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Focusing on BRAF(V600E) tumours, we found mechanisms of intrinsic resistance to BRAF(V600E)-targeted therapy in colorectal cancer, including targetable parallel activation of PDPK1 and PRKCA.
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PDK1, PLK1 and c-Myc were more commonly expressed in diffuse large B-cell lymphoma and the expression of each protein correlated positively with that of the other two molecules.
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the oncogenic effects of hsa_circ_0004015 was attributed to the regulation of miR-1183/PDPK1 axis.
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These results indicate that miR1623p may inhibit cell proliferation and migration, and promote apoptosis in MPMCs through repression of PDPK1 and may be a potential target for future clinical prevention and treatment of NSCL.
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miR-155-5p downregulation suppressed LC3 and promoted P62 protein expression in C33A cells through promoting the PDK1/mTOR pathway, whereas miR-155-5p overexpression recovered LC3 and suppressed P62 protein expression by suppressing PDK1/mTOR signaling
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PDPK1 expression is significantly associated with glioma progression. PDPK1 promotes the proliferation and inhibits the apoptosis of glioma cells.
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Studied role of 3-phosphoinositide dependent protein kinase (PDPK1) in gemcitabine resistance in pancreatic cancer stem-like cells.
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The present study strongly suggests that miR-718 inhibits papillary thyroid cancer cell proliferation, metastasis, and glucose metabolism...through PDPK1
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the combination of BX-912 and ABT-263, a BH3 mimetic, resulted in the enhancement of the induction of apoptosis. In conclusion, our results suggest that PDPK1 is a potential novel therapeutic target in Mantle cell lymphoma (MCL) and indicate that clinical development of PDPK1-targeted therapy for MCL is desirable.
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Our experimental results suggested that PDK1 may promote chondrocyte apoptosis in osteoarthritis via p38 MAPK signaling pathway
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our results offer significant insight into how PIK3CA overexpression drives squamous cell carcinoma (HNSCC) invasion and metastasis, providing a rationale for targeting PI3K/PDK1 and TGFb signaling in advanced HNSCC patients with PIK3CA amplification
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Ribociclib, in combination with GSK2334470 or the PI3Kalpha inhibitor alpelisib, decreased xenograft tumor growth more potently than each drug alone. Taken together, our results highlight a role for the PI3K-PDK1 signaling pathway in mediating acquired resistance to CDK4/6 inhibitors.
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Decreased PDK1 protein expression in A2058 cells.
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Together these results indicate a strong potential regulatory role for PDK1 in OC stimulatory pathways (Akt, ERK) and autophagy induction (via mTORC1), which may contribute to the OC phenotype in Paget's disease of bone.
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It targeted the 3-phosphoinositide-dependent protein kinase 1 gene that appeared to be a potent regulator of AKT.
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Highly expressed PDK1 could promote cell invasion and secretion of IL-1beta and IL-6 in human rheumatoid arthritis synovial MH7A cells. Inhibition of RSK2 reduced the PDK1-induced cell invasion and cytokines secretion in MH7A cells. In response to TNF-alpha, PDK1 could phosphorylate RSK2 and activated RSK2, then promoting the activation of NF-kappaB.
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In cancer cells resistant to PI3Kalpha inhibition, PDK1 blockade restores sensitivity to these therapies. SGK1, which is activated by PDK1, contributes to the maintenance of residual mTORC1 activity through direct phosphorylation and inhibition of TSC2.
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Results suggest that Ser-64 is an important phosphorylation site that is part of a positive feedback loop for human PDK1-PKCtheta;-mediated T cell activation.
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Elevated expression of PDK1 was an independent negative prognostic factor of gastric carcinoma.
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miR-138-1* played a critical role in aflatoxin B1-induced malignant transformation of B-2A13 cells by targeting PDK1.