WD repeat protein 54-mediator of ErbB2-driven cell motility 1 axis promotes bladder cancer tumorigenesis and metastasis and impairs chemosensitivity

Wei, Xiaosong; Wang, Beibei; Wu, Zixin; Yang, Xiaoming; Guo, Yufeng; Yang, Yang; Fang, Zhiwei; Yi, Chengzhi; Zhang, Liuhui; Fan, Xin; Zhang, Lirong; Song, Dongkui

doi:10.1016/j.canlet.2023.216058

Cited by 5 publications

(7 citation statements)

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“…WDR domain‐containing proteins have been shown to mediate protein–protein or protein–DNA interactions through their WDR domain 46,47 . As a WDR domain‐containing protein, WDR54 has been found to be elevated and associated with prognosis in colorectal cancer patients and bladder cancer patients 25,26 . Huang et al recently identified WDR54 as a hallmark gene of diabetes mellitus‐related atherogenesis using weight gene correlation network analysis 48 .…”

Section: Discussionmentioning

confidence: 99%

“…[20][21][22][23][24] WDR54 was recently identified as an oncogene in colorectal cancer and bladder cancer. 25,26 WDR54 could promote cell proliferation by activating AKT, ERK, and β-catenin signaling in cancers. 25,26 Mechanistically, the cross-linking and ubiquitination of WDR54 were found to regulate ERK activity in response to EGF stimulation.…”

Section: Introductionmentioning

confidence: 99%

“…WDR54 was recently identified as an oncogene in colorectal cancer and bladder cancer 25,26 . WDR54 could promote cell proliferation by activating AKT, ERK, and β‐catenin signaling in cancers 25,26 .…”

Section: Introductionmentioning

confidence: 99%

“… 25 , 26 WDR54 could promote cell proliferation by activating AKT, ERK, and β‐catenin signaling in cancers. 25 , 26 Mechanistically, the cross‐linking and ubiquitination of WDR54 were found to regulate ERK activity in response to EGF stimulation. 27 These studies suggest that WDR54 may be involved in the proliferation of tumors.…”

Section: Introductionmentioning

confidence: 99%

“…It has been widely reported that specific AKT inhibitor MK2206 and MEK-signaling inhibitor U0126 could effectively suppress T-ALL cell growth in a time-and dosedependent manner 36,41,42. A recent study reported that WDR54 could activate the AKT, ERK, or β-catenin signaling pathways and promote cell proliferation in colorectal cancer and bladder cancer 25,26. Mechanistically, WDR54 was found to be cross-linked by the action of transgluaminase, resulting in the activation of the EGF receptor-mediated signaling pathway 27.…”

mentioning

confidence: 99%

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WDR54 exerts oncogenic roles in T‐cell acute lymphoblastic leukemia

Li,

Zhang,

et al. 2023

Cancer Science

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WDR54 has been recently identified as a novel oncogene in colorectal and bladder cancers. However, the expression and function of WDR54 in T-cell acute lymphoblastic leukemia (T-ALL) were not reported. In this study, we investigated the expression of WDR54 in T-ALL, as well as its function in T-ALL pathogenesis using cell lines and T-ALL xenograft. Bioinformatics analysis indicated high mRNA expression of WDR54 in T-ALL. We further confirmed that the expression of WDR54 was significantly elevated in T-ALL. Depletion of WDR54 dramatically inhibited cell viability and induced apoptosis and cell cycle arrest at S phase in T-ALL cells in vitro. Moreover, knockdown of WDR54 impeded the process of leukemogenesis in a Jurkat xenograft model in vivo. Mechanistically, the expression of PDPK1, phospho-AKT (p-AKT), total AKT, phospho-ERK (p-ERK), Bcl-2 and Bcl-xL were downregulated, while cleaved caspase-3 and cleaved caspase-9 were upregulated in T-ALL cells with WDR54 knockdown.Additionally, RNA-seq analysis indicated that WDR54 might regulate the expression of some oncogenic genes involved in multiple signaling pathways. Taken together, these findings suggest that WDR54 may be involved in the pathogenesis of T-ALL and serve as a potential therapeutic target for the treatment of T-ALL.

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Section: Discussionmentioning

confidence: 99%