MAL2 interacts with IQGAP1 to promote pancreatic cancer progression by increasing ERK1/2 phosphorylation

被引：19
|
作者：
Zhang, Bin [1 ,2 ]
Xiao, Jun [1 ,2 ]
Cheng, Xiang [1 ,2 ]
Liu, Tao [1 ,2 ]
机构：
[1] Huazhong Univ Sci & Technol, Union Hosp, Dept Digest Surg Oncol, Tongji Med Coll, Wuhan 430022, Peoples R China
[2] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Canc Ctr, Wuhan 430022, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2021年 / 554卷
基金：
中国国家自然科学基金;
关键词：
MAL2; IQGAP1; ERK; Pancreatic cancer; EXPRESSION; RESISTANCE; PROTEIN; MACHINERY; CELL;
D O I：
10.1016/j.bbrc.2021.02.146
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：
Pancreatic cancer is a digestive tract malignancy characterized by an occult onset and rapid progression. The genetic heterogeneity of pancreatic cancer is closely related to its highly malignant biological behavior. The myelin and lymphocyte protein 2 (MAL2) is upregulated in multiple cancers at the transcriptional level. However, the exact role of MAL2 in pancreatic cancer remains elusive. In this study, we demonstrated that MAL2 protein and mRNA levels were upregulated in pancreatic cancer. MAL2 over expression was significantly associated with poor prognosis in patients with pancreatic cancer. We further showed that MAL2 interacted with IQGAP1 to increase ERK1/2 phosphorylation levels, which promoted pancreatic cancer progression. Therefore, these results suggest that MAL2 could be a novel therapeutic target for pancreatic cancer. ? 2021 Elsevier Inc. All rights reserved.
引用
收藏
页码：63 / 70
页数：8
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