research
Our research goal
To identify the molecular mechanisms
underlying MCS-C3-mediated apoptotic induction in prostate cancer.
Apoptosis, a programmed cell death, and
cell proliferation have been characterized as fundamental cellular events to
maintain the physiological balance and tissue homeostais of the organism.
Therefor, and imbalance between cell
proliferatio and death through deregulated cell cycle progression and impaired
apoptotic induction is involved in neoplastic cancer formation. Recently,
considerable attention has been focused onth discovery of small chemicals,
including natural products, which exert their anticancer effects by apoptotic
induction in various cancer cells.
Prostate cancer is the most frequently
diagnosed cancer and is the leading cause of cancer death in men.
Despite the initial efficacy of androgen
deprivation therapy, the advanced prostate cancer patients eventually develop
resistance to this therapy and progess to hormone-refactory prostate
cancer(HrPC), form which there is no curative therapy. Therefore, novel
targeted therapeutic approaches have to be developed for the treatment of HRPC
patients.
Androgen, such ad dihydrotestosterone(DHT),
exerts its biological effects by binding to AR. Upon binding to AR, androgen
activates AR through phosphorylation, dimerization and nuclear translocation,
which, in turn, interacts with androgen response elements(ARE) in the promoter
of target genes. Studies on the progression of prostate cancer have indicated
that an increase in AR at transcriptional and translational level is necessary
to convert prostate cancer from a hormone-sensitive to a hormone refractory state, and that
over-expressed AR linked to p21 silencing may be responsible for androgen
independence and resistance to apoptosis. Therefor, AR is a key target form the
treatment of both early stage prostate cancer and HRPC, and the discovery of AR
antagonist should be an important rational approach for the successful
treatment of HRPC.