G3BP1 Interact with JAK2 mRNA to Promote the Malignant Progression of Nasopharyngeal Carcinoma via Activating JAK2/STAT3 Signaling Pathway

被引:3
|
作者
Zhan, Yuting [1 ]
Wang, Weiyuan [2 ]
Wang, Haihua [1 ]
Xu, Yue [1 ]
Zhang, Yuting [1 ]
Ning, Yue [1 ]
Zheng, Hongmei [1 ]
Luo, Jiadi [1 ]
Yang, Yang [1 ]
Zang, Hongjing [1 ]
Zhou, Ming [3 ]
Fan, Songqing [1 ]
机构
[1] Cent South Univ, Xiangya Hosp 2, Dept Pathol, Changsha, Hunan, Peoples R China
[2] Cent South Univ, Xiangya Hosp, Dept Pathol, Changsha, Hunan, Peoples R China
[3] Cent South Univ, Canc Res Inst, Sch Basic Med Sci, Changsha, Hunan, Peoples R China
来源
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES | 2024年 / 20卷 / 01期
关键词
G3BP1; RNA binding protein; JAK2/STAT3 signaling pathway; malignant progression; CANCER-CELL-GROWTH; GASTRIC-CANCER; PROTEIN; APOPTOSIS; OVEREXPRESSION; CONTRIBUTES; METASTASIS; EXPRESSION; STABILITY; PROGNOSIS;
D O I
10.7150/ijbs.85341
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
Ras-GTPase-activating protein (GAP)-binding protein 1 (G3BP1) is an RNA-binding protein implicated in various malignancies. However, its role in nasopharyngeal carcinoma (NPC) remains elusive. This study elucidates the potential regulation mechanisms of G3BP1 and its significance in NPC advancement. Through knockdown and overexpression approaches, we validate G3BP1's oncogenic role by promoting proliferation, migration, and invasion in vitro and in vivo. Moreover, G3BP1 emerges as a key regulator of the JAK2/STAT3 signaling pathway, augmenting JAK2 expression via mRNA binding. Notably, epigallocatechin gallate (EGCG), a green tea-derived antioxidant, counteracts G3BP1-mediated pathway activation. Clinical analysis reveals heightened G3BP1, JAK2, and p-STAT3 as powerful prognostic markers, with G3BP1's expression standing as an independent indicator of poorer outcomes for NPC patients. In conclusion, the study unveils the oncogenic prowess of G3BP1, its orchestration of the JAK2/STAT3 signaling pathway, and its pivotal role in NPC progression.
引用
收藏
页码:94 / 112
页数:19
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