"Our findings showed that metformin in combination with quercetin synergistically inhibited the growth, migration and invasion of both PC-3 and LNCaP cells. Co-treatment of these two agents induced more apoptosis than single agent treatment."
...
The case for multiple agents is that the cancer might respond to the first by activating signaling pathways that the others inhibit. I tend to avoid mention of pathways such as "VEGF/Akt/PI3K", since I know that some already view my posts as TMI, but with a sense of what each supplement might do, one can tailor daily intake to block known escape paths.
Metformin combined with quercetin synergistically repressed prostate cancer cells via inhibition of VEGF/PI3K/Akt signaling pathway.
Sun S1, Gong F2, Liu P1, Miao Q3.
Author information
1
The Urology Center of the Affiliated Hospital of Medical School, Ningbo University, Ningbo, Zhejiang Province, People's Republic of China.
2
Ningbo Yinzhou No 2. Hospital, Ningbo, Zhejiang Province, People's Republic of China.
3
The Urology Center of the Affiliated Hospital of Medical School, Ningbo University, Ningbo, Zhejiang Province, People's Republic of China. Electronic address: drmiaoqilong@163.com.
Abstract
The aim of present study was to examine whether metformin in association with quercetin has any synergistically anti-tumor effects on prostate cancer. Our findings showed that metformin in combination with quercetin synergistically inhibited the growth, migration and invasion of both PC-3 and LNCaP cells. Co-treatment of these two agents induced more apoptosis than single agent treatment. The co-treatment-induced apoptosis was caspase-dependent and accompanied by the down-regulation of Bcl-2 family members. Our data also indicated that co-treatment of metformin and quercetin strongly inhibited the VEGF/Akt/PI3K pathway. Moreover, these two agents acted synergistically to repress the growth of human prostate cancer cell xenograft in vivo in nude mice. In conclusion, our findings indicate that the combination therapy of metformin and quercetin exerted synergistic antitumor effects in prostate cancers via inhibition of VEGF/Akt/PI3K pathway. Thus, combination treatment of metformin and quercetin would be a promising therapeutic strategy for prostate cancer patients.
Well, I take 2,000 mg Metformin (divided dose), as used in the Swiss intervention study that impressed Dr. Myers, & wouldn't go higher (or lower).
But it's anyone's guess as to the quercetin I would need to add for synergy. I have seen supplements up to 800 mg & am inclined to take two. Nalakrats would say I'm a sissy - that man is fearless!
Very interesting! Thanks for sharing the info, pj. I’ve been on Metformin for two years. Will add the Quercetin now based on the info you provided. Mark
Quercetin is yet another hormetic chemical, similar to sulforaphane - so at low dosage it's an antioxidant and in high dosage a ROS contributor. I'd be curious if the mechanism of action would be similar between the two.
Hi, wondering if there are people taking these combos with Xtandi? There seem to be supplements (and other drugs) which decrease metabolism of Xtandi - a good thing I guess - metform may decrease excretion rate of X resulting in higher serum level; Zolodex ditto; curcumin decreases metabolism of X; doxycycline ditto; quercetin ditto; whereas Xtandi increases metabolism of eg mebendazole, thus reducing its efficacy. I would be good to understand how everything interacts/synergises/counteracts.
I was looking through the Forum for stuff on Metabolic Pathways so please don't say that it's 'too much information' and that maybe you should back off.
We can never have too much info - whether individual members want to take it on board or not is up to them but as far as I am concerned publish and be damned! Please!
Whilst I come from the 'Mix and Match' brigade when it comes to TM, Supplementation and Alternative therapies, surely there needs to be more support for the principle of blocking off Metabolic Pathways to make the disease retreat, or stop it for a period of time, thus forcing it to try (as it will) to formulate a different route - thereby buying more TIME. After all that's what TM is doing.
I, though, have some difficulty in discovering at any given point in time which Pathways are being utilised by the disease.
I have seen suggestions that it could initially be the Fatty Acids and Glutamine Pathways, ultimately handing over to the Glucose Pathway in Advanced PCa but have you any thoughts on the subject, any blood markers, tests etc. to provide evidence one way or the other. Do you know whether this is something that Genetic Screening is geared to reflect?
One of the issues we have, is that without a more targeted approach, we run the risk of over medicating - if indeed we are able to get Scrips for repurposed drugs and buy all the supplements, which in turn may result in resistance further down the line, should it mutate again.
We seem to be increasingly told that our cancers are all different, yet the pathways used for survival are fairly common & have received a lot of research (& many are not unique to PCa.)
I once thought of going back over the polyphenol research from the viewpoint of pathway inhibition. I confess to feeling weary just thinking of the hours involved.
An area that I have neglected is that of gene polymorphisms. For the vitamin D receptor [VDR], I see 118 PCa papers on PubMed. Polymorphisms can affect PCa risk & perhaps survival. At first, I ignored these papers on the basis that tests were not available or affordable. & then there is the question of what one can realistically do with the information.
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