The active ingredient in cayenne peppers (hot chilli peppers - Capsicum annuum) is capsaicin.
Capsaicin, oddly, has a chemical structure similar to vanillin. There are vanilloid receptors in the body, & capsaicin is a ligand for them, i.e. can potentially bind to the receptors and activate them.
Anandamide, which is the natural ligand for cannabinoid receptors was also discovered to be a ligand for the TRPV1 vanilloid receptor in 2009. It had already been noted that there is a certain amount of promiscuity between ligands & the two families of receptors.
Also in 2009 : "Recently, functional cannabinoid receptor-1 (CB1) and vanilloid receptor-1 (TRPV1) have been described in human prostate and prostate cancer-derived cell lines where the activation of the receptors resulted in inhibition of cellular growth."
"We also found that the expression of CB1 and TRPV1 (both at the protein and mRNA levels) were significantly up-regulated in PCa. However, while the increased expression of TRPV1 showed a proper correlation with increasing PCa tumor grades, such phenomenon was not observed with CB1."
"Our findings strongly argue for ... the CB1 and TRPV1 molecules as well as their ligands may indeed possess a promising future role in the treatment of PCa ..."
It almost seems too good to be true that PCa would over-express these receptors. I suppose that the up-regulation of CB1 & TRPV1 has no relevance in the absence of therapeutic ligands. Anyway, cannabis (THC / CBD) & the cannabinoid receptors are a separate topic - I just wanted to note the connection with vanilloid receptors & their ligands.
 (2006 - Spain) "To study the in vivo effects of capsaicinoids, PC-3 cells were grown as xenografts in nude mice. Subcutaneous injection of either capsaicin or capsazepine (5 mg/kg body weight) in nude mice suppressed PC-3 tumor growth in all tumors investigated and induced apoptosis of tumor cells."
 (2006 - U.S.) "Capsaicin is the major pungent ingredient in red peppers. Here, we report that it has a profound antiproliferative effect on prostate cancer cells, inducing the apoptosis of both androgen receptor (AR)-positive (LNCaP) and -negative (PC-3, DU-145) prostate cancer cell lines associated with an increase of p53, p21, and Bax. Capsaicin down-regulated the expression of not only prostate-specific antigen (PSA) but also AR. Promoter assays showed that capsaicin inhibited the ability of dihydrotestosterone to activate the PSA promoter/enhancer even in the presence of exogenous AR in LNCaP cells, suggesting that capsaicin inhibited the transcription of PSA not only via down-regulation of expression of AR, but also by a direct inhibitory effect on PSA transcription. Capsaicin inhibited NF-κ activation by preventing its nuclear migration. In further studies, capsaicin inhibited tumor necrosis factor-α–stimulated degradation of IκBα in PC-3 cells, which was associated with the inhibition of proteasome activity. Taken together, capsaicin inhibits proteasome activity which suppressed the degradation of IκBα, preventing the activation of NF-κB. Capsaicin, when given orally, significantly slowed the growth of PC-3 prostate cancer xenografts as measured by size"
 (2010 - Canada) I hesitated to include this paper, since it involves a single case. But the patient's PSA doubling time was 4 weeks when he began using "2.5 mL of habaneros chili sauce" ....
 (2010 - Spain) This is the first to report: "In androgen-sensitive prostate cancer cells, capsaicin exerts a biphasic effect, promoting growth at low doses and inducing apoptosis at doses over 200 µM."
 (2015 - Canada) "Radio-sensitizing agents sensitize tumor cells to the lethal effects of radiotherapy (RT) allowing for use of lower doses of radiation to achieve equivalent cancer control, while minimizing adverse effects to normal tissues."
"Athymic mice (n = 40) were inoculated with human LNCaP cells. Once tumors reached 100 mm(3) , animals were randomized into four groups: control, capsaicin alone (5 mg/kg/d), RT alone (6 Gy), and capsaicin and RT."
"In vivo, oral administration of capsaicin with RT resulted in a 'greater than additive' growth delay and reduction in the tumor growth rate greater than capsaicin (P < 0.001) or RT (P < 0.03) alone. Immunohistochemical analysis revealed a reduction in proliferation and NFκB expression, and increase in DNA damage."
 (2015 - Canada) Another mouse study. "Mice in the control group expressed an overall trend of higher-grade disease". "The capsaicin group ... demonstrated a significant reduction ... in the metastatic burden compared to the controls ..."
 (2015 - China) A cell study that reported: "Capsaicin causes inactivation and degradation of the androgen receptor ..."
I didn't think there was much point in looking for a capsaicin clinical trial, but there is one [Ta]. It was supposed to be completed this month, but the status is given as: "This study is not yet open for participant recruitment."
The researcher is: "Dr. Laurence Klotz, Sunnybrook Health Sciences Centre". Dr. Myers has said nice things about him. He was also involved in  & . Also  is a Sunnybrook study.
Full study title: "CAPSAICIN Trial: A Prospective Study of Capsaicin in Subjects With Clinically Localized Prostate Cancer Undergoing Active Surveillance or Radical Prostatectomy".
"Dietary Supplement: Capsaicin Supplement (Cayenne by Nature's Way)
One capsule of the supplement to be taken twice daily.
Other Name: Naturesway Cayenne 40,000 H.U."
I use that brand, but the 100,000 H.U. (heat units) dose:
If you think it strange that there should be a PCa-capsaicin trial, there are 188 other capsaicin trials on ClinicalTrials.gov [Tb].