Japanese Rose (Rosa rugosa) as a tool for helping with Cancer (anticancer research)

This study elucidates the anti-colorectal cancer (CRC) mechanism of Rosa rugosa cv. Plena polysaccharide RPP1 against AOM/DSS-induced carcinogenesis. Purified via water extraction and chromatography, RPP1 was characterized as an eight-monosaccharide polymer by HPLC. In CRC mice, RPP1 administration reduced colonic polyp formation and ameliorated colon shortening while normalizing elevated serum IL-1β and TNF-α levels. Integrated multi-omics analyses revealed RPP1 remodeled gut microbiota composition through suppression of pro-inflammatory Bacteroides and Desulfovibrio concurrent with enrichment of beneficial Eubacterium and Muribaculum. These microbial shifts were associated with downregulation of fecal phosphatidylcholine (PC) and lysophosphatidylcholine (LPC), perturbing ether lipid, glycerophospholipid and sphingolipid metabolism. Mechanism correlation analysis further indicated Muribaculum/Clostridium modulation mediated RPP1's regulation of LPC levels. Transcriptomics confirmed suppression of lipid-metabolism pathways alongside activation of NOD-like receptor (NLR) and PPAR immune signaling. Collectively, RPP1 alleviates CRC through multifaceted modulation of gut microbiota, lipidomic remodeling, and immune pathway activation.

The aim of this study was to investigate the effect of a polysaccharide from Rosa rugosa Thunb. on human cervical cancer cells (HCCCs) and the underlying mechanism. Here, a novel Rosa rugosa polysaccharide, named as RRP, was purified from Rosa rugosa petals. RRP consisted of glucose, galacturonic acid, mannose, rhamnose, galactose, arabinose, xylose, and glucuronic acid (molar ratio: 7.78:7.59:4.23:3.22:3.15:1.65:1.00), with Mw of 327.92 kDa. RRP remarkably inhibited cell proliferation, migration, and cell cycle arrest in HeLa and SiHa cells. Furthermore, RRP induced apoptosis by activating the caspase family of proteins and mediating the reactive oxygen species (ROS)-mediated mitochondrial pathway. In addition, RRP was found to dose-dependently induce autophagy, which occurred prior to apoptosis. RRP also primarily induced autophagy-mediated apoptosis in HCCCs via the PI3K/AKT/mTOR pathway. Thus, RRP might serve as a legitimate therapeutic drug candidates against human cervical cancer.