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Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE144123 | GEO | 2022/01/10

REPOSITORIES: GEO

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Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hADSCs]

Project description:We implemented transcriptomic analyses of hADSCs treated with Licochalcone A 6 days

2022-01-21 | GSE144122 | GEO

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hippocampus]

Project description:We implemented transcriptomic analyses of hippocampus of 12M mice; These mice with the treatment of Licochalcone A for 30 days.

2022-01-10 | GSE144105 | GEO

Licochalcone A activation of glycolysis pathway has an anti-aging effect on human adipose stem cells.

Project description:Licochalcone A (LA) is a chalcone flavonoid of Glycyrrhiza inflata, which has anti-cancer, antioxidant, anti-inflammatory, and neuroprotective effects. However, no anti-aging benefits of LA have been demonstrated in vitro or in vivo. In this study, we explored whether LA has an anti-aging effect in adipose-derived stem cells (ADSCs). We performed β-galactosidase staining and measured reactive oxygen species, relative telomere lengths, and P16ink4a mRNA expression. Osteogenesis was assessed by Alizarin Red staining and adipogenesis by was assessed Oil Red O staining. Protein levels of related markers runt-related transcription factor 2 and lipoprotein lipase were also examined. RNA sequencing and measurement of glycolysis activities showed that LA significantly activated glycolysis in ADSCs. Together, our data strongly suggest that the LA have an anti-aging effect through activate the glycolysis pathway.

| S-EPMC8714166 | biostudies-literature

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice

Project description:Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice

| PRJNA602830 | ENA

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hippocampus]

Project description:Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hippocampus]

| PRJNA602809 | ENA

Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hADSCs]

Project description:Licochalcone A activate glycolysis by via PI3K / AKT pathway to play an anti-aging effect on adipose stem cells and aging mice [hADSCs]

| PRJNA602840 | ENA

PI3K/Akt signaling transduction pathway, erythropoiesis and glycolysis in hypoxia (Review).

Project description:The purpose of this review is to summarize the research progress of PI3K/Akt signaling pathway in erythropoiesis and glycolysis. Phosphatidylinositol?4,5?bisphosphate 3?kinase (PI3K) is activated by numerous genes and leads to protein kinase B (Akt) binding to the cell membrane, with the help of phosphoinositide?dependent kinase, in the PI3K/Akt signal transduction pathway. Threonine and serine phosphorylation contribute to Akt translocation from the cytoplasm to the nucleus and further mediates enzymatic biological effects, including those involved in cell proliferation, apoptosis inhibition, cell migration, vesicle transport and cell cancerous transformation. As a key downstream protein of the PI3K/Akt signaling pathway, hypoxia?inducible factor (HIF)?1 is closely associated with the concentration of oxygen in the environment. Maintaining stable levels of HIF?1 protein is critical under normoxic conditions; however, HIF?1 levels quickly increase under hypoxic conditions. HIF?1? is involved in the acute hypoxic response associated with erythropoietin, whereas HIF?2? is associated with the response to chronic hypoxia. Furthermore, PI3K/Akt can reduce the synthesis of glycogen and increase glycolysis. Inhibition of glycogen synthase kinase 3? activity by phosphorylation of its N?terminal serine increases accumulation of cyclin D1, which promotes the cell cycle and improves cell proliferation through the PI3K/Akt signaling pathway. The PI3K/Akt signaling pathway is closely associated with a variety of enzymatic biological effects and glucose metabolism.

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PLEKHG2 Promotes NSCLC Cell Growth by Increasing Glycolysis via Activated PI3K/AKT Pathway.

