Dishevelled-associated antagonist of β-catenin homolog 3 (DACT3) suppresses glioma progression though Notch1 signaling pathway in β-catenin-dependent manner

作者全名："Yue, Jianhe; Zhang, Jiqin; Huan, Renzheng; Zeng, Yu; Tan, Ying; Cheng, Yuan"

作者地址："[Yue, Jianhe; Huan, Renzheng; Cheng, Yuan] Chongqing Med Univ, Dept Neurosurg, Affiliated Hosp 2, Chongqing, Peoples R China; [Zhang, Jiqin] Guizhou Prov Peoples Hosp, Dept Anesthesiol, Guiyang, Peoples R China; [Zeng, Yu; Tan, Ying] Guizhou Prov Peoples Hosp, Dept Neurosurg, Guiyang, Peoples R China; [Cheng, Yuan] Chongqing Med Univ, Dept Neurol, Affiliated Hosp 2, 74 Linjiang Rd,Yuzhong Dist, Chongqing 400010, Peoples R China; [Tan, Ying] Guizhou Prov Peoples Hosp, Dept Neurosurg, 83 Zhongshandong Rd,Nanming Dist, Guiyang 400010, Peoples R China"

通信作者："Cheng, YN (通讯作者)，Chongqing Med Univ, Dept Neurol, Affiliated Hosp 2, 74 Linjiang Rd,Yuzhong Dist, Chongqing 400010, Peoples R China.; Tan, Y (通讯作者)，Guizhou Prov Peoples Hosp, Dept Neurosurg, 83 Zhongshandong Rd,Nanming Dist, Guiyang 400010, Peoples R China."

来源：HELIYON

ESI学科分类：　

WOS号：WOS:001155629400001

JCR分区：Q2

影响因子：4

年份：2024

卷号：10

期号：1

开始页：　

结束页：　

文献类型：Article

关键词：Glioma; DACT3; Notch1 signaling; beta-catenin; Progression

摘要："The disheveled-associated antagonist of beta-catenin homolog 3 (DACT3) has been recognized as a tumor suppressor in various cancers. However, the function of DACT3 on glioma malignant progression along with potential molecular mechanisms is poorly clarified. This research aimed to investigate how DACT3 contributes to suppressing the progression of glioma. In our investigation, a pronounced decrease in DACT3 expression was observed in glioma tissues. Through the overexpression of DACT3, we noted a significant suppression in the proliferation, invasion, and migration of glioma cells, while concurrently observing an increase in cell adhesion. Our exploration into the molecular mechanisms revealed that DACT3 executes its tumor-suppressive role by impeding the expression of notch 1 intracellular domain (NICD) and translocating into the nucleus by downregulating the expression of beta-catenin. Consequently, this process leads to the suppression of Notch1 signaling. To summarize, our findings reveal the function of DACT3 to inhibit glioma progression via the Notch1 signaling pathway in beta-catenin dependent manner. This study stands as the pioneer in examining the role of DACT3 in glioma progression and comprehensively elucidating its molecular mechanisms in glioma development. Therefore, our results suggest that DACT3 holds promise as both a prognostic factor and a potential biomarker for guiding treatment strategies in glioma patients (Graphical Abstract)."

基金机构："National Natural Science Foundation of China, China [81960454, 82260533, 82360482]; Guizhou Provincial Science and Technology Projects, China [[2020] 1Z066]; Guizhou Provincial People's Hospital Doctor Foundation, China [[2018] 06, [2018] 03]; Guizhou Provincial People's Hospital National Science Foundation, China [GPPH-NSFC-2019-13, GPPH-NSFC-D-2019-17]"

基金资助正文："This work was supported by the National Natural Science Foundation of China, China (81960454, 82260533, 82360482) , the Guizhou Provincial Science and Technology Projects, China ( [2020] 1Z066) , Guizhou Provincial People's Hospital Doctor Foundation, China ( [2018] 06 and [2018] 03) and Guizhou Provincial People's Hospital National Science Foundation, China (GPPH-NSFC-2019-13 and GPPH-NSFC-D-2019-17) ."