|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, we explored the relationship between PAR4 activation and the expression of p16, and elucidated the underlying mechanisms in PAR4 inducing the tumor suppressor role in ESCC.
|
30363984 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PAR4 may acts as a tumor suppressor in lung adenocarcinoma.
|
23886184 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor suppressor Par-4 is a novel integral player in the PTEN network.
|
19625770 |
2009 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Using an epigenome editing approach to reexpress Par-4 by specifically reversing the histone modifications found in recurrent tumors, we found that Par-4 reexpression sensitized recurrent tumors to chemotherapy in vitro and in vivo.
|
30148456 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
After several months the indolent WT1-LNCaP cells became proliferative forming small tumors lacking par-4 protein.
|
14767530 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Cancer-associated fibroblasts promote cancer cell growth through a miR-7-RASSF2-PAR-4 axis in the tumor microenvironment.
|
27901488 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Taken together, these results indicate that residual breast cancer tumor cell survival and recurrence requires circumventing Foxo-driven Par-4 upregulation and suggest that approaches to enforce Par-4 expression may prevent residual cell survival and recurrence.<i></i>.
|
29330285 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Par-4 is one such tumor suppressor which is unique in its ability to selectively induce apoptosis in cancer cells while leaving the normal cells unaffected.
|
25001535 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Chloroquine-Inducible Par-4 Secretion Is Essential for Tumor Cell Apoptosis and Inhibition of Metastasis.
|
28076793 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Breast cancer cell proliferation, cancer cell-induced endothelial tube formation in vitro, and tumour growth in vivo were studied in the presence of protease-activated receptor 1-stimulated platelet releasate (PAR1-PR; rich in pro-angiogenic factors) or PAR4-PR (rich in anti-angiogenic factors).
|
28697175 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Fbxo45-mediated degradation of the tumor-suppressor Par-4 regulates cancer cell survival.
|
24992930 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Par-4 but not Bcl-2 was detected in the secretory epithelium of benign prostatic tumors and in primary and metastatic prostate cancers that are apt to undergo apoptosis.
|
9989812 |
1999 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Analysis of tumor remnants showed that KPT-330 disrupted the interaction between CRM-1 and PAR-4, activated PAR-4 signaling, and reduced proliferation of tumor cells.
|
23089203 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The tumor suppressor Par-4 is an important negative regulator of the canonical NF-kappaB pathway and is highly expressed in prostate.
|
19470463 |
2009 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Importantly, restoration of Par-4 levels to normal in Ras-transformed cells makes these cells sensitive to the pro-apoptotic actions of tumor necrosis factor-alpha under conditions in which PI 3-kinase is inhibited and also severely impairs colony formation in soft agar and tumor development in nude mice, as well as increases the sensitivity of these tumors to camptothecin.
|
10562548 |
1999 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We discovered significantly low expression of Par-4 in the tumor tissue, which was positively correlated with high expression of GRP78 (glucose-regulated protein 78).
|
28720068 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We have uncovered a novel mechanism of 3-azidoWA induced extracellular pro-apoptotic candidate tumor suppressor Par-4 protein stimulation in conditioned media and also noticed a concomitant marked reduction in pAkt and pERK signaling by immunoblot analysis.
|
22962598 |
2012 |
|
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Par-4 drives trafficking and activation of Fas and Fasl to induce prostate cancer cell apoptosis and tumor regression.
|
11585763 |
2001 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Par-4 but not Bcl-2 was detected in the secretory epithelium of benign prostatic tumors and in primary and metastatic prostate cancers that are apt to undergo apoptosis.
|
9989812 |
1999 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
This review discusses salient features of molecules such as, Bcl-2, Bcl-(XL), NF-kappaB, Akt, PTEN and Par-4 that play a significant role in the regulation of prostate cancer and focuses on the prospects of effectively utilizing their potential for the therapy of hormone-sensitive and hormone-resistant prostate cancer.
|
14965337 |
2004 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results establish the cooperation between Par-4 and PTEN as relevant for the development of prostate cancer and implicate the NF-kappaB pathway as a critical event in prostate tumorigenesis.
|
19470463 |
2009 |
|
Malignant neoplasm of prostate
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The primary form of therapy for prostate cancer is androgen ablation resulting in apoptosis and expression of apoptotic genes (i.e. par-4).
|
14767530 |
2004 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
AKT inhibition and Par-4 induction suppressed prostate cancer progression in preclinical models.
|
28494348 |
2017 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Par-4 for molecular therapy of prostate cancer.
|
12643472 |
2003 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Par-4 deficiency cooperates with PTEN haploinsufficiency in prostate cancer initiation and progression and their simultaneous inactivation, in addition to enhancing Akt activation, sets in motion a unique mechanism involving the synergistic activation of NFkappaB.
|
19625770 |
2009 |