As cancer incidence continues to rise globally, conventional treatments like surgery, chemotherapy, and radiation remain the backbone of care. However, these approaches often come with severe side effects and limited efficacy in certain cancers. This has spurred interest in complementary therapies—particularly plant-based compounds that can provide multi-targeted, lower-toxicity options. Among them, Portulaca oleracea has recently gained attention for its broad-spectrum bioactivity.
Researchers have identified several classes of bioactive compounds in purslane, including:
These compounds were extracted using various solvents (ethanol, water, butanol) and structurally identified through HPLC, LC-MS, and NMR spectroscopy.
Purslane extracts significantly reduce tumor cell growth by downregulating proliferation markers such as PCNA and Ki-67. For example, portulacerebroside E (PCA-E) downregulates HIF-1α via the VHL pathway, while polysaccharides like POL suppress tumor volume in HeLa-bearing mice. Omega-3 fatty acids also disrupt membrane signaling by altering ω-3/ω-6 ratios.
Flavonoids like luteolin and kaempferol inhibit the PI3K/Akt and PKC/MAPK pathways, reducing expression of MMP-2 and MMP-9, which are enzymes crucial for cancer cell migration. PCA compounds enhance TIMP-2 expression to further suppress metastatic potential.
Purslane extracts induce cell cycle arrest at the S and G2/M phases. For example, alcohol extracts downregulate Notch1/Notch2 and β-catenin in HT-29 colon cancer cells, slowing their progression. Sulfated polysaccharide derivatives enhance this effect.
Both the intrinsic (mitochondrial) and extrinsic (death receptor) pathways are involved. Extracts modulate Bax/Bcl-2 ratios, activate Caspase-3, -8, and -9, and reduce mitochondrial membrane potential. These effects were confirmed by flow cytometry and Western blot assays in HepG2 and HeLa cells.
Tumor growth requires angiogenesis, often mediated by VEGF. POL and PCA reduce VEGF and CD34 expression in cervical and breast cancer models, disrupting tumor blood supply. Luteolin targets Wnt signaling to suppress microvessel formation in mouse models.
Polysaccharides activate dendritic cells and T lymphocytes, increasing IL-2, IFN-γ, and CD4+/CD8+ ratios. Purslane also improves thymus and spleen indices in immunosuppressed mice, suggesting systemic immune restoration.
Recent studies indicate that POL induces ferroptosis in ovarian cancer cells by upregulating ACSL4, PTGS2, and CHAC1 while decreasing glutathione levels. This disrupts redox balance and lipid metabolism.
Purslane extracts interfere with glycolysis and amino acid metabolism. Metabolomic studies in liver cancer mouse models show reduced tumor growth and altered profiles of tyrosine, lactic acid, and glycine derivatives.
Purslane helps restore gut microbial balance in colorectal cancer mouse models. It reduces pathogenic bacteria (e.g., E. coli, Salmonella) and increases beneficial genera like Bifidobacterium and Lactobacillus.
To improve bioavailability, researchers have chemically modified purslane polysaccharides through sulfation and selenization. Modified derivatives (e.g., SePSPO-1, POP1-s5) show higher immunomodulatory and cytotoxic activity, as confirmed by MTT and flow cytometry assays.
Early-stage clinical observations suggest that purslane extract may alleviate fatigue, pain, and immune suppression in patients undergoing chemotherapy. When used in combination with 5-fluorouracil, it enhances sensitivity and reduces side effects. However, more randomized controlled trials are needed to confirm efficacy and safety.
Purslane's multi-target, multi-pathway action and low toxicity make it a strong candidate for further development as a complementary anti-cancer therapy—especially in the context of integrative herbal medicine.
