HMGA2 overexpression activates IGF2BP2 to stabilize APLP2 via m6A modification and promote pancreatic cancer progression

被引：1
|
作者：
Liu, Ke [1 ]
Wei, Congbing [2 ]
Zhang, Qun [3 ]
机构：
[1] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Gastrointestinal Surg, Wuhan 430022, Peoples R China
[2] Hosp China Univ Geosci Wuhan, Wuhan 430074, Peoples R China
[3] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Canc Ctr, Wuhan 430022, Peoples R China
来源：
HELIYON | 2024年 / 10卷 / 05期
基金：
中国国家自然科学基金;
关键词：
HMGA2; IGF2BP2; APLP2; Pancreatic cancer; PROTEINS; GROWTH;
D O I：
10.1016/j.heliyon.2024.e27268
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Pancreatic cancer is a highly aggressive malignancy of the digestive system, with occult onset, rapid progression, and poor prognosis. The genetic heterogeneity of pancreatic cancer contributes to its highly malignant biological behavior. HMGA2 is overexpressed in tumors and is known to regulate tumor progression in various cancers through the HMGA2-IGF2BP2 axis, but its role and mechanism in pancreatic cancer remain unclear. In this study, we demonstrated that HMGA2 promotes pancreatic cancer progression. We further revealed that HMGA2 upregulates IGF2BP2, which stabilizes APLP2 mRNA via m6A modification, thereby promoting pancreatic cancer progression. These results indicate that HMGA2/IGF2BP2/APLP2 signaling axis regulates the progression of pancreatic cancer.
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收藏
页数：10
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