Search

Prostate cancer (PCa) is the leading cause of cancer death in men. With more therapeutic modalities available, the overall survival in PCa has increased significantly in recent years. Patients with relapses after advanced secondgeneration anti-androgen therapy however, often show poor disease prognosis. This group of patients often die from cancer-related complicacies. Multiple approaches have been taken to understand disease recurrence and to correlate the gene expression profile. In one such study, an 11-gene signature was identified to be associated with PCa recurrence and poor survival. Amongst them, a specific deubiquitinase called ubiquitin-specific peptidase 22 (USP22) was selectively and progressively overexpressed with PCa progression. Subsequently, it was shown to regulate androgen receptors and Myc, the two most important regulators of PCa progression. Furthermore, USP22 has been shown to be associated with the development of therapy resistant PCa. Inhibiting USP22 was also found to be therapeutically advantageous, especially in clinically challenging and advanced PCa. This review provides an update of USP22 related functions and challenges associated with PCa research and explains why targeting this axis is beneficial for PCa relapse cases., Competing Interests: Conflicts of interest Both authors declared that there are no conflicts of interest.

Non-small lung cancer (NSCLC) is one of the most common causes of cancer-associated death worldwide. Long noncoding RNAs (lncRNAs) regulate cancer initiation and progression through different mechanisms. In the present study, we characterized a novel lncRNA named lncKLF6, which was upregulated in NSCLC and associated with poor clinical outcomes. lncKLF6 inhibited Kruppel-like factor 6 (KLF6) transcription and then facilitated NSCLC growth. lncKLF6 is associated with the epigenetic repressor BMI1 and regulates its stability via recruiting deubiquitinase USP22. Moreover, it was revealed that lncKLF6 was a KLF6-responsive lncRNA, as KLF6 could occupy the lncKLF6 promoter to facilitate its transcription. The negative feedback loop of lncKLF6 and KLF6 continuously enhanced the oncogenic effects. Thus, our study elucidates the mechanism of lncKLF6-mediated growth via suppression of KLF6, which provides the promising target for developing new therapeutic strategy in NSCLC., Competing Interests: None.