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downregulation of lncRNA NEAT1_2 radiosensitizes hepatocellular carcinoma cells through regulation of miR-101-3p/WEE1 axis
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ATR inhibition synergizes with WEE1 inhibition in TNBC.
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Inhibition of Wee1 by its specific inhibitor MK1775 in combination with sorafenib restored the KRAS mutated cells' response to the multi-target tyrosine kinase inhibitor.
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miR-26b governed temozolomide (TMZ)-resistance-mediate epithelial-mesenchymal transition partly due to governing its target Wee1.
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the data suggest the importance of WEE1 as an enabler of branching vascularisation in colorectal cancer liver metastases.
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WEE1 is over-expressed and could enhance gastric cancer cell proliferation and metastasis
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Wee1 is identified as a novel direct target of miR-194. Ectopic expression of Wee1 at least in part overcomes the suppressive impacts of miR-194 on the malignant phenotypes of human laryngeal squamous cell carcinoma
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High WEE1 expression is associated with non-small cell lung cancer.
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miR-503 could function as an enhancer of radiation responses in laryngeal carcinoma cells by inhibiting WEE1
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Data suggest that SMURF1 is required for S phase progression; SMURF1 promotes ubiquitination-dependent degradation of WEE1; these functions of SMURF1 appear to be linked and may be important in cell proliferation and tumorigenesis. (SMURF1 = SMAD specific E3 ubiquitin protein ligase 1; WEE1 = wee 1 homolog [S pombe] protein)
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Date show that when Wee1 alone is inhibited, Chk1 suppresses CDC45 loading and thereby limits the extent of unscheduled replication initiation and subsequent S-phase DNA damage, despite very high CDK-activity.
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we overexpressed CKS1B in multiple cell lines and found increased sensitivity to PLK1 knockdown and PLK1 drug inhibition. Finally, combined inhibition of WEE1 and PLK1 results in less apoptosis than predicted based on an additive model of the individual inhibitors, showing an epistatic interaction and confirming a prediction of the yeast data.
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Wee1 staining intensity was a predictor of favorable metastasis-free and overall survival compared to strong intensity and no or weak staining
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These results highlight the key role of WEE1 suppression to combat glioblastomas. Moreover, it showed beneficial possibilities of WEE1 suppression with different anticancer approaches for neurological malignancies.
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Wee1 inhibition potentiates Wip1-dependent tumor sensitization effect by reducing levels of Hipk2 kinase, a negative regulator of Wip1 pathway.
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High nuclear expression of WEE1 protein is associated with all glioma grades and types.
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Consistent with these findings, a genome-scale pooled RNA interference screen revealed that toxic doses of MK-1775 are suppressed by CDK2 or Cyclin A2 knockdown. These findings support G2 exit as the more significant effect of Wee1 inhibition in pancreatic cancers.
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WEE1 is regulated at the translational level by CPEB1 and miR-15b in a coordinated and cell-cycle-dependent manner.
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Data show that proto-oncogene protein Mdm2 inactivation successfully protects tumor suppressor protein (p53)-proficient cells against the cytotoxic effects of Wee1 protein inhibition.
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nasopharyngeal carcinoma cells depend on CHK1 and WEE1 activity for growth
