2023
DOI: 10.1007/s13402-023-00779-9
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USP13 promotes breast cancer metastasis through FBXL14-induced Twist1 ubiquitination

Abstract: Purpose Epithelial-to-mesenchymal transition (EMT) is an important cause of high mortality in breast cancer. Twist1 is one of the EMT transcription factors (EMT-TFs) with a noticeably short half-life, which is regulated by proteasome degradation pathways. Recent studies have found that USP13 stabilizes several specific oncogenic proteins. As yet, however, the relationship between Twist1 and USP13 has not been investigated. Methods Co-Immunoprecipitation, G… Show more

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Cited by 4 publications
(3 citation statements)
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“…In fact, in addition to two key transcription factors, Snail and Twist, various signaling pathways could also be responsible factors such as Notch, tumor necrosis factor-alpha (TNFα), transforming growth factor beta (TGF-β), and hypoxia-inducible factor-1 alpha (HIF1α), which are involved in the induction of EMT in pancreatic cancer cells [65]. Quite interestingly, in the current study, all of the up-stream regulators and/or causal network master regulators estimated by the IPA analysis of the RNA sequencing, that is, STAT3 [42], GLI1 [43], ZNF367 [53], NKX3-2 [47], ZIC2 [51] IFIT2 [46], HEY1 [55] and FBXL14 [60] were identified as being directly or indirectly related to the EMT mechanisms of cancerous cells. Furthermore, among four factors, FABP5, IQSEC3, GASK1B, and SCN1A were identified as unique genes associated with their antisense RNA or pseudogene among the prominently altered DEGs (Log2 fold changes more than 6 or less than −6), FABP5 [66] and GASK1B [67] are also identified as modulators of cancerous EMT.…”
Section: Discussionmentioning
confidence: 57%
“…In fact, in addition to two key transcription factors, Snail and Twist, various signaling pathways could also be responsible factors such as Notch, tumor necrosis factor-alpha (TNFα), transforming growth factor beta (TGF-β), and hypoxia-inducible factor-1 alpha (HIF1α), which are involved in the induction of EMT in pancreatic cancer cells [65]. Quite interestingly, in the current study, all of the up-stream regulators and/or causal network master regulators estimated by the IPA analysis of the RNA sequencing, that is, STAT3 [42], GLI1 [43], ZNF367 [53], NKX3-2 [47], ZIC2 [51] IFIT2 [46], HEY1 [55] and FBXL14 [60] were identified as being directly or indirectly related to the EMT mechanisms of cancerous cells. Furthermore, among four factors, FABP5, IQSEC3, GASK1B, and SCN1A were identified as unique genes associated with their antisense RNA or pseudogene among the prominently altered DEGs (Log2 fold changes more than 6 or less than −6), FABP5 [66] and GASK1B [67] are also identified as modulators of cancerous EMT.…”
Section: Discussionmentioning
confidence: 57%
“…USP13 regulates DNA repair, senescence and proteasomal degradation via interactions with RAP80-BRCA1 complex, cell senescence related E3 ubiquitin ligase murine double minute 2 (MDM2) and inflammation regulation-associated protease inactive rhomboid protein 2 (IRHOM2), respectively, and via hydrolyzation of K63-linked ubiquitin chains ( 67 , 92 ). USP13 is also involved in the cleavage of K48-linked polyubiquitin chains in some cases, such as the upregulation of Twist1 ( 79 ). The regulatory function of USP13 in hydrolyzing different types of ubiquitin chains is complex and it may affect the tumor progression.…”
Section: Discussionmentioning
confidence: 99%
“…While the expression of Twist1 could be regulated by USP13, USP13 interacts with Twist1 and stabilizes its expression via the ubiquitin-proteasome pathway. High expression of USP13 promotes the migration and invasion of tumors such as breast cancer through Twist1 ( 79 ).…”
Section: Role Of Usp13 In Tumorsmentioning
confidence: 99%