Metformin combined with quercetin synergistically repressed prostate cancer cells via inhibition of VEGF/PI3K/Akt signaling pathway

Sun, Shuben; Gong, Fanger; Liu, Ping; Miao, Qun

doi:10.1016/j.gene.2018.04.045

Cited by 76 publications

(43 citation statements)

References 36 publications

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“…Phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway can be activated by growth factors and angiogenesis inducers such as VEGF and angiopoietins (32). A plenty of studies have demonstrated that PI3K/Akt was the main downstream cellular pathway mediating the biological effects of VEGF/VEGFR-2 (33)(34)(35), the VEGF/PI3K/Akt signaling pathway plays an significant role in various cellular processes including proliferation, migration, invasion, and metastasis (34,36). Vascular endothelial growth factor receptor-2 tyrosine kinase inhibitors such as apatinib might block the combination of VEGF and VEGFR-2, leading to suppressing the downstream PI3K/Akt signaling pathway by interrupting the phosphorylation of PI3K and Akt.…”

Section: Discussionmentioning

confidence: 99%

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

et al. 2020

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Background: The application of apatinib is immensely limited by its acquired drug resistance. This research investigates whether cordycepin, a component from Cordyceps could synergize with apatinib to improve its anticancer effect on non-small cell lung cancer (NSCLC) cells. Methods: The NSCLC cell lines A549, PC9, and H1993, and human bronchial epithelial (HBE) cell line Bears-2B were used in this study. Cell counting kit 8, colony formation assays, wound healing assay, transwell assay, and flow cytometry analysis were performed to assess the cell viability, the migration ability, and invasion ability of the cells. Kyoto encyclopedia of genes and genomes (KEGG), western blotting and molecular docking was applied to analyze the possible pathways affected by cordycepin. Results: The combination of cordycepin and apatinib in a ratio of 5:1 synergistically reduced proliferation of NSCLC cells, inhibited cell migration and invasion, increased cell apoptosis by altering cell cycle in NSCLC A549 and PC9 cells. The VEGF/PI3K/Akt pathway was inhibited after treatment with cordycepin and apatinib. Conclusion: Our findings demonstrated that the combination of cordycepin and apatinib has synergistically anticancer effect on NSCLC cells by down-regulating VEGF/PI3K/Akt signaling pathway. This result indicated that cordycepin and apatinib could be a promising drug combination against NSCLC.

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Section: Discussionmentioning

confidence: 99%

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

et al. 2020

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“…In a human hepatoma cell line, quercetin induced apoptosis via caspase activation, regulation of Bcl-2, and inhibition of PI-3-kinase/Akt and extracellular-signal-regulated kinase (ERK) pathways [118]. Quercetin was also able to suppress cancer cell proliferation due to inhibition of PI3K/Akt pathway [119]. Flavonol kaempferol, a phytoestrogen [120], induced intrinsic apoptosis in A2780/CP70, A2780wt and OVCAR-3 cell lines.…”

Section: Flavonoids In Apoptosismentioning

confidence: 99%

Flavonoids as Anticancer Agents

et al. 2020

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Flavonoids are polyphenolic compounds subdivided into 6 groups: isoflavonoids, flavanones, flavanols, flavonols, flavones and anthocyanidins found in a variety of plants. Fruits, vegetables, plant-derived beverages such as green tea, wine and cocoa-based products are the main dietary sources of flavonoids. Flavonoids have been shown to possess a wide variety of anticancer effects: they modulate reactive oxygen species (ROS)-scavenging enzyme activities, participate in arresting the cell cycle, induce apoptosis, autophagy, and suppress cancer cell proliferation and invasiveness. Flavonoids have dual action regarding ROS homeostasis—they act as antioxidants under normal conditions and are potent pro-oxidants in cancer cells triggering the apoptotic pathways and downregulating pro-inflammatory signaling pathways. This article reviews the biochemical properties and bioavailability of flavonoids, their anticancer activity and its mechanisms of action.

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“…In animal studies, quercetin inhibited tumor growth and improved the lifespan of tumor-bearing mice 23 , 24 . Furthermore, the anticancer effects of quercetin are enhanced in combination with chemotherapeutic agents or other drugs 25 – 27 .…”

Section: Introductionmentioning

confidence: 99%

Inhibition of glioblastoma cell proliferation, invasion, and mechanism of action of a novel hydroxamic acid hybrid molecule

et al. 2018

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Glioblastoma multiforme is one of the most aggressive brain tumors and current therapies with temozolomide or suberoylanilide hydroxamic acid (SAHA, vorinostat) show considerable limitations. SAHA is a histone deacetylase (HDAC) inhibitor that can cause undesirable side effects due to the lack of selectivity. We show here properties of a novel hybrid molecule, sahaquine, which selectively inhibits cytoplasmic HDAC6 at nanomolar concentrations without markedly suppressing class I HDACs. Inhibition of HDAC6 leads to significant α-tubulin acetylation, thereby impairing cytoskeletal organization in glioblastoma cells. The primaquine moiety of sahaquine reduced the activity of P-glycoprotein, which contributes to glioblastoma multiforme drug resistance. We propose the mechanism of action of sahaquine to implicate HDAC6 inhibition together with suppression of epidermal growth factor receptor and downstream kinase activity, which are prominent therapeutic targets in glioblastoma multiforme. Sahaquine significantly reduces the viability and invasiveness of glioblastoma tumoroids, as well as brain tumor stem cells, which are key to tumor survival and recurrence. These effects are augmented with the combination of sahaquine with temozolomide, the natural compound quercetin or buthionine sulfoximine, an inhibitor of glutathione biosynthesis. Thus, a combination of agents disrupting glioblastoma and brain tumor stem cell homeostasis provides an effective anti–cancer intervention.

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Metformin combined with quercetin synergistically repressed prostate cancer cells via inhibition of VEGF/PI3K/Akt signaling pathway

Cited by 76 publications

References 36 publications

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway

Flavonoids as Anticancer Agents

Inhibition of glioblastoma cell proliferation, invasion, and mechanism of action of a novel hydroxamic acid hybrid molecule

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