Prostatecancer is relatively critical and major disease among men especially those above40 years old which is death-causing disease (Claudio, 2016). In2004, an estimated 230110 men were diagnosed with prostate cancer and 29900 ofthem were died from this cancer in United States. There are some symptoms forthe patients who suffered from prostate cancer such as frequent urination,blood in urine or semen, burning sensation during ejaculation and urination andetc. In fact, several pre-determinantfactors could be led to prostate cancer initiation such as genetic preferences,inflammation and increased the rate of cell proliferation(Ramalingam, Ramamurthy and Njar, 2017).
Prostate cancer always associated withdysregulation of PI3K/AKT/mTOR pathway caused by genetic, functional, post-translationaland epigenetic modifications (Claudio, 2016). All those pathways are crucial tobe activated which can reduce apoptotic rate, malignant transformation, tumourprogression and metastasis (Claudio, 2016) and establishment of chemo andradio-resistance. Theprocesses that cause the epithelium of normal prostate initiate the cascading,which induce the lesions to form. This directly gives a primary prostate canceror proliferative inflammatory atrophy (PIA) or stimulates an intermediate stageknown as prostatic intraepithelial neoplasia (PIN)(Ramalingam,Ramamurthy and Njar, 2017). As a result, basal cell layers lost the capacity ofproliferation and elevated the activity of luminal secretory cells.
There isscientific proof via molecular and pathological analysis with prostate cancerof human and animal model which indicated that infectious agents, estrogenichormone, age, race, genetic factor and other environmental issues can lead todeterioration in the prostate epithelium and provoke inflammation which mightbe attributed to chronic and recurrent condition of prostate cancer. To treat prostate cancer, androgendeprivation therapy (ADT) through chronic administration ofgonadotropin-releasing hormone, anti-androgenic drugs or their combination isstandard choice of treatment. But, most of the prostate cancer patients relapseand worsen their situation as developing castration resistant prostate cancer(CRPC) within two years. This is because of the amplification or mutation inandrogen receptors which lead to happening of hormones such as progesterone andestrogens activation.
Besides, a sequential of molecular changes in the pathwaycan form androgen-independence prostate cancer and induce cancer progression.Lastly, prostate cancer is supposed thatinitiation and progressive growth of the cancerous cells contributed by cascadeof genetic mutations coupled with epigenetic factors. Androgen receptor, eitherhormone dependent or hormone independent is playing vital role in controllingthe prostate cancer, which have to be further investigated to reduce themortality rate.