate cancer (PC) is a clinically and biologically heterogeneous disease that lacks effective treatment. Heat shock protein B8 (HSPB8) is an important factor in the progression of various types of cancer. However, the clinical significance and biological role of HSPB8 in PC are still unclear. In this study, we determined HSPB8 expression in PC tissues by immunohistochemical staining and explored the in vitro functions of HSPB8 using HSPB8 knockdown DU145 and LNcap PC cell lines. The in vivo effect of HSPB8 was explored by a subcutaneous xenograft mice model. The human phospho-kinase array and signal trans-ducer and activator of transcription (STAT) 3 activator were utilized to explore the potential mechanism of HSPB8-induced PC progression. As a result, we found that HSPB8 was abundantly expressed in PC tissues and cell lines. HSPB8 knockdown in-hibited cell proliferation and migration, promoted apoptosis and cycle repression, as well as weakened tumorigenesis ability. Mechanistically, we demonstrated that HSPB8 facilitates the malignant phenotypes of PC by activating the Janus kinase/STAT3 signaling pathway. These results proposed that HSPB8 seems to be an attractive therapeutic target for PC patients.
引用
收藏
页码:1 / 11
页数:11
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