Recently, the research team led by Professor Jun Pang from the Department of Urology at The Seventh Affiliated Hospital of Sun Yat-sen University discovered that cyclin-dependent kinase 12 (CDK12) can directly phosphorylate the pioneer transcription factor FOXA1, thereby activating a critical new pathway that drives prostate cancer progression. This study is the first to identify a novel phosphorylation site (S234) on the FOXA1 protein and elucidates the complete mechanism by which phosphorylation at this site upregulates the expression of the oncogene MDM2, leading to the degradation of the tumor suppressor protein p53, ultimately promoting tumor cell survival and proliferation. Targeted inhibition of CDK12 can effectively block this pathway, restore p53 function, and induce cancer cell apoptosis, providing a highly promising new strategy for the treatment of advanced prostate cancer. The related findings have been published in Research under the title "CDK12-Mediated Phosphorylation of FOXA1 Promotes Prostate Cancer Progression via the MDM2–p53 Axis."

Overcoming tumor resistance to chemotherapy drugs has long been a challenge for oncology clinicians and researchers. Now, a new study suggests that blocking a key protein, p300, may force damaged cancer cells into a state of uncontrolled transcriptional activity, thereby creating a novel form of cellular stress that can make even chemo-resistant tumors sensitive again to treatment.

The new method developed by Rutgers researchers distinguishes between existing microbes and contamination in tissue samples.