PI3K/AKT phosphorylation activates ERRα by upregulating PGC‑1α and PGC‑1β in gallbladder cancer

Wang, Lei; Jin, Huihan

doi:10.3892/mmr.2021.12252

Cited by 6 publications

(4 citation statements)

References 41 publications

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“…PI3K can directly cause phosphorylation of the downstream effector molecule Akt. When the PI3K/ Akt pathway is activated, the Akt phosphorylation level increases, and when the PI3K/Akt pathway is inhibited, the Akt phosphorylation level decreases [30][31][32]. In this study, compared with the model group, the expression levels of PI3K, p-PI3K, Akt, and p-Akt proteins in the tumor tissues of the rats in each group were decreased in a dosedependent manner after afuresertib intervention.…”

mentioning

confidence: 58%

The Protective Mechanism of Afuresertib against Esophageal Cancer

et al. 2022

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Esophageal cancer (EC) is a common malignant tumor of the digestive system. Exploring the molecular biological mechanism of EC will help to clarify its carcinogenesis mechanism, find important molecular targets in the process of carcinogenesis, and provide new ideas for the diagnosis and treatment of EC. Phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway is one of the signal transduction pathways most closely related to cell proliferation and apoptosis. The regulation of various downstream molecules affects the proliferation and growth of tumor cells. In this study, we determined the effect of different concentrations of afuresertib on cell viability by MTT assay and determined the effect of afuresertib on cell apoptosis by Annexin V-FITC/PI dual staining. Animal experiments verified the effects of afuresertib on VEGF, bFGF, and PI3K/Akt. Our results indicated that afuresertib is closely related to the survival, proliferation, and apoptosis of esophageal cancer cell lines. More importantly, we found that afuresertib could reduce tumor volume and mass in EC rats through in vivo experiments. In conclusion, afuresertib may exert its antitumor effect by inhibiting the expression of PI3K and Akt-related proteins in rat tumor tissues.

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confidence: 58%

The Protective Mechanism of Afuresertib against Esophageal Cancer

et al. 2022

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“…The upregulation of PPARG may result from the disrupted lipid balance caused by the inhibition of the PI3K/AKT pathway. It is worth noting that PGC1α , a downstream target of the PI3K/AKT signaling pathway, is positively influenced by the phosphorylated PI3K/AKT signaling pathway, which enhances its activity [ 47 ]. Conversely, when the PI3K/AKT pathway was inhibited, the expression of PGC1α decreased; this conclusion is consistent with the results of our analysis.…”

Section: Discussionmentioning

confidence: 99%

miR-129 Regulates Yak Intramuscular Preadipocyte Proliferation and Differentiation through the PI3K/AKT Pathway

Qin,

Wang,

Zhong

et al. 2024

IJMS

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miR-129 plays a crucial role in regulating various cellular processes, including adipogenesis; however, its downstream molecular mechanisms remain unclear. In this study, we demonstrated that miR-129 promotes yak adipogenesis in vitro via the PI3K/AKT pathway. Overexpression and interference of miR-129 in yak intramuscular preadipocytes (YIMAs) enhanced and inhibited cell differentiation, respectively, with corresponding changes in cell proliferation. Further investigation revealed that miR-129 enhances AKT and p-AKT activity in the AKT pathway without affecting cell apoptosis, and a specific inhibitor (LY294002) was used to confirm that miR-129 regulates YIMAs proliferation and differentiation through the PI3K/AKT pathway. Our findings suggest that miR-129 promotes yak adipogenesis by enhancing PI3K/AKT pathway activity. This study provides the foundation to precisely elucidate the molecular mechanism of miR-129 in YIMAs adipogenesis and develop advanced miRNA-based strategies to improve meat nutrition and obesity-related ailments in beef production.

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“… 40 PGC1α also acts as the co‑activators of ERRα and activates ERRα via promoting PI3K/Akt phosphorylation to promote the proliferation and invasion of gallbladder cancer cells. 41 Another study in human colorectal cancer revealed that knockdown PGC1α inhibited cell proliferation via the AKT/GSK-3β/β-catenin pathway. 42 …”

Section: Discussionmentioning

confidence: 99%

Knockdown of PGC1α suppresses dysplastic oral keratinocytes proliferation through reprogramming energy metabolism

Liu,

Huang,

Qiao

et al. 2023

Int J Oral Sci

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Oral potentially malignant disorders (OPMDs) are precursors of oral squamous cell carcinoma (OSCC). Deregulated cellular energy metabolism is a critical hallmark of cancer cells. Peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC1α) plays vital role in mitochondrial energy metabolism. However, the molecular mechanism of PGC1α on OPMDs progression is less unclear. Therefore, we investigated the effects of knockdown PGC1α on human dysplastic oral keratinocytes (DOKs) comprehensively, including cell proliferation, cell cycle, apoptosis, xenograft tumor, mitochondrial DNA (mtDNA), mitochondrial electron transport chain complexes (ETC), reactive oxygen species (ROS), oxygen consumption rate (OCR), extracellular acidification rate (ECAR), and glucose uptake. We found that knockdown PGC1α significantly inhibited the proliferation of DOKs in vitro and tumor growth in vivo, induced S-phase arrest, and suppressed PI3K/Akt signaling pathway without affecting cell apoptosis. Mechanistically, downregulated of PGC1α decreased mtDNA, ETC, and OCR, while enhancing ROS, glucose uptake, ECAR, and glycolysis by regulating lactate dehydrogenase A (LDHA). Moreover, SR18292 (an inhibitor of PGC1α) induced oxidative phosphorylation dysfunction of DOKs and declined DOK xenograft tumor progression. Thus, our work suggests that PGC1α plays a crucial role in cell proliferation by reprograming energy metabolism and interfering with energy metabolism, acting as a potential therapeutic target for OPMDs.

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PI3K/AKT phosphorylation activates ERRα by upregulating PGC‑1α and PGC‑1β in gallbladder cancer

Cited by 6 publications

References 41 publications

The Protective Mechanism of Afuresertib against Esophageal Cancer

The Protective Mechanism of Afuresertib against Esophageal Cancer

miR-129 Regulates Yak Intramuscular Preadipocyte Proliferation and Differentiation through the PI3K/AKT Pathway

Knockdown of PGC1α suppresses dysplastic oral keratinocytes proliferation through reprogramming energy metabolism

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