Project description:Purpose: PLEKHG2 is a member of the diffuse B-cell lymphoma family. The function of PLEKHG2 in NSCLC was still unclear. This study aimed to investigate the relationship between the upregulated expression of PLEKHG2 and the prognosis of NSCLC and to revealed its mechanisms. Materials and methods: The expression of PLEKHG2 in NSCLC patients and its relationship with prognosis were first determined by analyzing public databases. Validation was performed in NSCLC cell lines and patient`s tumor tissues. PLEKHG2-silenced H1299 cells and PLEKHG2 overexpressing PC9 cells were constructed and used to validate its function. Glycolysis was evaluated by assaying cellular metabolites, glucose uptake and the expression levels of biomarkers of glycolysis. The relationship of PLEKHG2 and the PI3K/Akt pathway was demonstrated by small molecule inhibitors. The function of PLEKHG2 was evaluated in vivo by a H1299 cell derived xenograft (CDX) model. Results: PLEKEHG2 was highly expressed in NSCLC tissues and associated with poor prognosis. In PLEKHG2 knockdown H1299 cells, ATP and lactate production and glucose uptake were significantly inhibited. The opposite results were observed in PC9 cells with PLEKHG2 overexpression. The increased glycolysis following PLEKHG2 overexpression was abolished by adding the PI3K/AKT pathway inhibitor LY294002, suggesting that PLEKHG2 promotes glycolysis in NSCLC cells via activation of the PI3K/AKT pathway. Finally, we found that PLEKHG2 knockdown inhibited the tumor growth in the H1299 CDX model. Conclusion: PLEKHG2 contributed to NSCLC development by promoting glycolysis via activation of the PI3K/AKT pathway. PLEKHG2 was a potential therapeutic target and biomarker for poor prognosis of NSCLC.

| S-EPMC10647195 | biostudies-literature

Proteasome inhibitors activate autophagy involving inhibition of PI3K-Akt-mTOR pathway as an anti-oxidation defense in human RPE cells.

Project description:The two major intracellular protein degradation systems, the ubiquitin-proteasome system (UPS) and autophagy, work collaboratively in many biological processes including development, apoptosis, aging, and countering oxidative injuries. We report here that, in human retinal pigment epithelial cells (RPE), ARPE-19 cells, proteasome inhibitors, clasto-lactacystin?-lactone (LA) or epoxomicin (Epo), at non-lethal doses, increased the protein levels of autophagy-specific genes Atg5 and Atg7 and enhanced the conversion of microtubule-associated protein light chain (LC3) from LC3-I to its lipidative form, LC3-II, which was enhanced by co-addition of the saturated concentration of Bafilomycin A1 (Baf). Detection of co-localization for LC3 staining and labeled-lysosome further confirmed autophagic flux induced by LA or Epo. LA or Epo reduced the phosphorylation of the protein kinase B (Akt), a downstream target of phosphatidylinositol-3-kinases (PI3K), and mammalian target of rapamycin (mTOR) in ARPE-19 cells; by contrast, the induced changes of autophagy substrate, p62, showed biphasic pattern. The autophagy inhibitor, Baf, attenuated the reduction in oxidative injury conferred by treatment with low doses of LA and Epo in ARPE-19 cells exposed to menadione (VK3) or 4-hydroxynonenal (4-HNE). Knockdown of Atg7 with siRNA in ARPE-19 cells reduced the protective effects of LA or Epo against VK3. Overall, our results suggest that treatment with low levels of proteasome inhibitors confers resistance to oxidative injury by a pathway involving inhibition of the PI3K-Akt-mTOR pathway and activation of autophagy.

| S-EPMC4111584 | biostudies-literature

MAP2K4 interacts with Vimentin to activate the PI3K/AKT pathway and promotes breast cancer pathogenesis.

Project description:Mitogen-activated protein kinase kinase 4 (MAP2K4) is a member of the mitogen-activated protein kinase (MAPK) activator family. MAPK signaling plays a significant role in cell proliferation, differentiation, transcriptional regulation, and development. However, specific function and mechanism of MAP2K4 in breast cancer have not been clarified. According to our study, overexpressed MAP2K4 in breast cancer cells increased proliferation, migration, and invasion in vivo and in vitro, while MAP2K4 knockdown restored the effects. Subsequent mechanistic analyses demonstrated that MAP2K4 promoted cell proliferation, migration, and invasion by activating phosphoinositide-3-kinase (PI3K)/AKT signaling, the downstream proteins, c-JUN, the G1/S cell cycle, and the epithelial-to-mesenchymal transition (EMT). Meanwhile, MAP2K4 interacted with Vimentin and further propagated the malignant phenotype. Furthermore, patients with high MAP2K4 and Vimentin expression levels had poorer overall survival rates than those with low expression levels of both proteins. Our studies demonstrated that MAP2K4 has the potential to serve as an oncogene in breast cancer and it activates the phosphorylated PI3K/AKT signaling pathway to activate downstream cycle-associated proteins and EMT signals while interacting with Vimentin to promote breast cancer cells proliferation, migration, and invasion. In our study, MAP2K4 and Vimentin co-expression is confirmed to be an unfavorable factor in breast cancer.

| S-EPMC6914392 | biostudies-literature

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