Prostate cancer is a common type of cancer in men, with an estimated 32,000 deaths from prostate cancer in the United States alone in 2010. In the past few decades, suppression of androgen (especially testosterone) function has been the main strategy for the treatment of metastatic prostate cancer. Commonly used clinical approaches include surgical denervation (because the testes are the primary site of androgen synthesis); and chemical denervation, which is the application of drugs that target gonadotropin-releasing hormones to regulate androgen synthesis. However, although denervation is effective in most patients with this disease at the beginning of treatment, often denervation resistance occurs in tumors as treatment progresses. Currently, the standard of care for patients with metastatic desmoplastic-resistant prostate cancer is the paclitaxel anticancer drug docetaxel combined with the steroid prednisone. As a new class of androgen biosynthesis inhibitors, abiraterone acetate has attracted attention because it was recently approved by the U.S. Food and Drug Administration in combination with prednisone for the treatment of metastatic desmoid-resistant prostate cancer previously treated with docetaxel chemotherapy. It is believed that the clinical findings of this drug confirm that androgen signaling pathways play an important role in advanced destructive-resistant prostate cancer. Mechanism of action Testosterone, and its potent metabolite dihydrotestosterone, bind to androgen receptors (which belong to the family of cytosolic receptors), which in turn promote the broad expression of genes associated with prostate cell growth and survival. However, depot does not completely inhibit androgen production, as adrenal and prostate tumors can also produce small amounts of androgens. It has been found that denervation resistance in prostate cancer cells involves alterations in multiple androgen receptor signaling pathways, with persistent activation of androgen receptor signaling through androgen denervation levels. Assuming sustained specific inhibition of cytochrome P450 C17 (CYP17), a key enzyme in androgen biosynthesis, a therapeutic effect could be achieved by blocking androgen production in patients with destructive-resistant prostate cancer. Abiraterone acetate is converted in vivo to abiraterone, which is active and selectively inhibits CYP17, thereby reducing testosterone and other androgen levels in patients with prostate cancer. Clinical Studies A randomized, placebo-controlled clinical study of 1195 patients with metastatic decompensated resistant prostate cancer previously treated with docetaxel chemotherapy evaluated the efficacy and safety of abiraterone acetate. These patients were randomized in a 2:1 ratio to receive abiraterone acetate (1000 mg orally) and placebo once daily in combination with bonisone (5 mg twice daily) until disease progression or discontinuation due to the development of unacceptable toxic effects. The primary endpoint of this study was overall survival, with secondary endpoints of time to specific antigen (PSA) re-elevation, progression-free survival, and PSA response rate. Of the deaths in this study, 42% (333/797) were in the abiraterone acetate treatment group and 55% (219/398) were in the placebo group. This indicates that abiraterone acetate reduced the risk of death by 35% compared to placebo. The median overall survival time was 14.8 months in the abiraterone acetate group and 10.9 months in the placebo group. In addition, the time to PSA re-elevation, median progression-free survival and PSA response rates were 10.2 months and 6.6 months, 5.6 months and 3.6 months, and 29% and 6% in the two groups, respectively. For the most recent survival analysis (excluding 775 deaths), median overall survival was 15.8 months and 11.2 months in the abiraterone acetate and placebo groups, respectively. Academic Discussion Researchers from the Division of Genitourinary Medical Oncology at The University of Texas M. D. Anderson Cancer Center who participated in the clinical study of abiraterone acetate noted that conventional wisdom once agreed that the application of endocrine agents was the best treatment for prostate cancer and that chemotherapeutic agents should be preferred for metastatic desmoid-resistant prostate cancer, even when the disease is initiated early. However, although docetaxel and cabazitaxel are effective in patients with metastatic desmoplastic-resistant prostate cancer, premature administration of chemotherapy does not improve patient prognosis. The results of numerous preclinical studies over the past 15 years have provided the rationale for a shift in the direction of prostate cancer treatment from endocrine to paracrine. More recently, the hypothesis has been proposed that the shift from endocrine to paracrine therapy involves the development of a “microenvironmental dependency” that is primarily influenced by networks including androgen signaling and osteogenic pathways. The development of a microenvironment-dependent state is strongly associated with distal metastasis and predicts disease recurrence after surgery and disease progression after denervation and chemotherapy. Mechanisms associated with altered androgen signaling in this process include altered androgen metabolite biosynthesis, abnormal androgen receptor activity, and disruption of androgen signaling with other mesenchymal-epithelial interaction pathways. Recently developed relevant drugs have begun to take into account mechanisms that target the androgen signaling pathway. The survival benefit to patients demonstrated in phase III clinical trials of a new class of androgen biosynthesis inhibitor, abiraterone acetate, confirms that the androgen signaling pathway plays an important role in advanced denervation-resistant prostate cancer. In the past 2 years, the new prostate cancer drugs sipuleucel-T, cabazitaxel, and abiraterone acetate have been approved for their survival benefits in patients with metastatic denervation-resistant prostate cancer in phase III trials. There is a need to determine the optimal therapeutic area for these drugs so that they can be optimally effective. Today, it is important to look not only at the benefit of the drugs in terms of survival time, but also at the sequencing of their use or the effects of their combination, so that the patient receives the maximum therapeutic benefit. Therefore, it is important to explore more individualized treatment options for prostate cancer treatment and to determine treatment guidelines based on the results in order to significantly prolong the survival of patients.