|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Par-4 induces apoptosis selectively in various types of cancer cells but not normal cells.
|
29695515 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Many studies have highlighted the importance of Par-4 not only in preventing cancer development/recurrence but also as a promising anticancer therapeutic agent.
|
25001535 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Transcripts for genes (<i>F2RL3, EMILIN1</i> and <i>CDC42BPA</i>) previously identified as being differentially methylated or expressed in smoking or smoking-related cancers were overexpressed in smokers compared to non-smokers and the expression of transcripts for genes (<i>HERPUD1, GAB2, FAM167A</i> and <i>GLS</i>) previously associated with stress response, autoimmune disease and cancer were associated with telomere length.
|
29207374 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The unique ability of Par-4 to induce apoptosis in cancer cells but not normal cells and the ability of Par-4 antisense or dominant-negative mutant to abrogate apoptosis in neurodegenerative disease paradigms makes it an appealing candidate for molecular therapy of cancer and neuronal diseases.
|
12565819 |
2003 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Fbxo45-mediated degradation of the tumor-suppressor Par-4 regulates cancer cell survival.
|
24992930 |
2014 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In this study, differential expression of PAR4 in esophageal squamous cancer was measured by real-time PCR (n = 28), western blot and tissue microarrays (n = 78).
|
25030438 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Experimental evidence indicates that prostate apoptosis response-4 (Par-4, also known as PAWR) is a key regulator of cancer cell survival and may be a target for cancer-selective targeted therapeutics.
|
23760770 |
2013 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Previous study revealed that the expression of PAR4 was increased in colorectal cancer tissues compared with the associated normal tissues, particularly in positive lymph node and poorly differentiated types of cancer.
|
30333860 |
2018 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
PAR mRNA expression was higher in cancer, and protein expression was increased in PAR-1 (45%), PAR-2 (42%), and PAR-4 (68%), compared to normal glands.
|
17373694 |
2007 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We report that the anti-malarial drug, chloroquine (CQ), is a robust inducer of Par-4 secretion from normal cells in mice and cancer patients in a clinical trial.
|
28076793 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Endoplasmic reticulum-stress and higher levels of protein kinase A in tumor cells confer the coveted feature of cancer selective response to extracellular and intracellular Par-4, respectively.
|
22552839 |
2012 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This mutant AATF along with its interactome consisting of SP1, DNMT3B and Par-4 ensures cancer cell DNA methylation required for down-regulation of tumor suppressor genes.
|
25231211 |
2015 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Par-4 down-regulation is often observed in cancer while up-regulation is characteristic of neurodegenerative conditions such as Alzheimer's disease.
|
30518159 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A novel MMP-2 inhibitor 3-azidowithaferin A (3-azidoWA) abrogates cancer cell invasion and angiogenesis by modulating extracellular Par-4.
|
22962598 |
2012 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Par-4 activity and levels can be downregulated in several tumors and cancer cell types, indicating poor prognosis and treatment resistance.
|
30474528 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Par-4 drives trafficking and activation of Fas and Fasl to induce prostate cancer cell apoptosis and tumor regression.
|
11585763 |
2001 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
However, WIN effects were not associated with a canonical apoptotic pathway, as demonstrated by the absence of specific features, and only the addition of TRAIL to WIN-treated cells led to apoptotic death probably mediated by up-regulation of the tumor suppressor factor PAR-4, whose levels increased after WIN treatment, and by the translocation of GRP78 on cell surface.
|
24795528 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our results therefore identify a key strd-1/STRAD-independent function of par-4/LKB1 in polarity establishment that is likely to be important for tumour suppression in humans.
|
20110331 |
2010 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Par-4-overexpressing tumors exhibited a bystander effect on wild-type tumors growing distally in the same mouse.
|
21555373 |
2011 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This review emphasizes the role of Par-4/SAC in apoptosis and tumor resistance.
|
18836307 |
2008 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Moreover, recombinant Par-4 inhibits the growth of tumors in mice.
|
22552839 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Inactivation of the candidate tumor suppressor par-4 in endometrial cancer.
|
17332319 |
2007 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
For instance, we demonstrate using ChIP-seq analysis that estrogen downregulate tumor suppressor Par-4 in hormone-dependent cells by directly binding to its DNA regulatory elements and inhibiting estrogen signaling could reinstate Par-4 apoptosis-inducing abilities.
|
28008141 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Oral administration of WA to mice with xenograft tumors restores FOXO3a-mediated Par-4 functions and results in inhibited tumor growth.
|
26913603 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, IKM5 amplified the expression and nuclear translocation of tumor suppressor Par-4 to control NF-kB-mediated pro-EMT activities.
|
31175498 |
2019 |