Alexandre Tavartkiladze, Tolga Sutlu, Gaiane Simonia, Ruite Lou, Nana Okrostsvaridze, Pati Revazishvili, Givi Tavartkiladze
Cancer progression and metastasis are strongly influenced by the disruption of key tumor suppressor proteins, including E-cadherin and PTEN. E-cadherin, an essential cell adhesion molecule, maintains epithelial tissue integrity by preventing epithelial-to-mesenchymal transition (EMT), a process that enables tumor invasion and metastasis. PTEN, a phosphatase and tumor suppressor, controls cell growth and survival by negatively regulating the PI3K/AKT signaling pathway. The loss or inactivation of these proteins in many cancers, including breast, non-small cell lung cancer (NSCLC), and prostate cancer, contributes to increased malignancy, tumor growth, and resistance to apoptosis.
This study investigates the effects of Soulager, a biologically active remedy derived from Polygonum Cuspidatum, on the expression of E-cadherin, PTEN, and apoptotic pathways in aggressive cancer models. Soulager is known to contain bioactive compounds, including resveratrol, flavonoids, melatonin, and polyphenols, which are recognized for their antitumor and antioxidant activities. Using the highly invasive MDA-MB-231 (breast), H1299 (NSCLC), and PC-3 (prostate) cancer cell lines, we evaluated the impact of Soulager across three concentrations—low (10 µg/mL), medium (50 µg/mL), and high (100 µg/ mL).
Our experiments included Western blot analysis, immunofluorescence imaging, and apoptosis assays to monitor the changes in protein expression and the rate of apoptosis following Soulager treatment. We found that Soulager induced a dosedependent increase in apoptosis, particularly at the highest concentration, without compromising the viability of healthy epithelial cells used as controls. Importantly, Soulager treatment significantly upregulated E-cadherin expression in breast and NSCLC cell lines, restoring epithelial integrity and preventing EMT. In prostate cancer cells, PTEN levels were markedly increased, correlating with reduced PI3K/AKT signaling and enhanced apoptosis. These effects suggest that Soulager exerts its antitumor activity by reactivating key tumor suppressor pathways that are often silenced in aggressive cancers.
The results underscore the potential of Soulager as a promising adjunctive therapy in cancer treatment, capable of targeting cancer progression through multiple pathways. Its ability to restore E-cadherin expression, enhance PTEN activity, and promote apoptosis positions it as an attractive candidate for future clinical applications, particularly in cancers where current therapies are insufficient. The selectivity of Soulager toward tumor cells, combined with its minimal cytotoxicity in normal epithelial cells, highlights its safety profile and therapeutic potential. Further in vivo and clinical studies are warranted to validate these findings and explore Soulager’s role in precision oncology