Berberine inhibits gastric cancer development and progression by regulating the JAK2/STAT3 pathway and downregulating IL-6.
Berberine (BBR), an alkaloid from Chinese herbal medicines, inhibits the proliferation of various cancers.
Gastric Cancer · LIVING RESEARCH LIBRARY
Ongoing Research for Gastric Cancer Using Advanced Alternative Medicine
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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Research organized by substance and finding
Browse 26 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.
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(-)-Epigallocatechin-3-gallate induced apoptosis by dissociation of c-FLIP/Ku70 complex in gastric cancer cells.
Anti-cancer properties of (-)-epigallocatechin-3-gallate (EGCG) are mediated via apoptosis induction, as well as inhibition of cell proliferation and histone deacetylase.
EGCG targeting STAT3 transcriptionally represses PLXNC1 to inhibit M2 polarization mediated by gastric cancer cell-derived exosomal miR-92b-5p.
EGCG derived from HDI inhibits GC cell proliferation and targets STAT3 to inhibit M2 polarization induced by PLXNC1-mediated exosomes derived from GC cells, which may be a multi-target therapeutic agent for GC cell proliferation and immune microenvironment.
Pancreatic enzyme supplementation after gastrectomy for gastric cancer: a randomized controlled trial
Pancreatic enzyme supplementation improved nutritional-status measures and produced an early quality-of-life improvement after gastrectomy for gastric cancer.
20(S)-ginsenoside Rg3 suppresses gastric cancer cell proliferation by inhibiting E2F-DP dimerization.
Ginsenoside Rg3, a bioactive compound derived from ginseng, has shown promise in inhibiting the growth of various tumor types, including GC.
Ginsenoside Rb1 carbon nanodots: A green and promising nanomedicine for effective gastric cancer treatment.
This remarkable improvement in drug delivery characteristics, combined with the inherent bioactivity of ginsenosides, resulted in potent anti-gastric cancer effects, achieving approximately 74.0 % tumor growth inhibition in vivo with minimal systemic toxicity.
Glutathione peroxidase 2 knockdown suppresses gastric cancer progression and metastasis via regulation of kynurenine metabolism.
Glutathione peroxidase-2 (GPx2) plays various roles in tumor progression and patient survival.
Inhibition of glutathione peroxidase 4 suppresses gastric cancer peritoneal metastasis via regulation of RCC2 homeostasis.
Glutathione peroxidase 4 (GPx4), a key regulator of ferroptosis and redox homeostasis, contributes to progression and influences patient survival.
Melatonin Inhibits Gastric Cancer Cell Proliferation by Suppressing Exosome miR-27b-3p Expression.
In addition to its established role in regulating circadian rhythms and reducing inflammation, melatonin has been demonstrated to possess anti-cancer properties.
Characterization of the landscape of the intratumoral microbiota reveals that Streptococcus anginosus increases the risk of gastric cancer initiation and progression.
Further assays revealed that Streptococcus anginosus (SA) promoted tumour cell proliferation and metastasis while suppressing the differentiation and infiltration of CD8+ T cells.
Feasibility of antibiotic-assisted fecal microbiota transplantation with immunotherapy for esophageal and gastric cancer.
Recent evidence suggests that modulation of the intestinal microbiota may influence the therapeutic response to ICIs.
Gut microbiota-dependent modulation of pre-metastatic niches by Jianpi Yangzheng decoction in the prevention of lung metastasis of gastric cancer.
Mechanically, JPYZ treatment not only prevented the alteration in gut microbiota structure, but also restored the SCFAs content induced by GC cells administration.
Intratumoral microbiome is associated with gastric cancer prognosis and therapy efficacy.
After adjusting for clinical features, prognostic analysis revealed 2 phyla, 14 genera, and 5 species associated with the overall survival of patients with GC.
Mucin-microbiome signatures shape the tumor microenvironment in gastric cancer.
Gastric adenocarcinomas with an intestinal mucin environment or high-level MUC13 expression are associated with poor survival.
The gut microbiome affects response of treatments in HER2-negative advanced gastric cancer.
Patients with higher relative abundance of Lactobacillus possessed higher microbiome diversity and significantly better response to anti-PD-1/PD-L1 immunotherapy and had a trend to achieve better progression-free survival.
A Bioinformatic Assay of Quercetin in Gastric Cancer.
Quercetin (QRC), a flavonoid present in various plants and foods, has demonstrated multiple health benefits, including anticancer properties.
Quercetin induces immunogenic cell death against gastric cancer by targeting NR3C1.
Quercetin significantly reduced the viability and proliferation of gastric cancer cells while promoting apoptosis, ER stress and ICD.
Quercetin Inhibits the Progression of Gastric Cancer Through the AKT/MAPK Signaling Pathway.
In vitro, quercetin dose-dependently inhibited cell proliferation, suppressed migration, and induced apoptosis through increasing Bax while decreasing Bcl-2 expression.
Resveratrol Decreases the Invasion Potential of Gastric Cancer Cells.
The cancer-preventive agent Resveratrol (RSV) [3,5,4'-trihydroxytrans-stilbene] is a widely recognized antioxidant molecule with antitumoral potential against several types of cancers, including prostate, hepatic, breast, skin, colorectal, and pancreatic.
Resveratrol induces apoptosis in SGC-7901 gastric cancer cells.
In conclusion, the results of the present study revealed that resveratrol was able to inhibit viability and induce apoptosis in SGC-7901 cells by suppressing NF-κB activation.
Resveratrol inhibits TGF-β1-induced EMT in gastric cancer cells through Hippo-YAP signaling pathway.
RSVL inhibited the migration, invasion, and growth of gastric cancer cells in concentration- and time-dependent manners.
Resveratrol reverses Doxorubicin resistance by inhibiting epithelial-mesenchymal transition (EMT) through modulating PTEN/Akt signaling pathway in gastric cancer.
Resveratrol (RES) as a kind of phytoalexin has demonstrated anti-tumor functions in breast cancer and myeloid leukemia, but its function and mechanism are still unknown in gastric cancer treatment.
Resveratrol targets mitochondrial USP36-SOD2 to induce autophagy-ferroptosis and inhibit gastric cancer progression.
In vitro, resveratrol significantly inhibited gastric cancer cell proliferation and migration; in vivo, it suppressed tumor growth.
Retraction Note: Sulforaphane induces S-phase arrest and apoptosis via p53-dependent manner in gastric cancer cells.
The study reports retraction Note: Sulforaphane induces S-phase arrest and apoptosis via p53-dependent manner in gastric cancer cells.
Sulforaphane inhibits gastric cancer progression by regulating the YY1/PSMB8-AS1/miR-888-5p/SLC4A7 axis.
Subsequently, using gastric cancer data from TCGA and 11 pairs of clinical samples from gastric and paracancerous tissues, we found that PSMB8-AS1 was upregulated in gastric cancer, and high expression of PSMB8-AS1 was associated with low survival of patients with gastric cancer.
Sulforaphane targets STAT3-CKMT2-AS1 to suppress gastric cancer via PSMB8 downregulation and AIMP1 stabilization.
Sulforaphane (SFN), a natural isothiocyanate, exhibits antitumor activity; however, its molecular mechanisms of action in GC remain unclear.
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