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miR-375 and its probable PDK1 target may be utilized for the management of Kidney cancer.
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The importance of PDK1 in tumor growth and progression.A role of PDK1 in tumor microenvironment.[review]
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MiR-138 inhibits glycolysis but promotes mitochondrial respiration through directly targetting PDK1, and that contributes to cardiac cells' survival.
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Study shows higher expression level of PDK1 in non-small cell lung cancer (NSCLC) and its promoter region targeted by miR- 145.
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These results indicate that the immunohistochemistry analysis of the protein expression of PDK1, PHD3, and HIF-1alpha defines the hypoxic status of Neuroblastoma tumors.
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The pyruvate dehydrogenase kinases (PDKs) PDK1 and PDK3 are direct targets of KDM4A and E2F1 and modulate the switch between glycolytic metabolism and mitochondrial oxidation.
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dicumarol potently inhibited the kinase activity of PDK1, shifted the glucose metabolism from aerobic glycolysis to oxidative phosphorylation, generated a higher level of reactive oxygen species (ROS), attenuated the mitochondrial membrane potential (MMP), induced apoptosis, and reduced cell viability in vitro.
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miR-379 could function as a tumour-suppressing miRNA via targeting PDK1 in osteosarcoma.
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These results also suggest that inhibition of HIF-1a with 2-MeOE2 sensitizes radioresistant melanoma cells 435R to X-ray irradiation through targeting the glycolysis that is regulated by PDK1
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PDK1 is frequently upregulated in primary nasopharyngeal carcinoma and may serve as a prognostic marker.
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A new function for PDK1 in metabolic reprogramming, which could be used to indicate the prognosis of Non small cell lung cancer and provide targeted therapeutic strategy for clinical treatment.
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Our results demonstrated that down-regulation of SDHB and up-regulation of PDK1 may be novel biomarkers for predicting advanced tumor progression and unfavorable prognosis in recurrent nasopharyngeal carcinoma patients
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n the conditon of miR- 128b over-expression, we also observed spontaneous inactivation of the Akt/NF-kappaB signalling, implying PDK1 was a potential regulator of this pathway. In conclusion, our study shed some novel light on miR-128b-PDK1/Akt/NF-kappaB axis onGastric cancer (GC) progression
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Dichloroacetate, an Iihibitor of PDK1, can reverse the mitochondrial suppression of renal cell carcinoma and decrease HIF transcriptional activity, decreasing tumor growth and angiogenesis.
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Tergeting PDK1 with dichloroacetophenone inhibited acute myeloid leukemia cell growth via multiple signaling pathways.
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PDK1 was specifically required for metabolic adaptation to nutrient limitation and hypoxia.
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High expression of PDK1 is associated with Colon Cancer.
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both PDK 1 and 2 isoforms are overexpressed in cutaneous melanoma compared to nevi, this expression being associated with the expression of the mTOR pathway effectors and independent of the BRAF mutational status
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Lin28A and Lin28B enhance, whereas let-7 suppresses, aerobic glycolysis via targeting pyruvate dehydrogenase kinase 1, or PDK1.
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Follow-up replication analyses in up to an additional 21,345 participants identified three new fasting plasma glucose loci reaching genome-wide significance in or near PDK1-RAPGEF4, KANK1, and IGF1R.