|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Together, our findings provide a novel mechanism of tumor growth that acts through intracellular Ca<sup>2+</sup> levels to modulate JNK-mediated Hippo signaling.
|
31649333 |
2020 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We further demonstrated that MEX3C regulated lipid metabolism and promoted tumor development and progression through activation of JNK signaling and upregulating the JNK downstream protein levels of sterol regulatory element-binding proteins-1, fatty acid synthase and acetyl-CoA carboxylase-1.
|
31118679 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Meanwhile, the leucine-rich diet modulated key steps of the mTOR pathway by triggering the increased activation of RAG and mTOR and maintaining JNK, STAT-3 and STAT-6 levels in muscle, leading to an increased muscle protein synthesis, reducing the degradation during tumour evolution in a host, minimising the cancer-induced damages in the cachectic state.
|
30975087 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Silymarin was revealed to reduce tumor growth through inhibition of p‑ERK and activation of p‑p38 and p‑JNK in human gastric cancer cells.
|
31485597 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results highlight the functional significance of the JNK pathway in epithelial cells with defective cytokinesis and elucidate a mechanism used by emerging tumor cells to bypass this tumor-suppressive barrier and develop into tumors.
|
29719260 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Matrine promoted the expression of GADD45B, a tumor suppressive gene that is involved in the regulation of cell cycle, DNA damage repair, cell survival, aging, apoptosis and other cellular processes through p38/JNK, ROS-GADD45B-p38, or other signal pathways.
|
29356020 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This tumor suppressive function was not mediated by a role of JNK in the growth of established tumors, but by a requirement of JNK to prevent tumor initiation.
|
29856313 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
JNK drives the transcriptional induction of mitogenic molecules, matrix metalloproteases and systemic signals that lead to tumor growth, tissue invasiveness and malignancy.
|
29451063 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Akt-S6K1 inhibition and JNK activation were observed in ABC294640-treated tumors.
|
29428730 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Collectively, ω-HUA-induced intracellular ROS generation induced breast cancer cell apoptosis through JNK and p38 signaling pathway activation, resulting in tumor regression.
|
28681938 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To determine the role of the MEKK1/SEK1/JNK1/AP-1 pathway in the action of Xihuang pill (XHP) in reducing regulatory T (Treg) cell numbers in the tumor microenvironment in a 4T1 mouse breast cancer model, and to clarify the anti-tumor mechanism of XHP in breast cancer.
|
29710529 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Piperine functions as a tumor suppressor for human ovarian tumor growth via activation of JNK/p38 MAPK-mediated intrinsic apoptotic pathway.
|
29717031 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
TIPE attenuates the apoptotic effect of radiation and cisplatin and promotes tumor growth via JNK and p38 activation in Raw264.7 and EL4 cells.
|
29620232 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Diallyl trisulfide suppresses tumor growth through the attenuation of Nrf2/Akt and activation of p38/JNK and potentiates cisplatin efficacy in gastric cancer treatment.
|
28344324 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Ex vivo tumor analysis indicated significant molecular activity such as changes in the level of phosphoproteins JNK, Akt, and inflammation markers IL-6 and IFN-γ.
|
28135100 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Combining <i>in vitro</i> and <i>in vivo</i> functional analyses, we demonstrate that JNK inhibition both promotes tumor cell cytostasis and blocks activation of the proapoptotic protein Bax, thereby antagonizing chemotherapy-mediated cytotoxicity.
|
28611109 |
2017 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Liver-specific JNK1/2 deletion led to tumor reduction and enhanced survival in Akt/Notch- or p53/Kras-induced ICC models.
|
28609656 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
c-Jun N-terminal kinase in pancreatic tumor stroma augments tumor development in mice.
|
28837246 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Interestingly, CRC patients expressing high levels of the cysteinyl leukotriene 2 (CysLT2) receptor have a good prognosis; therefore, we investigated a potential link between CysLT2 signaling and the tumor suppressor 15-PGDH in colon cancer cells.We observed a significant up-regulation of 15-PGDH after treatment with LTC4, a CysLT2 ligand, in colon cancer cells at both the mRNA and protein levels, which could be reduced by a CysLT2 antagonist or a JNK inhibitor.
|
28402256 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We show that <i>SMAD4</i> depletion in an HNSCC cell line induces cetuximab resistance and results in worse survival in an orthotopic mouse model <i>in vivo</i> We implicate JNK and MAPK activation as mediators of cetuximab resistance and provide the foundation for the concomitant EGFR and JNK/MAPK inhibition as a potential strategy for overcoming cetuximab resistance in HNSCCs with SMAD4 loss.<b>Conclusions:</b> Our study demonstrates that loss of SMAD4 expression is a signature characterizing the cetuximab-resistant phenotype and suggests that SMAD4 expression may be a determinant of sensitivity/resistance to EGFR/MAPK or EGFR/JNK inhibition in HPV-negative HNSCC tumors.<i></i>.
|
28522603 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Immunohistochemical assessment of the phosphorylated levels of STAT3(tyrosine/ serine), ERK1/2 and JNK was performed in 60 OSCC, including well, moderately and poorly differentiated tumors.
|
28090628 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, a xenograft assay showed that CT significantly inhibited MKN-45 cell-induced tumor growth <i>in vivo</i> by increasing expression of pro-apoptotic proteins (p-JNK, p-38 and cleaved-caspase-3) and reducing expression of anti-apoptotic proteins (p-ERK and p-STAT3) without adverse effects on nude mice weight.
|
29383168 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Forkhead transcription factor (Foxo3a) is a downstream effector of JNK-induced tumor suppression.
|
28099944 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
However, a number of studies have implicated JNK in malignant transformation and tumor growth.
|
28639904 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Taken together we show that Ets21C is a crucial player in regulating the transcriptional program of the JNK pathway and enhances our understanding of the mechanisms that govern neoplastic growth.
|
27713480 |
2016 |