Concanavalin A promotes angiogenesis and proliferation in endothelial cells through the Akt/ERK/Cyclin D1 axis

Zhou, Xiaoxia; Wu, Wei‐Yin; Qiang, Haifeng; Xiao, Guosheng; Li, Gang

doi:10.1080/13880209.2021.2013259

Cited by 17 publications

(11 citation statements)

References 46 publications

(39 reference statements)

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“…These findings open a new insight on the ConA potential as an anti-neoplastic agent that might arise different responses in different cells, whether or not by modulating the same signaling pathways. Therefore, the lectin can even be used as an anti-atherosclerosis agent to repair myocardium in acute MI (myocardial infarction) [ 55 ].…”

Section: Molecular Modulation Of Angiogenesis By Conamentioning

confidence: 99%

Concanavalin A as a promising lectin-based anti-cancer agent: the molecular mechanisms and therapeutic potential

et al. 2022

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Concanavalin A (ConA), the most studied plant lectin, has been known as a potent anti-neoplastic agent for a long time. Since initial reports on its capacity to kill cancer cells, much attention has been devoted to unveiling the lectin's exact molecular mechanism. It has been revealed that ConA can bind to several receptors on cancerous and normal cells and modulate the related signaling cascades. The most studied host receptor for ConA is MT1-MMP, responsible for most of the lectin's modulations, ranging from activating immune cells to killing tumor cells. In this study, in addition to studying the effect of ConA on signaling and immune cell function, we will focus on the most up-to-date advancements that unraveled the molecular mechanisms by which ConA can induce autophagy and apoptosis in various cancer cell types, where it has been found that P73 and JAK/STAT3 are the leading players. Moreover, we further discuss the main signaling molecules causing liver injury as the most significant side effect of the lectin injection. Altogether, these findings may shed light on the complex signaling pathways controlling the diverse responses created via ConA treatment, thereby modulating these complex networks to create more potent lectin-based cancer therapy.

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Section: Molecular Modulation Of Angiogenesis By Conamentioning

confidence: 99%

Concanavalin A as a promising lectin-based anti-cancer agent: the molecular mechanisms and therapeutic potential

et al. 2022

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“…Our results suggest that DGS can stimulate the secretion of VEGFA to upregulate VEGFR2, thereby accentuating the binding of VEGFA to VEGFR2. ERK and Akt are located downstream of the VEGF/VEGFR2 pathway, and it has been shown that the phosphorylation of Erk and Akt can further mediate the proliferation and migration of HUVECs, thereby promoting angiogenesis [46]. The results allude that DGS may promote angiogenesis and vasodilation by promoting the phosphorylation of Akt and Erk.…”

Section: Discussionmentioning

confidence: 74%

Investigation Driven by Network Pharmacology on Potential Components and Mechanism of DGS, a Natural Vasoprotective Combination, for the Phytotherapy of Coronary Artery Disease

Zhang

Liu²,

Zong³

et al. 2022

Molecules

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Phytotherapy offers obvious advantages in the intervention of Coronary Artery Disease (CAD), but it is difficult to clarify the working mechanisms of the medicinal materials it uses. DGS is a natural vasoprotective combination that was screened out in our previous research, yet its potential components and mechanisms are unknown. Therefore, in this study, HPLC-MS and network pharmacology were employed to identify the active components and key signaling pathways of DGS. Transgenic zebrafish and HUVECs cell assays were used to evaluate the effectiveness of DGS. A total of 37 potentially active compounds were identified that interacted with 112 potential targets of CAD. Furthermore, PI3K-Akt, MAPK, relaxin, VEGF, and other signal pathways were determined to be the most promising DGS-mediated pathways. NO kit, ELISA, and Western blot results showed that DGS significantly promoted NO and VEGFA secretion via the upregulation of VEGFR2 expression and the phosphorylation of Akt, Erk1/2, and eNOS to cause angiogenesis and vasodilation. The result of dynamics molecular docking indicated that Salvianolic acid C may be a key active component of DGS in the treatment of CAD. In conclusion, this study has shed light on the network molecular mechanism of DGS for the intervention of CAD using a network pharmacology-driven strategy for the first time to aid in the intervention of CAD.

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“…Through analyzing the KEGG map, Akt, Erk1/2, and BAD were taken into measurement. According to the existing references, LY294002, an inhibitor for the PI3K/Akt signaling pathway, has been confirmed that could also inhibit the phosphorylation of Akt, ERK1/2, and BAD in human or rat cells [65][66][67]. Phosphorylated Akt, Erk1/2, and BAD protein were raised by EPO and suppressed by TNF-α or PI3K/ Akt specific inhibitor-LY294002, denoting that the Akt/ Erk1/2/BAD signaling pathway was activated through phosphorylation.…”

Section: Discussionmentioning

confidence: 92%

Erythropoietin Activates Autophagy to Regulate Apoptosis and Angiogenesis of Periodontal Ligament Stem Cells via the Akt/ERK1/2/BAD Signaling Pathway under Inflammatory Microenvironment

Huang

Lei

et al. 2022

Stem Cells International

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Background. Angiogenic tissue engineering is a vital problem waiting to be settled for periodontal regeneration. Erythropoietin, a multieffect cytokine, has been reported as a protective factor for cell fate. According to our previous study, erythropoietin has a significantly angiogenic effect on periodontal ligament stem cells. To further explore its potential effects and mechanism, we studied biological behaviors of periodontal ligament stem cells under inflammatory microenvironment induced by different concentrations (0, 10, 20, 50, and 100 ng/mL) of tumor necrosis factor-α (TNF-α) and examined how different concentrations (0, 5, 10, 20, and 50 IU/mL) of erythropoietin changed biological behaviors of periodontal ligament stem cells. Materials and Methods. Cell Counting Kit-8 was used for cell proliferation assay. Annexin V-PI-FITC was used for cell apoptosis through flow cytometry. Matrigel plug was adopted to measure the angiogenic capacity in vitro. RNA sequencing was used to detect the downstream signaling pathway. Quantitative real-time polymerase chain reaction was conducted to examine mRNA expression level. Western blot and immunofluorescence were applied to testify the protein expression level. Results. Periodontal ligament stem cells upregulated apoptosis and suppressed autophagy and angiogenesis under inflammatory microenvironment. Erythropoietin could activate autophagy to rescue apoptosis and angiogenesis levels of periodontal ligament stem cells through the Akt/Erk1/2/BAD signaling pathway under inflammatory microenvironment. Conclusions. Erythropoietin could protect periodontal ligament stem cells from inflammatory microenvironment, which provided a novel theory for periodontal regeneration.

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Concanavalin A promotes angiogenesis and proliferation in endothelial cells through the Akt/ERK/Cyclin D1 axis

Cited by 17 publications

References 46 publications

Concanavalin A as a promising lectin-based anti-cancer agent: the molecular mechanisms and therapeutic potential

Concanavalin A as a promising lectin-based anti-cancer agent: the molecular mechanisms and therapeutic potential

Investigation Driven by Network Pharmacology on Potential Components and Mechanism of DGS, a Natural Vasoprotective Combination, for the Phytotherapy of Coronary Artery Disease

Erythropoietin Activates Autophagy to Regulate Apoptosis and Angiogenesis of Periodontal Ligament Stem Cells via the Akt/ERK1/2/BAD Signaling Pathway under Inflammatory Microenvironment

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