RETRACTED: Targeting USP1‐dependent KDM4A protein stability as a potential prostate cancer therapy
The histone demethylase lysine‐specific demethylase 4A (KDM4A) is reported to be overexpressed and plays a vital in multiple cancers through controlling gene expression by epigenetic regulation of H3K9 or H3K36 methylation marks. However, the biological role and mechanism of KDM4A in prostate cancer...
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| Veröffentlicht in: | Cancer science 2020-05, Vol.111 (5), p.1567-1581 |
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| container_title | Cancer science |
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| creator | Cui, Shu‐Zhong Lei, Zi‐Ying Guan, Tian‐Pei Fan, Ling‐Ling Li, You‐Qiang Geng, Xin‐Yan Fu, De‐Xue Jiang, Hao‐Wu Xu, Song‐Hui |
| description | The histone demethylase lysine‐specific demethylase 4A (KDM4A) is reported to be overexpressed and plays a vital in multiple cancers through controlling gene expression by epigenetic regulation of H3K9 or H3K36 methylation marks. However, the biological role and mechanism of KDM4A in prostate cancer (PC) remain unclear. Herein, we reported KDM4A expression was upregulation in phosphatase and tensin homolog knockout mouse prostate tissue. Depletion of KDM4A in PC cells inhibited their proliferation and survival in vivo and vitro. Further studies reveal that USP1 is a deubiquitinase that regulates KDM4A K48‐linked deubiquitin and stability. Interestingly, we found c‐Myc was a key downstream effector of the USP1‐KDM4A/androgen receptor axis in driving PC cell proliferation. Notably, upregulation of KDM4A expression with high USP1 expression was observed in most prostate tumors and inhibition of USP1 promotes PC cells response to therapeutic agent enzalutamide. Our studies propose USP1 could be an anticancer therapeutic target in PC. |
| doi_str_mv | 10.1111/cas.14375 |
| format | Article |
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However, the biological role and mechanism of KDM4A in prostate cancer (PC) remain unclear. Herein, we reported KDM4A expression was upregulation in phosphatase and tensin homolog knockout mouse prostate tissue. Depletion of KDM4A in PC cells inhibited their proliferation and survival in vivo and vitro. Further studies reveal that USP1 is a deubiquitinase that regulates KDM4A K48‐linked deubiquitin and stability. Interestingly, we found c‐Myc was a key downstream effector of the USP1‐KDM4A/androgen receptor axis in driving PC cell proliferation. Notably, upregulation of KDM4A expression with high USP1 expression was observed in most prostate tumors and inhibition of USP1 promotes PC cells response to therapeutic agent enzalutamide. 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| source | DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Wiley Online Library Open Access; PubMed Central |
| subjects | Androgen receptors Androgens Cancer therapies Cell proliferation Deoxyribonucleic acid DNA DNA methylation Enzymes Gene expression Lung cancer Lysine Mass spectrometry Myc protein Pheochromocytoma cells Plasmids Prostate cancer Proteins PTEN protein Scientific imaging Tensin Therapeutic applications Tumors |
| title | RETRACTED: Targeting USP1‐dependent KDM4A protein stability as a potential prostate cancer therapy |
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