Collectively, our results highlight elevated CDK7 expression as a candidate biomarker of poor prognosis in TNBC, and they offer a preclinical proof of concept for combining CDK7 and BCL-2/BCL-XL inhibitors as a mechanism-based therapeutic strategy to improve TNBC treatment.<i></i>.
Exploiting the dependence of cancer cells on transcription can be used as an effective strategy for targeting aggressive and therapeutically recalcitrant tumors.Wang et al. show that inhibiting transcription using THZ1, a small-molecule inhibitor of cyclin-dependent kinase CDK7, induces apoptotic cell death in triple-negative breast cancers.
We conclude that CDK7 mediates transcriptional addiction to a vital cluster of genes in TNBC and CDK7 inhibition may be a useful therapy for this challenging cancer.