PLCB1 Enhances Cell Migration and Invasion in Gastric Cancer Via Regulating Actin Cytoskeletal Remodeling and Epithelial-Mesenchymal Transition

被引:7
|
作者
Wang, Yulin [2 ]
Tu, Zhiyue [1 ]
Zhao, Wei [3 ]
Wang, Liping [2 ]
Jiang, Jing [2 ]
Gu, Lili [3 ]
Li, Meng [2 ]
Jiang, Lujian [2 ]
Wang, Yibin [2 ]
Bi, Yinglu [2 ]
机构
[1] Tianjin Canc Hosp Airport Hosp, Dept Endoscopy, Tianjin, Peoples R China
[2] Tianjin Acad Tradit Chinese Med Affiliated Hosp, Digest Med Dept, 354 North Rd, Tianjin 300120, Peoples R China
[3] Tianjin Acad Tradit Chinese Med Affiliated Hosp, Dept Digest Endoscopy Ctr, Tianjin, Peoples R China
关键词
Phospholipase C beta 1; Gastric cancer; Actin cytoskeletal remodeling; Epithelial-Mesenchymal transition; PHOSPHOLIPASE-C; PROLIFERATION; EXPRESSION; BETA-1;
D O I
10.1007/s10528-023-10396-8
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
Phospholipase C Beta 1 (PLCB1) regulates the abundance of PI(4,5)P2 in the plasma membrane and is implicated in various kinds of cancers. This study aimed to investigate the role and underlying mechanisms of PLCB1 in gastric cancer. Herein, it was found that PLCB1 mRNA and protein were highly expressed in gastric cancer, and high levels of PLCB1 were correlated with poor outcomes of patients with gastric cancer via the GEPIA database. Moreover, our results revealed that PLCB1 depletion inhibited gastric cancer cell proliferation, migration, and invasion. Meanwhile, PLCB1 overexpression resulted in an inverse result. Furthermore, PLCB1 mediated actin cytoskeleton rearrangement and activated the RhoA/LIMK/Cofilin pathway. Besides, PLCB1 promoted the Epithelial-Mesenchymal transition process via activating ATK signaling. In conclusion, PLCB1 promoted gastric cancer cell migratory and invasive abilities via regulating actin cytoskeleton rearrangement and Epithelial-Mesenchymal transition process. These findings imply that targeting PLCB1 may be a potential strategy to improve the prognosis of gastric cancer patients.
引用
收藏
页码:2618 / 2632
页数:15
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