Prostate cancer is relatively critical and major diseaseamong men especially those above 40 years old which is secondleading cause-related death (Claudio,2016). In 2004, an estimated 230110 men were diagnosed with prostate cancer and29900 of them were died from this cancer in United States.
There are somesymptoms for the patients who suffered from prostate cancer such as frequenturination, blood in urine or semen, burning sensation during ejaculation and urinationand etc. 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-translational and epigenetic modifications (Claudio, 2016). All thosepathways are crucial to be activated which can reduce apoptotic rate, malignanttransformation, tumour progression and metastasis (Claudio, 2016) andestablishment of chemo and radio-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.