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 80 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.
Bioinforma-tics analysis showed that the survival rate of patients with extracapsular spread and metastasis in tumor tissues was lower than that of patients without such phenomena (P<0.05).
Artesunate (ART) a derivative of artemisinin, used in Traditional Chinese Medicine, shows anti-tumor activity extending over a broad spectrum of human cancers.
The mechanism of dihydroartemisinin (DHA) inhibiting the migration and invasion of glioma in an ROS-DSB-dependent manner has been revealed.
This study investigated the role and mechanism of galectin-1 within the GC microenvironment in promoting PM and evaluated the inhibitory effects of dihydroartemisinin(DHA) on galectin-1-induced PM.
Dihydroartemisinin (DHA), an artemisinin derivative extracted from the traditional Chinese medicinal herb Artemisia annua, has the potential to suppress head and neck squamous cell carcinoma (HNSCC) progression.
It has been demonstrated from previous studies about the killing effect of dihydroartemisinin (DHA) on glioblastoma, which involves multiple aspects: cytotoxicity, cell cycle arrest and invasion inhibition.
In clinic, the berberine (BBR) compound has widely been in NPC therapy to decrease metastasis and disease recurrence, and BBR was documented as a main component with multiple anti-NPC effects.
In previous studies, we demonstrated that berberine inhibits glioma cell proliferation by inhibiting mutant p53 protein and promoting mitochondrial damage.
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.
Here, we showed that BBR exerted its anti-metastasis role by inhibiting system Xc-/GSH/GPX4 axis-driven ferroptosis.
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 treatment significantly inhibited the proliferation and invasion of C6661-IR cells, promoted apoptosis and enhanced radiosensitivity.
Finally, AKT, MMP14, E-cadherin and N-cadherin were analyzed by Western blot assay to confirm whether curcumin could inhibit bladder cancer by inhibiting invasion via AKT/MMP14 pathway.
In conclusion, the results of the present study demonstrated that curcumin was able to reverse HGF-induced EMT, possibly by inhibiting c-Met expression in oral cancer cells, providing a strong basis for the development of novel approaches for the treatment of oral cancer.
Curcumin significantly accelerated cell apoptosis, and inhibited cell proliferation and invasion in LoVo and HCT-116 cells.
Modern pharmacological studies have found that curcumin has many kinds of pharmacological activities of anti-inflammatory, anti-tumor, anti-angiogenesis, anti-metastasis and anti-multidrug resistance.
Curcumin (20 and 30 μM) inhibited the proliferation, migration and invasion, and promoted the apoptosis of MCF-7 and MDA-MB-231 cells.
Comparative analyses of three anti-cancer natural products, including curcumin, gingerol, and allicin, revealed that only curcumin robustly inhibited HNSCC cell proliferation, invasion, and cancer stem cell self-renewal, with potency comparable or superior to cisplatin.
This multimodal mechanism significantly inhibited primary tumor growth and metastasis in HNC models, while extending survival.
In conclusion, we have shown that nano micelles curcumin effectively prevent proliferation, and invasion of GBM cells through perturbation of Wnt/β-catenin and NF-κB pathways, suggesting further investigations on the therapeutic application of this novel anticancer drug in in vivo models.
Experimental analyses revealed that PSMG1 was markedly upregulated in bladder cancer (BCa), progressively upregulated from normal tissue to MIBC, and PSMG1 silencing reduced cell proliferation, invasion, and clonogenic capacity in vitro, while attenuating tumor growth in vivo.
Because it has chemopreventive and anti-invasive effect against various cancer cells, EGCG can be used to inhibit proliferation and invasion of cholangiocarcinoma (CCA) cells.
The results revealed that EGCG considerably inhibited the migration abilities of three NPC cells.
Here, cellular experiments showed that EGCG significantly promoted OS cell apoptosis and inhibited proliferation, migration and invasion, and cell and animal experiments demonstrated that the Wnt/β-catenin pathway played an indispensable role in the antitumour effects of EGCG.
Ginsenosides can reportedly induce tumor cell death, invasion, and metastasis; however, poor water solubility, low oral absorption rate, and rapid blood clearance limit their clinical application.
