Explore positive published findings by substance, cancer biology, treatment interaction and quality-of-life outcome.
Every entry includes the original study title, year, concise finding and a direct PubMed link.
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Browse 33 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked substance to move directly to its corresponding Sunridge page.
This study demonstrated that BBR inhibited HFD-associated CRC directly through modulating gut microbiota-regulated LPC levels, thereby providing a promising microbiota-modulating therapeutic strategy for the clinical prevention and treatment of Western diet-associated CRC.
Berberine was discovered to suppress the proliferation, migration, invasion and clonogenesis of HCT116 cells and SW480 cells.
In conclusion, berberine can reverse the tumorigenic function of colon cancer exosomes and, thus, exert a remarkable suppressive impact against the survival and metastatic ability of colon cancer cells.
Berberine (BBR) has a long history in the treatment of intestinal diseases, which has been reported to inhibit colitis and CRC.
In conclusion, turmeric spice and curcumin may affect the metabolomics of probiotics in intestinal flora which could subsequently influence their anticancer properties.
Deletion of miR-34a and miR-34b/c significantly reduced curcumin-induced apoptosis and senescence, and prevented the inhibition of migration and invasion by curcumin or ectopic NRF2.
Curcumin significantly reduced CRC cell viability, migration and invasion in a dose‑dependent manner.
Curcumin significantly accelerated cell apoptosis, and inhibited cell proliferation and invasion in LoVo and HCT-116 cells.
Curcumin reduced the MACC1 expression, restricted the MACC1-induced proliferation, and was able to reduce the MACC1-induced cell motility as one of the crucial steps for the distant dissemination of the tumor.
DMC-BH, a curcumin analog, has been reported to possess anticancer properties against human gliomas.
Curcumin (CUR), a natural phenolic compound, has been increasingly investigated in several malignancies due to its safe profile and ability to affect a wide range of oncogenic targets.
EGCG induced apoptosis and significantly suppressed the proliferation of colon cancer cells, both in vitro and in vivo.
At week 12, high-dose EGCG treatment significantly reduced the tumor formation rate, total number of tumors, cancerous and non-cancerous tumors, tumor volume, ascites formation, and aberrant crypt foci count.
In this study, we observed the antitumor activity following combinatorial therapy with anti-CTLA4 antibody and epigallocatechin-3-gallate (EGCG) in CT26 tumors.Indeed, EGCG triggered colon cancer cells ICD with the secretion of high-mobility group protein B1 (HMGB1) and the surface expression of calreticulin (CRT) and heat shock protein 70 (HSP70).
The study underscores the potential of nanoparticles in enhancing EGCG delivery for colorectal cancer therapy, aiming to minimize side effects and improve therapeutic outcomes.
These results suggest that fenbendazole may be a potential alternative treatment in 5-fluorouracil-resistant cancer cells, and the anticancer activity of fenbendazole does not require p53 in 5-fluorouracil-resistant SNU-C5 cells.
Ginsenoside Rh1, the main metabolite of a steroidal saponin extracted from Panax ginseng, improves memory and learning and to inhibit tumor growth.
Our results confirm that Rh4 inhibits CRC in a gut microbiota-dependent manner by modulating gut microbiota-mediated bile acid metabolism and promoting the production of UDCA, which further activates the FXR receptor and regulates the TLR4-NF-κB signaling pathway.
To address this challenge, it is vital to identify traditional Chinese medicine components that modulate COX-2 and PD-1/PD-L1: rosmarinic acid (RA) exerts striking inhibitory effect on COX-2, while ginsenoside Rg1 (GR) possesses the potential to suppress the binding of PD-1/PD-L1.
Furthermore, the incorporation of sulforaphane, recognized for its ability to scavenge glutathione, in combination with quercetin and oxaliplatin, substantially suppressed tumor growth in an HCT116 xenograft mouse model.
Insulin pretreatment increased colorectal-cancer-cell susceptibility to several chemotherapies; insulin plus 5-FU also inhibited tumor growth and reduced circulating tumor cells in the reported model.
Insulin increased the growth-inhibitory response of two colorectal-cancer cell lines to 5-fluorouracil and increased the proportion of cells in S phase.
The results demonstrated that ivermectin dose-dependently inhibited colorectal cancer SW480 and SW1116 cell growth, followed by promoting cell apoptosis and increasing Caspase-3/7 activity.
Little is known about the role of mitochondria in the survival and metastatic ability of CSCs.
Furthermore, ECH-reshaped or F.p-colonized microbiota with a high butyrate-producing capability inhibited liver metastasis by suppressing PI3K/AKT signaling and reversing the epithelial-mesenchymal transition (EMT) process, whereas this anti-metastatic ability was abrogated by the butyrate synthase inhibitor heptanoyl-CoA.
Our study demonstrates that probiotics might have great therapeutic potential via modulation of the gut microbiota, and they can exert anti-tumor effects in murine models of CRC with distinct compositions showing differential efficacy depending on the model.
The mechanisms include the change in intestinal microbiota, the metabolic activity of microbiota, the binding and degradation of the carcinogenic compounds present in the lumen of the intestine, the production of compounds with anticancer activity, immune system modification, intestinal dysfunction, changes in host physiology, and inhibition of cell proliferation and induction of apoptosis in cancerous cells.
The results showed that the probiotic powder improved the intestinal barrier integrity, survival rate, and reduced tumor size in CRC mice.
Microbial dysbiosis is a colorectal cancer (CRC) hallmark and contributes to inflammation, tumor growth, and therapy response.
Quercetin (QCT) and luteolin (LTL) are anticancer herbal compounds.
The combination of circ_0001766 or PPP1R3C with rapamycin markedly inhibits CRC cell proliferation and induces apoptosis by reducing rapamycin-induced Myc phosphorylation.
Raf-1 kinase inhibitory protein (RKIP) acts as a tumor cell metastasis suppressor and prognostic indicator for survival in various cancers.
Resveratrol, a polyphenolic compound has been shown to inhibit colorectal cancer metastasis in recent studies.
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