|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, KLF4 was shown to activate the p38 MAPK signaling pathway to promote cancer stemness.
|
29930276 |
2019 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
On the other hand, in adult males, a number of genes with significant expression alterations were found to be associated with cancer and tumors. p38 mitogen-activated protein kinase (p38 MAPK) was also indicated as an upstream regulator of observed gene expression changes.
|
29074346 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A detailed mechanistic understanding of how p38 MAPK family members function is urgently warranted for cancer targeted therapy.
|
31828036 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
NRP-1 interacts with GIPC1 and SYX to activate p38 MAPK signaling and cancer stem cell survival.
|
30456845 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, simultaneous Fas ligation and low-dose p38 inhibition may be an effective approach for T<sub>H</sub>9 cell induction and cancer therapy.
|
31266950 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data suggest the importance of p38alpha kinase in the regulation of ROS metabolism in embryonic stem cells and the significance of the observed phenomena of cancer cell-like phenotypes, which is discussed.
|
31176685 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These differentially abundant proteins were related to nuclear factor κB (NF-κB) and p38 mitogen-activated protein (MAP) kinase pathways and were involved in cellular compromise, inflammatory response, and cancer.
|
31623319 |
2019 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
MAPKAPK2 (MK2), the direct substrate of p38 MAPK, has been well-acknowledged as an attractive drug target for cancer therapy.
|
31440466 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We demonstrate that IKKα signaling promotes increased cell malignancy of NSCLC cells as well as lung tumor progression and metastasis in either subcellular localization, through activation of common protumoral proteins, such as Erk, p38 and mTor.
|
30867890 |
2019 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Increased expression and activity of p38 MAPK is correlated with poor prognosis in cancer, including glioblastoma multiforme; however, the toxicity of p38 MAPK inhibitors limits their clinical use.
|
29316898 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Role of p38 MAPK in disease relapse and therapeutic resistance by maintenance of cancer stem cells in head and neck squamous cell carcinoma.
|
29575240 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The nuclear translocation of the kinases p38 and JNK promotes inflammation-induced cancer.
|
29636389 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The signaling pathway driven by p38 and MAPKAPK2 alias MK2 is activated as part of stress responses, and these kinases represent attractive drug targets for cancer therapy.
|
29704518 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Knockdown of BMPR1a of breast cancer cells suppresses their production of RANKL via p38 pathway and inhibits cancer-induced osteoclastogenesis, which indicates that BMPR1a might be a possible target in breast cancer-induced osteolytic metastasis.
|
29495003 |
2018 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These surprising results delineate a mechanism by which a transcription factor switches cells from ERK to p38 signaling in response to chemotherapy and suggest that therapeutic targeting of HIF1 or the p38 pathway in combination with chemotherapy will block BCSC enrichment and improve outcome in TNBC.<b>Significance:</b> These findings provide a molecular mechanism that may account for the increased relapse rate of women with TNBC who are treated with cytotoxic chemotherapy and suggest that combining chemotherapy with an inhibitor of HIF1 or p38 activity may increase patient survival.<i>Cancer Res; 78(15); 4191-202.©2018 AACR</i>.
|
29880481 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, two cancer cell lines were used to evaluate the cytotoxicity and apoptotic effect of Sg-AgNP along with the determination of the role of the Caspase-3 / p38 MAPK pathways.
|
29331758 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
As p38 and E-cadherin also serve a key role in epithelial-to-mesenchymal transition (EMT) and cancer metastasis, we hypothesized that the combination of aspirin and erlotinib may significantly inhibit tumor metastasis.
|
30013667 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The p38 MAPK signaling pathway is a key signal transduction cascade that cancer cells employ to sense and adapt to a plethora of environmental stimuli, and has attracted much attention as a promising target for cancer therapy.
|
27725227 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
PI3K/AKT and p38 are important signaling pathways to modulate cancer cell apoptosis and proliferation through caspase-3, NF-κB and mTOR signal pathways.
|
28677816 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Western blot and real-time PCR analyses were used to assess ANP32A expression and the activity of Akt and p38 in cancer and normal tissues.
|
28731192 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Inhibition of p38 MAPK phosphorylation by SB203580 treatment increased number of migratory cancer cells in CT-26 and HT-1080 cells, indicating that blue LED irradiation inhibited cancer cell migration via phosphorylation of p38 MAPK.
|
28098340 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data reveal that elevated <i>O</i>-GlcNAcylation in the TME reduces the production of inflammatory cytokines and promotes cancer progression through downregulation of p38 MAPK activity and subsequent upregulation of the ERK1/2 signaling pathway.<b>Implications:</b> The reduced production of inflammatory cytokines by augmented <i>O</i>-GlcNAcylation in the TME, mainly macrophages, promotes tumor proliferation through the inhibition of p38 MAPK and suggests a possible cause of increased morbidity and mortality rates for various cancers in diabetic patients.<i>Mol Cancer Res; 15(9); 1287-98.©2017 AACR</i>.
|
28536142 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These findings have demonstrated a novel mechanism by which cancer stem cell properties are acquired and maintained in a cancer cell population, and have revealed a new function of the p38 pathway in suppressing cancer development.
|
28460458 |
2017 |
|
Malignant Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
We also found that PI3K (Phoshoinositide 3-kinase) inhibition and p38 MAPK (p38 mitogen-activated protein kinase) activation leads to reduction in phosphorylation of BCNP1 at serine residues, suggesting that BCNP1 phosphorylation is PI3K and p38MAPK dependent and that it might be involved in cancer.
|
27680505 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The N-Terminal Phosphorylation of RB by p38 Bypasses Its Inactivation by CDKs and Prevents Proliferation in Cancer Cells.
|
27642049 |
2016 |