Ginsenoside Rd inhibits tongue cancer cell migration and invasion via the H19/miR-675-5p/CDH1 axis.
We aim to study whether ginsenoside Rg5 exerted inhibitory effects on crucial aspects of glioma stem cells, including cell viability, tumor initiation, invasion, self-renewal ability, neurosphere formation, and stemness.
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.
Glutathione peroxidase-2 (GPx2) plays various roles in tumor progression and patient survival.
Glutathione peroxidase 4 (GPx4), a key regulator of ferroptosis and redox homeostasis, contributes to progression and influences patient survival.
Tumor growth and metastasis were markedly suppressed in melatonin alone and in combination with doxorubicin.
Restoration of these factors suppressed glioma cell proliferation, migration and invasion while promoting apoptosis.
We found that melatonin treatment significantly reduced the viability and colony formation ability of SCC-25 cells, impairing cell migration and invasion.
Melatonin and taxol clearly decreased cell migration and invasion at low doses, especially those matching the normal physiological concentration at night.
The mechanisms of action of melatonin against tumor progression involve cellular apoptosis, antimetastatic activity, antioxidant and mutagenic effects, antiangiogenic activity, and the restoration of cancer immune surveillance.
Overall, The beneficial roles of melatonin in retarding OSCC metastasis were implicated with inhibition of TANs.
Little is known about the role of mitochondria in the survival and metastatic ability of CSCs.
The results of this study show that melatonin in the presence of EGF does not show the anti-cancer properties previously described for this substance.
Here, we integrated multiomics integration of 16S rRNA sequencing and circulating microbial DNA (cmDNA) profiling to investigate intratumoral microbiome dynamics in osteosarcoma pulmonary metastasis.
Further assays revealed that Streptococcus anginosus (SA) promoted tumour cell proliferation and metastasis while suppressing the differentiation and infiltration of CD8+ T cells.
Higher tumor microbial α diversity was associated with lymph node metastasis and predicted shortened overall survival (OS) and recurrence-free survival (RFS).
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.
Gut microbiota has been shown to initiate tumorigenesis and cancer metastasis in multiple cancer types.
In vitro experiments showed that GCDC inhibited breast cancer cell proliferation, migration, and invasion while inducing cell death.
Mechanically, JPYZ treatment not only prevented the alteration in gut microbiota structure, but also restored the SCFAs content induced by GC cells administration.
PEA suppressed EJ and T24 BC cell migration, invasion, and proliferation, while inhibiting BC development in a BBN-induced mouse model.
Taken together, we show that modulating the gut microbiota through antibiotics, HFD-FMT, or by administering LPS influenced TNBC chemotherapy responsiveness, lung metastasis, and intestinal inflammation.
Further mice investigations demonstrated that TFENs after intravenous (i.v.) injection or oral administration could accumulate in breast tumors and lung metastatic sites, inhibit the growth and metastasis of breast cancer, and modulate gut microbiota.
The relationship between intratumor microbiomes and cervical cancer metastasis, however, remains unclear.
The study reports eRRATUM: Quercetin Inhibits Intrahepatic Cholangiocarcinoma by Inducing Ferroptosis and Inhibiting Invasion via the NF-[Formula: see text]B Pathway.
Quercetin (QCT) and luteolin (LTL) are anticancer herbal compounds.
Multiple lines of evidence have shown that Quercetin has anti-tumor effects, documenting this natural compound exerts its pharmacological effects by targeting a variety of cellular and molecular processes, i.e., apoptosis, metastasis, and autophagy.
Quercetin significantly suppressed the growth and migration of human GBM T98G cells, induced apoptosis, and arrested cells in the S-phase cell cycle.
The migration distance and the number of invasive cells were significantly reduced in the 10 μg/mL quercetin group.
In vitro, quercetin dose-dependently inhibited cell proliferation, suppressed migration, and induced apoptosis through increasing Bax while decreasing Bcl-2 expression.
Our results showed that quercetin markedly suppressed the viability of glioblastoma cells in vitro and in vivo, and significantly inhibited glioblastoma cell migration and invasion.
