JNK1/2 |
Promotes development |
Negative cross-talk with the carcinogenic STAT3 signaling pathway. Chemical inhibition or selective targeting (via siRNA) downregulated STAT3 serine phosphorylation, accompanied by a modest increase in p-tyrstat3 levels. JNK activation could downregulate cell proliferation and viability and reduce cyclin D1 expression levels. |
STAT3 |
[54] |
ERK1/2, JNK1/2, p38 |
Promotes apoptosis |
Protein G induces OSCC apoptosis by activating Akt, ERK1/2, p38, and JNK1/2, and JNK1/2 activation is associated with autophagy in tumor cells. |
Protein G |
[55] |
JNK |
Promotes development |
Abnormal ubiquitination affects the corresponding JNK-dependent signaling pathway through the autophagy regulation mechanism. |
Abnormal ubiquitination |
[56] |
JNK |
Promotes apoptosis |
C-Jun mediates Nur77 in the orphan nuclear receptor superfamily of glioblastoma multiforme, which plays a key role in ahpn/cd437-induced apoptosis. PC drugs promote Nur77 transfer from nucleus to cytoplasm in OSCC and induce cell apoptosis. Other apoptotic stimuli that induce Nur77 nuclear output, including TPA, VP16, and cisplatin, can activate JNK. |
Nur77 |
[57] |
JNK |
Promotes apoptosis |
JNK is involved in activating Bax, a pro-apoptotic Bcl-2 protein, after sunitinib treatment. |
Bcl-2 protein |
[58] |
JNK |
Promotes apoptosis |
ROS production also mediates docetaxel-induced apoptosis of OSCC cells. ROS activates upstream kinase ASK1 of JNK. ASK1 activation must be tightly regulated according to the intensity and duration of stress (ROS), and various post-translational modifications, such as ubiquitination and methylation, participate in this tight regulation of activity and phosphorylation. |
ROS, ASK |
[59,60,61] |
JNK |
Promotes apoptosis |
JNK activation is also involved in activating caspase induced in OSCC. It can activate caspase and reduce necrosis, apoptosis, cell cycle, and mito_x001e_chondrial membrane potential (∆Ψm), thus inducing OSCC cell apoptosis. |
Caspase |
[62] |