Lipoic Acid vs Cancer

If you are going to do it, make sure it is at least R Lipoic Acid, better yet, Liposomal Lipoic Acid.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10707055/

Abstract

Alpha-lipoic acid (ALA) is a natural antioxidant dithiol compound, exerting antiproliferative and antimetastatic effects in various cancer cell lines.

In our study, we demonstrated that ALA reduces the cell growth of prostate cancer cells LNCaP and DU-145. Western blot results revealed that in both cancer cells, ALA, by upregulating pmTOR expression, reduced the protein content of two autophagy initiation markers, Beclin-1 and MAPLC3. Concomitantly, MTT assays showed that chloroquine (CQ) exposure, a well-known autophagy inhibitor, reduced cells’ viability.

This was more evident for treatment using the combination ALA + CQ, suggesting that ALA can reduce cells’ viability by inhibiting autophagy. In addition, in DU-145 cells we observed that ALA affected the oxidative/redox balance system by deregulating the KEAP1/Nrf2/p62 signaling pathway. ALA decreased ROS production, SOD1 and GSTP1 protein expression, and significantly reduced the cytosolic and nuclear content of the transcription factor Nrf2, concomitantly downregulating p62, suggesting that ALA disrupted p62-Nrf2 feedback loop. Conversely, in LNCaP cells, ALA exposure upregulated both SOD1 and p62 protein expression, but did not affect the KEAP1/Nrf2/p62 signaling pathway.

In addition, wound-healing, Western blot, and immunofluorescence assays evidenced that ALA significantly reduced the motility of LNCaP and DU-145 cells and downregulated the protein expression of TGFβ1 and vimentin and the deposition of fibronectin.

Finally, a soft agar assay revealed that ALA decreased the colony formation of both the prostate cancer cells by affecting the anchorage independent growth. Collectively, our in vitro evidence demonstrated that in prostate cancer cells, ALA reduces cell growth and counteracts both migration and invasion. Further studies are needed in order to achieve a better understanding of the underlined molecular mechanisms.

Keywords: alpha-lipoic acid, prostate cancer cells, ROS, KEAP1, Nrf2, p62, autophagy, cell migration

»In recent decades, several researchers have demonstrated that some nutraceuticals can counteract tumor development and progression by targeting the cancerous cells at multiple levels, such as by promoting cell cycle arrest or apoptosis, suppressing metastasis, invasion, angiogenesis, and by modifying the redox status and the tumor microenvironment Furthermore, some natural bioactive compounds are able to resensitize drug-resistant tumors via their pleiotropic capability to affect different intra-cellular pathways [8]. Interestingly, a recent extensive review by Hitesh Chopra et al. described the main experimental evidence demonstrating the effectiveness of nanonutraceutical approaches in the management of prostate cancer, highlighting that nutraceuticals could represent a promising therapeutic tool in prostate cancer therapy [9].

A growing number of studies have demonstrated that α-lipoic acid (ALA), a natural dithiol compound with marked antioxidant properties, displays antiproliferative and antimetastatic potential in various cancer cell lines by affecting different oncogenic signaling pathways. Furthermore, favorable results emerging from a few preclinical cancer models and human studies with ALA and its derivatives have opened promising scenarios for their potential application either alone or in combination with anticancer drugs in the management of tumors of different origins [10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26].«