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Research articles

ScienceAsia 50 (2024):ID 2024016 1-9 |doi: 10.2306/scienceasia1513-1874.2024.016


CD142 inhibits BCL2-dependent autophagic cell death and apoptosis in Wilms' tumor


Linshan Zenga, Qiang Zengb, Haifeng Zhangc, Mingfeng Xiea, Xiaojun Zhangd,*

 
ABSTRACT:     It is known that cluster of differentiation 142 (CD142) is closely related to the tumorigenesis of Wilms? tumor (WT). However, the underlying mechanism of CD142-regulated WT tumorigenesis remains unknown. CD142 can upregulate the expression of autophagy and apoptosis-inhibiting factor B-cell lymphoma-2 (BCL2). This study aimed to investigate whether CD142 regulates the WT tumorigenesis through the inhibition of BCL2-dependent autophagic cell death and apoptosis. Our results showed that CD142-positive sorting WT cell line WiT49 had stronger survival capacity and migratory function, while CD142-negative WiT49 cells were contrary. Moreover, xenogeneic tumor experiments showed that nude mice with CD142+ WiT49 cells had stronger tumorigenicity in vivo. Importantly, CD142+ WiT49 cells had higher protein level of BCL2, weaker autophagy, weaker apoptosis, and more significant interaction of BCL2 with Beclin1 and BAX; whereas CD142? WiT49 cells showed the opposite effects. However, BCL2 inhibition with ABT737 intervention rescued the inhibited autophagy and apoptosis and promoted the survival and migratory function in CD142+ WiT49 cells. Overall, this study demonstrated that CD142 inhibits the autophagic death and apoptosis by the overexpressed BCL2, which enhances the tumorigenesis of WT.

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a Department of Pediatric Surgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000 China
b Department of Pediatric Surgery, Jiangxi Maternal and Child Health Hospital, Nanchang 330000 China
c Department of Urology, The First People?s Hospital of Jiujiang City, Jiujiang 332000 China
d Department of Medical Oncology, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000 China

* Corresponding author, E-mail: ZXJgnyxy@163.com

Received 21 Oct 2022, Accepted 18 Aug 2023