combining THZ1 with a BCL2/BCL-XL inhibitor ABT-263 synergized in impairing cell growth and driving apoptosis. Our results demonstrate CDK7 as a potential target in treating CCA. Combinations of CDK7 inhibition and BCL2/BCL-XL inhibition may offer a novel therapeutic strategy for CCA.
In this study Hep3B and Huh7 cells were infected with two CDK7 shRNAs both of which reduced CDK7 levels. Inhibition of CDK7 impaired proliferation of Hep3B and Huh7 cells in both short-term IncuCyte(R) cell proliferation assays and long-term colony formation assays.
Our studies have demonstrated the essential role of endogenous PRL and CDK7 in the upregulation of PRLR by E2 and provide insights for therapeutic approaches that will mitigate the transcription/expression of PRLR and its participation in breast cancer progression fueled by E2 and PRL via their cognate receptors.
Taken together these findings elucidated a novel mechanism of prostate cancer progression. Thus SNHG1 might serve as a potential target for prostate cancer therapies.
Study demonstrate that CDK7 activity is necessary to maintain the transcriptional program induced by STAT proteins that are activated both aberrantly by mutation and by extracellular cues in T-cell lymphomas.
MYC promotes mRNA cap methylation and protein production of Wnt/beta-catenin signaling transcripts through recruitment of cyclin-dependent kinase 7 (CDK7) and consequently RNMT to gene promoters.
Study shows that triple-negative but not hormone receptor-positive breast cancer cells are exceptionally dependent on CDK7 a transcriptional cyclin-dependent kinase.
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