The results of this study demonstrate reduced signal transduction; increased cell death; reduced cell proliferation, migration, invasion, and vascular endothelial growth factor production in vitro; as well as reduced tumor growth and greater survival times with inhibition of PI3K-AKT-mTOR signaling in a xenograft mouse model.
Rapamycin treatment significantly inhibited OSCC cell proliferation and migration, increased apoptotic cell death, and upregulated cell surface expression of several immune accessory and adhesion molecules, including CD40, CD83, PD-L1, PD-L2, MHC class I, P-selectin, and VCAM-1.
Rsv-AuNPs treatment significantly suppressed proliferation, migration, and invasion of U87 cells (all P < 0.05) and increased the apoptosis rate (P < 0.05).
Resveratrol increases cytotoxic activity in the PE/CA-PJ15 cell line and reduces cell migration capacity, while the combination of resveratrol and irradiation exerts a synergic effect.
Resveratrol inhibited the adhesion, migration, and invasion of OSCC cells in vitro, suggesting that it might serve as a chemopreventive agent for reducing the invasion and metastasis of OSCC.
We found (1) a cell growth inhibition due to an increase in cell distress, which was, in part, due to the involvement of the AKT and caspase-3 pathways, (2) an increase in cellular differentiation due to major gene expression levels of the osteoblastic differentiation genes, (3) an inhibition of IL-6 secretion due to an epigenetic effect on the IL-6 promoter, and (4) an inhibition of OS cells migration related to the decrease in IL-8 secretion levels due to an epigenetic effect on its promoter.
Among the herb-based components, resveratrol has several beneficial effects given its anticancer activities (e.g., anti-angiogenesis, anti-proliferation, anti-metastatic and pro-apoptotic).
Raf-1 kinase inhibitory protein (RKIP) acts as a tumor cell metastasis suppressor and prognostic indicator for survival in various cancers.
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 can affect numerous signaling pathways in vitro, leading to the induction of cell cycle arrest and apoptosis, suppression of proliferation, reduction of inflammatory responses, and the inhibition of angiogenesis and metastasis.
CCK-8, scratch wound, and transwell assays were employed to confirm the inhibitory effect of resveratrol on the proliferation, migration, and invasion of nasopharyngeal carcinoma cells.
RSVL inhibited the migration, invasion, and growth of gastric cancer cells in concentration- and time-dependent manners.
Resveratrol, a polyphenolic compound has been shown to inhibit colorectal cancer metastasis in recent studies.
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.
In vitro, resveratrol significantly inhibited gastric cancer cell proliferation and migration; in vivo, it suppressed tumor growth.
Notably, we provide evidence that resveratrol (REV) strongly inhibits RCP-induced Zeb1 expression through blocking β1 integrin endosome recycling and EGFR activation, leading to suppression of RCP-induced OSCC invasion, demonstrating the important role of RCP in OSCC invasion and its reversion by REV.
In conclusion, the silibinin inhibited the urinary bladder tumor cell proliferation independently of TP53 status; however, cell cycle effects, gene expression changes, and alteration of cell migration are dependent on TP53 status. © 2020 Wiley Periodicals, Inc.
Here, we unravel the effects of sulforaphane (SFN), an isothiocyanate in cruciferous vegetables, on the assembly of pseudopodia and BC metastasis, and its molecular mechanism in the process.
Here, we showed that SFN, including its two isomers of R-SFN and S-SFN, significantly inhibited TGF-β1-induced migration and invasion in breast cancer cells.
Sulforaphane has been demonstrated to exert numerous biological effects, such as neuroprotective, anti-inflammatory, and anticancer effects.
Finally, orthotopic xenografts induced in immunocompetent guinea pigs showed that vitamin C deficiency retained collagen, reduced blood vessel invasion, and affected glomeruloid vasculature formation, all pathological conditions associated with malignancy.
When administered to mice, this nanosystem demonstrates high calcitriol doses in breast tumor cells, significant tumor growth inhibition and antimetastasis capability, as well as good biocompatibility.
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