Photoactivation of Akt1/GSK3β Isoform‐Specific Signaling Axis Promotes Pancreatic β‐Cell Regeneration

Huang, Lei; Jiang, Xiaoxiao; Gong, Longlong; Xing, Da

doi:10.1002/jcb.25133

Cited by 15 publications

(8 citation statements)

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“…GSK3 has been demonstrated to be a downstream target of multiple signaling pathways and is associated with cell proliferation and cell cycle regulation ( 17 ). It has been reported that stimulation of GSK3 negatively regulates β-cell function by maintaining the sub-cellular localization and stability of Pdx1 ( 18 ).…”

Section: Insulin Signaling Pathwaysmentioning

confidence: 99%

Cellular signaling pathways regulating β‑cell proliferation as a promising therapeutic target in the treatment of diabetes (Review)

2018

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It is established that a decrease in β-cell number and deficiency in the function of existing β-cells contribute to type 1 and type 2 diabetes mellitus. Therefore, a major focus of current research is to identify novel methods of improving the number and function of β-cells, so as to prevent and/or postpone the development of diabetes mellitus and potentially reverse diabetes mellitus. Based on prior knowledge of the above-mentioned causes, promising therapeutic approaches may include direct transplantation of islets, implantation and subsequent induced differentiation of progenitors/stem cells to β-cells, replication of pre-existing β-cells, or activation of endogenous β-cell progenitors. More recently, with regards to cell replacement and regenerative treatment for diabetes patients, the identification of cellular signaling pathways with related genes or corresponding proteins involved in diabetes has become a topic of interest. However, the majority of pathways and molecules associated with β-cells remain unresolved, and the specialized functions of known pathways remain unclear, particularly in humans. The current article has evaluated the progress of research on pivotal cellular signaling pathways involved with β-cell proliferation and survival, and their validity for therapeutic adult β-cell regeneration in diabetes. More efforts are required to elucidate the cellular events involved in human β-cell proliferation in terms of the underlying mechanisms and functions.

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Section: Insulin Signaling Pathwaysmentioning

confidence: 99%

Cellular signaling pathways regulating β‑cell proliferation as a promising therapeutic target in the treatment of diabetes (Review)

2018

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“…The STRING database was applied to perform PPI network analysis on the 51 selected intersected targets, among which the top 3 targets of degree were AKT1, CASP3, and IL6. AKT1, a member of the serine/tyrosine family, is a critical downstream molecule in the PI3K/AKT/mTOR pathway, and is involved in significant immune pathways such as cytokine activation [ 30 ]. An existing report unveiled that the deletion of AKT1 accelerated kidney fibrosis through the activation of TGF-β1/STAT3 signaling in a mouse model of unilateral ureteral obstruction (UUO) [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Forecast and verification of the active compounds and latent targets of Guyuan decoction in treating frequently relapsing nephrotic syndrome based on network pharmacology

et al. 2023

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Background Our study majorly utilizes network pharmacology combined with molecular docking to explore the latent active components and associated pivotal targets of Guyuan Decoction (GYD) in the treatment of frequently relapsing nephrotic syndrome (FRNS). Methods All active components and latent targets of GYD were retrieved from TCMSP database. The target genes for FRNS in our research were obtained from the GeneCards database. The drug-compounds-disease-targets (D-C-D-T) network was established using Cytoscape 3.7.1. STRING database was applied to observe the protein interaction. Pathway enrichment analyses (GO and KEGG) were conducted in R software. Moreover, molecular docking was employed to further validate the binding activity. MPC-5 cells were treated with adriamycin to mimic FRNS in vitro and to determine the effects of luteolin on modeled cells. Results A total of 181 active components and 186 target genes of GYD were identified. Meanwhile, 518 targets related to FRNS were also revealed. Based on the intersection using a Venn diagram, 51 common latent targets were recognized to be associated with active ingredients and FRNS. Additionally, we identified the biological processes and signaling pathways involved in the action of these targets. Molecular docking analyses illustrated that AKT1 and CASP3 interacted with luteolin, wogonin, and kaempferol, respectively. Moreover, luteolin treatment enhanced the viability but inhibited the apoptosis of adriamycin-treated MPC-5 cells via regulating AKT1 and CASP3. Conclusion Our study forecasts the active compounds, latent targets, and molecular mechanisms of GYD in FRNS, which helps us to understand the action mechanism of GYD in FRNS comprehensive treatment.

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“…LPLI suppresses tumor growth and induces apoptosis in ASTC-a-1 human lung adenocarcinoma cells [ 7 ]. These results demonstrate that the antitumor effects of LPLI treatment involve in the induction of apoptosis [ 8 , 9 ], which is the preferred way to manage cancer.…”

Section: Introductionmentioning

confidence: 93%

RelA-Mediated BECN1 Expression Is Required for Reactive Oxygen Species-Induced Autophagy in Oral Cancer Cells Exposed to Low-Power Laser Irradiation

Shu¹,

Chang²,

Wu³

et al. 2016

PLoS ONE

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Low-power laser irradiation (LPLI) is a non-invasive and safe method for cancer treatment that alters a variety of physiological processes in the cells. Autophagy can play either a cytoprotective role or a detrimental role in cancer cells exposed to stress. The detailed mechanisms of autophagy and its role on cytotoxicity in oral cancer cells exposed to LPLI remain unclear. In this study, we showed that LPLI at 810 nm with energy density 60 J/cm2 increased the number of microtubule associated protein 1 light chain 3 (MAP1LC3) puncta and increased autophagic flux in oral cancer cells. Moreover, reactive oxygen species (ROS) production was induced, which increased RelA transcriptional activity and beclin 1 (BECN1) expression in oral cancer cells irradiated with LPLI. Furthermore, ROS scavenger or knockdown of RelA diminished LPLI-induced BECN1 expression and MAP1LC3-II conversion. In addition, pharmacological and genetic ablation of autophagy significantly enhanced the effects of LPLI-induced apoptosis in oral cancer cells. These results suggest that autophagy may be a resistant mechanism for LPLI-induced apoptosis in oral cancer cells.

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Photoactivation of Akt1/GSK3β Isoform‐Specific Signaling Axis Promotes Pancreatic β‐Cell Regeneration

Cited by 15 publications

References 50 publications

Cellular signaling pathways regulating β‑cell proliferation as a promising therapeutic target in the treatment of diabetes (Review)

Cellular signaling pathways regulating β‑cell proliferation as a promising therapeutic target in the treatment of diabetes (Review)

Forecast and verification of the active compounds and latent targets of Guyuan decoction in treating frequently relapsing nephrotic syndrome based on network pharmacology

RelA-Mediated BECN1 Expression Is Required for Reactive Oxygen Species-Induced Autophagy in Oral Cancer Cells Exposed to Low-Power Laser Irradiation

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