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data confirm the key role of MDA-9/Syntenin in Human Liver Carcinoma biology. The presence of a regulation loop among MDA-9/Syntenin, NF-kappaB and RKIP provide new pharmacological approaches.
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these findings indicated that RKIP suppresses apoptosis and inflammation in MPP(+)-treated microglial cells through the inactivation of NF-kappaB and MEK/ERK signaling pathways. Thus, RKIP may be a promising target molecular involving in the pathogenesis of Parkinson's disease (PD).
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overexpression of RKIP inhibited prostate cancer cell proliferation, migration and invasion
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isruption of the TROY/RKIP interaction using the TAT-TROY (234-371 aa) protein reduced the glioma development in xenografted mice. This suggests the TROY/RKIP interaction is a potential target for therapy of gliomas.
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Loss of RKIP is associated with myeloid sarcoma.
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Low RKIP Expression is associated with asthma.
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our studies demonstrate how KRAS inhibits the tumor suppressor RKIP, thus offering novel justification for targeting RKIP as a strategy to overcome KRAS-induced tumor metastasis and chemoresistance in PDAC.
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RKIP expression in gastrointestinal stromal tumors is associated with tumor size, NIH risk grade, and mucosal invasion, and low or no expression of RKIP predicts a high malignancy potential.
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Octreotide may weaken invasion and metastasis through the upregulation of PEBP1. Octreotide may reduce the risk of recurrence and metastasis after surgery for liver cancer.
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Knockdown of RKIP increased phosphorylated ERK and thus suppressed sorafenib-mediated cell death.
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Baseline urinary RKIP, evaluated in an independent cohort of 56 Clear cell Renal Cell Carcinoma patients and 28 healthy subjects, successfully distinguished both groups and, most importantly, a cut-off value of 10 ng/mg/g Pr/uCr enabled a highly accurate prediction of Cancer-specific survival and Progression-free survival.
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we found that the RKIP expression was decreased significantly in HBV infected tumor tissues compared to normal adjacent tissues, suggesting the reduction or absence of RKIP expression was closely related to liver carcinogenesis.
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downregulation of RKIP plays an important role in the breast neoplastic progression and correlates with poor prognosis in patients with breast carcinoma (BC). Aberrant RKIP methylation is one of the mechanisms that lead to downregulation of RKIP in BC.
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can act as a negative mediator in autophagy through stimulation of the AKT-MTORC1 pathway and direct interaction with LC3.
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PEBP1, a scaffold protein inhibitor of protein kinase cascades, complexes with two 15LO isoforms, 15LO1 and 15LO2, and changes their substrate competence to generate hydroperoxy-phosphatidylethanolamines (PE). Inadequate reduction of hydroperoxy-PE due to insufficiency or dysfunction of a selenoperoxidase, GPX4, leads to ferroptosis.
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miR-23a as a negative regulator of RKIP expression in AML.
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Knockdown of RKIP promotes LX-2 cell proliferation.
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RKIP contributes to colitis development by promoting inflammation and mediating intestinal epithelial cell apoptosis.
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The study demonstrates that miR-543 promotes the proliferation and metastasis of prostate cancer via targeting RKIP.
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RKIP inhibitors locostatin reduces extracellular matrix production as well as the migration and proliferation of myometrial and leiomyoma cells.