Matches in SemOpenAlex for { <https://semopenalex.org/work/W4386422191> ?p ?o ?g. }
- W4386422191 abstract "Abstract Background Accumulating evidence has demonstrated that aberrant expression of deubiquitinating enzymes is associated with the initiation and progression of Triple-negative breast cancer (TNBC). The publicly available TCGA database of breast cancer data was used to analyze the OTUD deubiquitinating family members that were correlated with survival of breast cancer and ovarian tumor domain-containing 2 (OTUD-2), or YOD1 was identified. The aim of present study was to assess YOD1 expression and function in human TNBC and then explored the underlying molecular events. Methods We detected the expression of YOD1 in 32 TNBC and 44 NTNBC samples by qRT-PCR, Western blot and immunohistochemistry. Manipulation of YOD1 expression was assessed in vitro and in vivo for TNBC cell proliferation, migration, invasion, cell-cycle and drug resistance, using colony formation assay, transwell assay, CCK8 assay, TUNEL assay, flow cytometric analysis and xenograft tumor assay. Next, proteomic analysis, Western blot, proximity ligation assay, Immunoprecipitation, and Immunofluorescence were conducted to assess downstream targets. Results It was found that YOD1 was significantly upregulated in TNBC tissues compared with non-triple-negative breast cancer (NTNBC), which was positively correlated with poor survival in TNBC patients. Knockdown of YOD1 effectively inhibited TNBC cell migration, proliferation, cell cycle and resistance to cisplatin and paclitaxel. Mechanistically, YOD1 promoted TNBC progression in a manner dependent on its catalytic activity through binding with CDK1, leading to de-polyubiquitylation of CDK1 and upregulation of CDK1 expression. In addition, YOD1 overexpression was found to be correlated with CDK1 overexpression in human TNBC specimens. Finally, in vivo study demonstrated that YOD1 knockdown or YOD1 inhibitor could inhibit CDK1 expression and suppress the growth and metastasis of TNBC tumors. Conclusion Our study highlights that YOD1 functions as an oncogene in TNBC via binding to CDK1 and mediated its stability and oncogenic activity. Interfering with YOD1 expression or YOD1 inhibitor could suppress TNBC cells in vitro and in vivo, suggesting that YOD1 may prove to be a promising therapeutic target for TNBC." @default.
- W4386422191 created "2023-09-05" @default.
- W4386422191 creator A5001331259 @default.
- W4386422191 creator A5001525752 @default.
- W4386422191 creator A5003261759 @default.
- W4386422191 creator A5009601612 @default.
- W4386422191 creator A5012488321 @default.
- W4386422191 creator A5033647915 @default.
- W4386422191 creator A5049132248 @default.
- W4386422191 creator A5059083216 @default.
- W4386422191 creator A5070015170 @default.
- W4386422191 creator A5077632892 @default.
- W4386422191 creator A5078099916 @default.
- W4386422191 creator A5083338149 @default.
- W4386422191 creator A5084023767 @default.
- W4386422191 creator A5085142676 @default.
- W4386422191 creator A5088059015 @default.
- W4386422191 creator A5088575306 @default.
- W4386422191 date "2023-09-04" @default.
- W4386422191 modified "2023-10-17" @default.
- W4386422191 title "Deubiquitylase YOD1 regulates CDK1 stability and drives triple-negative breast cancer tumorigenesis" @default.
- W4386422191 cites W2023587394 @default.
- W4386422191 cites W2036565476 @default.
- W4386422191 cites W2056402768 @default.
- W4386422191 cites W2072130349 @default.
- W4386422191 cites W2089353165 @default.
- W4386422191 cites W2148390144 @default.
- W4386422191 cites W2151049734 @default.
- W4386422191 cites W2594511910 @default.
- W4386422191 cites W2621171915 @default.
- W4386422191 cites W2755529729 @default.
- W4386422191 cites W2773915736 @default.
- W4386422191 cites W2887119856 @default.
- W4386422191 cites W2889389988 @default.
- W4386422191 cites W2900128053 @default.
- W4386422191 cites W2900847633 @default.
- W4386422191 cites W2910383048 @default.
- W4386422191 cites W2941601461 @default.
- W4386422191 cites W2973871067 @default.
- W4386422191 cites W2980122850 @default.
- W4386422191 cites W2983982331 @default.
- W4386422191 cites W3004925426 @default.
- W4386422191 cites W3008017784 @default.
- W4386422191 cites W3019964615 @default.
- W4386422191 cites W3021330263 @default.
- W4386422191 cites W3029166518 @default.
- W4386422191 cites W3033869790 @default.
- W4386422191 cites W3037864935 @default.
- W4386422191 cites W3048260453 @default.
- W4386422191 cites W3084395085 @default.
- W4386422191 cites W3088233290 @default.
- W4386422191 cites W3098975119 @default.
- W4386422191 cites W3106631616 @default.
- W4386422191 cites W3112585650 @default.
- W4386422191 cites W3120597199 @default.
- W4386422191 cites W3127549549 @default.
- W4386422191 cites W3130271765 @default.
- W4386422191 cites W3164428180 @default.
- W4386422191 cites W3165239292 @default.
- W4386422191 cites W3165723818 @default.
- W4386422191 cites W3190030088 @default.
- W4386422191 cites W3198835038 @default.
- W4386422191 cites W3209399935 @default.
- W4386422191 cites W3210998084 @default.
- W4386422191 cites W3213834237 @default.
- W4386422191 cites W3215820950 @default.
- W4386422191 cites W4207033714 @default.
- W4386422191 cites W4281756586 @default.
- W4386422191 cites W4283710601 @default.
- W4386422191 cites W4304196204 @default.
- W4386422191 doi "https://doi.org/10.1186/s13046-023-02781-3" @default.
- W4386422191 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37667382" @default.
- W4386422191 hasPublicationYear "2023" @default.
- W4386422191 type Work @default.
- W4386422191 citedByCount "0" @default.
- W4386422191 crossrefType "journal-article" @default.
- W4386422191 hasAuthorship W4386422191A5001331259 @default.
- W4386422191 hasAuthorship W4386422191A5001525752 @default.
- W4386422191 hasAuthorship W4386422191A5003261759 @default.
- W4386422191 hasAuthorship W4386422191A5009601612 @default.
- W4386422191 hasAuthorship W4386422191A5012488321 @default.
- W4386422191 hasAuthorship W4386422191A5033647915 @default.
- W4386422191 hasAuthorship W4386422191A5049132248 @default.
- W4386422191 hasAuthorship W4386422191A5059083216 @default.
- W4386422191 hasAuthorship W4386422191A5070015170 @default.
- W4386422191 hasAuthorship W4386422191A5077632892 @default.
- W4386422191 hasAuthorship W4386422191A5078099916 @default.
- W4386422191 hasAuthorship W4386422191A5083338149 @default.
- W4386422191 hasAuthorship W4386422191A5084023767 @default.
- W4386422191 hasAuthorship W4386422191A5085142676 @default.
- W4386422191 hasAuthorship W4386422191A5088059015 @default.
- W4386422191 hasAuthorship W4386422191A5088575306 @default.
- W4386422191 hasBestOaLocation W43864221911 @default.
- W4386422191 hasConcept C104317684 @default.
- W4386422191 hasConcept C120504264 @default.
- W4386422191 hasConcept C121608353 @default.
- W4386422191 hasConcept C127561419 @default.
- W4386422191 hasConcept C173396325 @default.
- W4386422191 hasConcept C190283241 @default.
- W4386422191 hasConcept C2775975398 @default.