•Thirteen different neoplasms were shown to be susceptible to the antidepressant drug sertraline.
•The mechanisms of action through which sertraline can kill tumor cells are apoptosis, autophagy, and drug synergism.
•Sertraline inhibits TCTP, a tumor protein involved in cell survival pathways, responsible for reducing p53 levels.
•The testing of sertraline in vitro and in vivo resulted in reduced cell counting, shrinking of tumoral masses and increased survival rates.
•Dose extrapolation from animals to humans has shown a therapeutic index of sertraline that could support future clinical trials.
Abstract
Sertraline hydrochloride is a first-line antidepressant with potential antineoplastic properties because of its structural similarity with other drugs capable to inhibit the translation-controlled tumor protein (TCTP), a biomolecule involved in cell proliferation. Recent studies suggest it could be repositioned for cancer treatment. In this review, we systematically map the findings that repurpose sertraline as an antitumoral agent, including the mechanisms of action that support this hypotesis. From experimental in vivo and in vitro tumor models of thirteen different types of neoplasms, three mechanisms of action are proposed: apoptosis, autophagy, and drug synergism. The antidepressant is able to inhibit TCTP, modulate chemotherapeutical resistance and exhibit proper cytotoxicity, resulting in reduced cell counting (in vitro) and shrunken tumor masses (in vivo). A mathematical equation determined possible doses to be used in human beings, supporting that sertraline could be explored in clinical trials as a TCTP-inhibitor.
Written by
Graham49
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I switched my anti-depressant to Sertraline about1 year ago. I had read that it appeared to HELP in apoptosis (PCa stem cells specifically).
My 'other' anti-depressant wasn't doing much, so I asked my GP if he'd let me switch.
He asked me to send him the 'link' to the article I was mentioning.
My GP has also been a huge beneficial resource for me and has allowed me to get some 'off label' drugs as part of my fight against PCa.
He was surprised (about Zoloft) , but noted that the side effects were lessened and the results (anti-depression) might be better - a 'win-win'.
Here's where it gets 'tricky' ....
I am currently 'undetectable' (after a BCR) on bicalutamide mono-therapy. It took ONE year to go from a PSA of 12+ to my last reading of <0.02 - 3 MONTHS ago,
My original Dx (5.5 yrs. ago) was G9, node positive (aka advanced / aggressive) with a PSA in the 3 digits (xxx.xx).
My current medical 'team' are quite surprised at my reaction to this latest round of treatment, seeing as it is NOT the SOC. I appear to be an 'oddball' who has had some impressive success - based on my original Dx and BCR.
The last scans ( CRT / bone ) all show a 'shrinking' of the previous 'hot spots', including a vertebrae (L5). I had a PSMA scan about a year ago - before I started the monotherapy.
I am NOT suggesting that what works for me works for others - but I have learned a LOT from these forums and have used some of the SOCs and some 'alternative' off-label supplements / drugs that have shown some promise.
Time will tell IF I'll remain on this positive track, but keep up digging + researching - there are options, ideas and possibilities out 'there' that MIGHT make a huge difference for some or many of us.
Clinical TRIALS and or published 'Studies' should be part of the research - it's NOT good enough to bounce around taking this and that without knowing what you're doing.
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