-
we determined that increased miR-17-3P level plays crucial role in CRC cells survival by targeting Par4, contributing to colorectal carcinogenesis.
-
PAR4 is the target of mir-107 in colorectal cancer cells.
-
we confirmed that the RASSF2-PAR-4 axis was mainly responsible for miR-7 functions in CAFs using bioinformatics methods. Overexpression of miR-7 in CAFs led to down-regulation of RASSF2, which dramatically decreased the secretion of PAR-4 from CAFs and then enhanced the proliferation and migration of the co-cultured cancer cells.
-
we investigated in the present study the mechanisms regulating the accumulation of a 25kDa cleaved-Par-4 (cl-Par-4) fragment in ovarian and endometrial cancer cell lines
-
Authors demonstrate that TRIM21 expression predicts survival in pancreatic cancer patients. This work highlights a novel mechanism of Par-4 regulation, and identifies a novel prognostic marker and potential therapeutic target for pancreatic cancer.
-
Data suggest that PAR4 and P2Y12 heterodimer internalization/endocytosis is required for beta-arrestin-2 recruitment to endosomes and up-regulation of Akt signaling; activation of PAR4 but not of P2Y12 drives internalization of the PAR4-P2Y12 heterodimer. (PAR4 = protease-activated receptor 4; P2Y12 = purinergic receptor P2Y, G-protein coupled, 12 protein; Akt = proto-oncogene protein c-akt)
-
In this review, we will focus on the therapeutic perspective of Par-4 with a special reference to its (Par-4) virgin prospect of devastating metastasis control.
-
in vitro and in vivo upregulation of Par-4 expression is indispensable for the trafficking of GRP78 to the cell membrane and subsequent apoptosis of cancer cell
-
Prostate apoptosis response 4 (PAR4) expression modulates WNT signaling pathways in MCF7 breast cancer cells: A possible mechanism underlying PAR4-mediated docetaxel chemosensitivity.
-
Decreased PAR4 expression in breast cancer is associated with shorter survival. PAR4 suppresses growth and invasiveness of breast cancer cells.
-
Authors determined that PAR-4 induces cell apoptosis in response to stimuli, in vitro, but is also involved in the relocation of GRP78 from endoplasmic reticulum to the cell surface of ovarian cancer cell line.
-
These results suggest that Porphyromonas gingivalis activates PAR4 signaling pathways, leading proMMP9 over-expression and cellular invasion in oral squamous cell carcinoma cells.
-
PAR1-platelet releasate enhances vasculogenesis more potently than PAR4-platelet releasate, and the enhancements require a cooperation of multiple platelet-derived angiogenic regulators.
-
A novel long non-coding RNA T-ALL-R-LncR1 knockdown and Par-4 cooperate to induce cellular apoptosis in T-cell acute lymphoblastic leukemia cells.
-
Data indicate that PAR1 and PAR4 activate common promigratory signalling pathways in Hep3B liver carcinoma cells including activation of the receptor tyrosine kinases Met and PDGFR, the formation of ROS and the inactivation of PTP1B.
-
a Par-4 mutant that is unable to bind Fbxo45 is stabilized and further enhances staurosporine-induced apoptosis.
-
C-terminus of the rat homologue of Par-4 was crystallized and a 3.7 A resolution X-ray diffraction data set was collected
-
These results indicate that the expression of PAR1 and PAR2 in esophageal squamous cell carcinoma is increased but PAR4 is decreased.
-
our results indicate that the mechanism by which PAR-4 orchestrates the apoptotic process requires cleavage by caspase-8.
-
Par-4 is expressed in trophoblastic cells and is involved in transport of GRP78 to the cell surface.
