"Long-Term Treatment with Simvastatin Leads to Reduced Migration Capacity of Prostate Cancer Cells"
pubmed.ncbi.nlm.nih.gov/366...
-Patrick
"Long-Term Treatment with Simvastatin Leads to Reduced Migration Capacity of Prostate Cancer Cells"
pubmed.ncbi.nlm.nih.gov/366...
-Patrick
OK, I looked at the article. This is the first sentence:
"Statins have been shown to improve survival of metastatic prostate cancer (mPCa). "
I am confused. Do statins improve the survival of the person or the survival of the cancer?
Scratching my head,
Capt Dave
I haven’t read the whole paper, and hope it’s not out of context, but is states:
Our data showed that the three statins expressed highly diverse short-term effects, with the strongest growth-inhibitory effect from simvastatin in PC-3 cells and almost no effect from rosuvastatin in any of the cell lines.
I read that as simvastatin leading the pack in inhibiting, or opposing, the growth of PCa in PC-3 lines whereas the others had no effect across all the cell lines.
I think you’ll need to read the whole paper to see how much it inhibits growth. If the other two statins have no effect I would look at that.
"Our data showed that the three statins expressed highly diverse short-term effects, with the strongest growth-inhibitory effect from simvastatin in PC-3 cells and almost no effect from rosuvastatin in any of the cell lines. "
That's most significant.
Thanks PJ.......sounds like Simvastatin will slow down PCa.
Patrick, I recall that you’ve been using atorvastatin. Is that correct? Do you plan to switch to simvastatin?
In your opinion, is this research good enough to make a switch to simvistatin.
Myers put me on rosuvastatin because he thought it specifically had the strongest effect on prostate cancer.
But that was not informed by the most current research.
"In the present study, we investigated the short-term effects of three different statins (simvastatin, atorvastatin and rosuvastatin) in various PCa cell lines mimicking androgen-sensitive and -insensitive PCa.
Moreover, we generated three new PCa cell lines (LNCaPsim, ABLsim, PC-3sim) that were cultured with simvastatin over several months.
(What does "cultured with simvastatin" mean with respect to the other two stations?)
Our data showed that the three statins expressed highly diverse short-term effects, with the strongest growth-inhibitory effect from simvastatin in PC-3 cells and almost no effect from rosuvastatin in any of the cell lines.
Long-term treatment with simvastatin resulted in a loss of response to statins in all three cell lines, which was associated with an upregulation of cholesterol and fatty acid pathways as revealed through RNA sequencing.
Despite that, long-term treated cells exhibited diminished spheroid growth and significantly reduced migration capacity per se and to differentiated osteoclasts.
These findings were strengthened by reduced expression of genes annotated to cell adhesion and migration after long-term simvastatin treatment. Notably, mPCa patients taking statins were found to have lower numbers of circulating tumor cells in their blood with reduced levels of PSA and alkaline phosphatase. Our data suggest that long-term usage of simvastatin hampers the metastatic potential of PCa cells and may therefore be a potential therapeutic drug for mPCa."
Maybe this is not quite actionable yet?
I just got this off the internet:
"We elected to use rosuvastatin in an EOD regimen because its half-life of approximately 19 hours is the longest of available statins, and it is the most potent statin at reducing LDL-C levels."
I don't know why Myers preferred Rosuvastatin. Maybe specifically because it is hydrophilic?
Maybe the longer life cycle?
Compelling...
Suitable to our findings, Harshman et al. recently
showed a significant prolonged time to progression (27.5 months vs. 17.4 months) in patients with hormone-sensitive PCa who had a co-medication with a statin at the start of ADT as compared to non-statin users [31]. A reduced risk of progression and even death of PCa in statin users was also demonstrated in other retrospective cohort studies [32,33]. Of note, long-term treatment with simvastatin did not alter the response to chemotherapeutics in our study.
And at the same time, concerning...
Altogether, long-term simvastatin treatment resulted in loss of response to statins and an upregulation of cholesterol and fatty acid synthesis, which let us assume that long-term statin medication would render the tumor cells more aggressive.
Like most of these studies that offer confliction as much as confounding evidence, always a conundrum as well...
Very interesting, I like it... The ideology of keeping things dynamic rather than static! Same as BAT!!! Definitely an excellent path to travel in our journey!
I couldn't tolerate simvastatin. I take omeprazole for GERD/heartburn. The simvastatin completely negated the effect of omeprazole and left me with horrible heartburn. I switched to atorvastatin. I hope it works as well as simvastatin in inhibiting prostate cancer progress.
Be careful if using a high dose of Rosuvastatin. I switched to atorvastatin after this. Why take the chance.
we’ve had this discussion many times. Different studies showed that the most effective were atorvastatin, simvastatin and rousvastain. They didn’t test livalo. Crestor can’t be taken with nubeqa, so I’m content with ator or simva, although, one study has ator about 40% more effective at extending life, than simva, but that was only one study.
There have been a lot of statin cohort studies over the years, but few differentiatiate between the different statin types. This one does:
Statin use and incident prostate cancer risk: does the statin brand matter? A population-based cohort study
A Lustman, S Nakar, AD Cohen, S Vinker
Prostate cancer and prostatic diseases 17 (1), 6-9, 2014
Background:
Statins have known anticarcinogenic effects; evidence for long-term statin use as effective chemoprevention for prostate cancer is inconsistent.
Methods:
We conducted a population-based cohort study to examine the association between statin use and risk of prostate cancer using the Database of Clalit Health Services. A total of 66 741 eligible participants were identified at 1 January 2001 and followed through to 31 December 2009. Cox proportional hazard models were used to compute hazard ratios (HRs) of incident prostate cancer associated with statin therapy controling for patients’ clinical and sociodemographic characteristics.
Results:
A total of 1813 cases of prostate cancer were diagnosed. Statin use was associated with a decreased incidence of prostate cancer, the association was stronger with increasing total dose, hydrophobic statins use and longer periods of treatment. When comparing statin use of over 6 months, this association was strongest for simvastatin (HR 0.51, 95% confidence interval (CI) 0.47–0.56), atorvostatin (HR 0.48, 95% CI 0.33–0.68) and rosuvastatin (HR 0.22, 95% CI 0.08–0.75).
Conclusions:
Our findings suggest that prolonged statin use is associated with a reduced risk of prostate cancer; however, this was not true for all types of statin.
no mention of Pitavastatin
Patrick, I recall that you’ve been using atorvastatin. Is that correct? Do you plan to switch to simvastatin?