USP22调控肿瘤中信号转导通路的研究进展

Advances in USP22 Regulation of Signal Transduction Pathways in Tumors

USP22作为肿瘤干细胞标志物之一,在几种类型的人类癌症中已被观察到,这表明USP22可能参与各种生理和病理过程,并作为致癌基因在癌症进展中起作用。然而,导致USP22转录激活的机制,特别是USP22介导人类肿瘤进展的机制,至今仍然未知。前期研究表明USP22主要通过调节正常T细胞和B细胞中丝裂原的激活诱导肿瘤发生。而最新研究发现,仅USP22过表达不足以诱导肿瘤发生,USP22是通过肿瘤相关信号通路的激活参与肿瘤进展的,该理论的出现为肿瘤机制的研究提出了新见解,也为USP22介导肿瘤治疗耐药性提供了新思路。该文对USP22参与肿瘤进展的相关信号通路进行概述和总结,以期发现USP22介导肿瘤发生发展的分子机制及不同信号通路之间的串扰对肿瘤进展的影响,为癌症治疗提供新思路。

USP22,as one of the tumor stem cell markers,has been observed in several types of human cancers,suggesting that USP22 may be involved in various physiological and pathological processes and act as an oncogene in cancer progression.However,the mechanisms leading to the transcriptional activation of USP22,especially the mechanism by which USP22 mediates human tumor progression,remain unknown.Previous studies have shown that USP22 induces tumorigenesis mainly by regulating mitogen-stimulated activation in normal T cells and B cells or by viral infection.However,recent studies have shown that USP22 overexpression alone is not sufficient to induce tumorigenesis,and that USP22 is involved in tumor progression through the activation of tumor-associated signaling pathways,which provides new insights into the tumor mechanism and a new way of thinking about USP22-guided tumor therapeutic resistance.This article summarizes the relevant signaling pathways of USP22 involved in tumor progression,in order to find the molecular mechanism of USP22-mediated tumor development and the crosstalk between different signaling pathways on tumor progression,and provide new ideas for cancer treatment.