Expression of MYSM1 is associated with tumor progression in colorectal cancer

MYSM1 的表达与结直肠癌的肿瘤进展相关

阅读:13
作者:Yongmin Li, Jingwen Li, He Liu, Yanlong Liu, Binbin Cui

Abstract

Colorectal cancer, the third most common cancer in both men and women, has gradually increased in recent years. MYSM1has been investigated as a regulator of hematopoiesis and lymphocyte development in human. It has been reported that some tumor-related genes were modulated by MYSM1. However, its exact role in cancer development remains unclear. Herein, we aimed to examine the expression level of MYSM1 in tumor tissues and its correlation with clinicopathology and survivals of patients with colorectal cancer (CRC).MYSM1expressions in tumor specimens resected from 123 CRC patients were detected by immunochemistry and Western blot analysis. The results showed that MYSM1 was significantly highly expressed in carcinoma tissues compared with adjacent normal mucosa tissues (P<0.05). Correlation analyses by Pearson's chi-square test demonstrated that MYSM1 in tumors was positively correlated with tumor status (pathological assessment of the primary tumor (pT, P<0.001), regional lymph nodes (pN, P = 0.013), distant metastasis (pM, P<0.001)) and clinic stage (P<0.001); Whereas, MYSM1 was not associated with tumor size of CRC patients and was positively associated with tumor differentiation grade (P = 0.015). Patients with positiveMYSM1expression showed poor survival compared with the MYSM1 negative group (P<0.001).Simultaneously, multivariate Cox regression analysis indicated thatMYSM1 expression in tumor cells was an independent factor for reduced overall survival in CRC patients (P<0.001).Additionally,MYSM1 in CRC SW480 cells was silenced by small interference RNA (siRNA) technology. Scratch assay and Transwell assay showed that MYSM1 silencing decreased migration and invasion abilities of SW480 cells. These data suggested that expression of MYSM1 was associated with the progression of CRC and might be a potential biomarker for clinical prognosis.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。