New meta-analysis below.
This analysis of published PCa-Metformin studies is specifically to survival (which is why I began using Metformin >5 years ago).
I am not aware of statistics, but I expect that most Metformin users with PCa are diabetic. I know of a number of non-diabetic men with PCa (including myself) who were initially turned down by their GPs.
A few years ago, Life Extension suggest that Metformin might be a drug that everyone should be on as they age. LEF members received considerable resistance from their doctors, so LEF began pushing an over-the-counter AMPK activator [2] as an alternative. See also Swanson's AMPK Stimulator [3]. {AMPK = 5' adenosine monophosphate-activated protein kinase [4]}
{The role of AMPK in PCa is too big a topic to cover here.}
It might be a long while before we see a PCa survival study that reports on non-diabetic Metformin users, & also AMPK activator users.
...
"DISCUSSION
Principal findings of this study
This present systematic review and meta-analysis
represents the most comprehensive review to date on the association between metformin use and PCa prognosis by
including 13 cohort studies enrolling 177,490 individuals.
Overall, we find that metformin intake has a trend to
improve survival for patients with PCa in terms of OS {overall survival},
CSS {cancer-specific
survival} and RFS {recurrence-free survival}. Significant CSS benefits were noted in
studies conducted in USA/Canada with prospective, large
sample size, multiple-centered study design."
...
For those interested in potential mechanisms, the following is included (without helpful comments):
"Potential mechanisms
Several potential mechanisms for the antineoplastic
action of metformin have been noted.
Metformin, as an activator of AMP-activated protein
kinase (AMPK), may play an important role in cancer
metabolism. AMPK pathway is reported to inhibit mTOR
signaling and result in fatty acid synthesis, inhibition of
protein synthesis, and cell proliferation [26]. It has been
reported that fatty acid synthase is overexpressed in PCa,
breast cancer and pancreatic cancer, which is necessary for de novo fatty acid biosynthesis and malignant
phenotype. AMPK activation can reduce the expression
of fatty acid synthase and acetyl-CoA carboxylase, which
diminishes the metabolization and growth of PCa cells
[27]. Zadra et al [28] also suggested that suppression of
de novo lipogenesis affected AMPK-mediated inhibition
of PCa growth. In addition, metformin plays a role in
cyclin-dependent kinase (CDK) induction of autophagy,
cell cycle arrest, and apoptosis. Metformin can reduce
the activity of cyclin D1, leading to the inhibition of
PCa cell lines [29]. It has been verified that the cyclin
D1 pathway can serve as a regulator of androgen dependent
transcription and cell cycle progression in
PCa cells [30]."
...
{I came across the paper by chance - it hadn't appeared in my daily PubMed search for new PCa papers. Turns out that the journal OncoTarget has been delisted by MedLine. Papers going back to Vol. 1 (2010) are still available, but nothing since August.
OncoTarget is a peer-reviewed open-access publication, where authors pay to be published. Presumably, there is a question as to how much peer-reviewing occurs. The authors submitted the paper before the delisting & may now regret their choice of journal.}
-Patrick
[1] impactjournals.com/oncotarg...
[2] lifeextension.com/Vitamins-...
Statin Use May Reduce Mortality in High-Risk Prostate Cancer 
Study: Cannabidiol Inhibits the Proliferation and Invasiveness of Prostate Cancer Cells 
Vasectomy and Risk of Prostate Cancer: A Systematic Review and Meta-Analysis. significant association between vasectomy and any-grade PCa 
