gemcitabine-induced apoptosis in human non-small cell lung cancer H1299 cells requires activation of the JNK1 signaling pathway

Thermotherapy in combination with chemotherapy showed a stronger inhibitory effect than thermotherapy or chemotherapy alone on lung tumor cell growth by activation of c-Jun N-terminal kinase and inhibition of heat shock protein70.

JNK pathway (p = 6.10(-6)) as a key event in response to high linear energy transfer ionizing radiation induced apoptosis in a non-small cell lung cancer cell line.

Results suggest that Tgase-2/PP2A/JNK might be a novel axis that affects N-cadherin switching in the epithelial-mesenchymal-transition (EMT) of A549 lung cancer cells.

JNK is specifically involved in the maintenance of the tumor initiating capacity of A549 Non-small cell lung cancer cells.

These findings suggest for the first time that FOXO1 is a promising candidate substrate for JNK, and the FOXO1-dependent DNA damage repair may be regulated positively by the JNK pathway in H1299 lung cancer cells.

Phloretin is able to inhibit NSCLC A549 cell growth by inducing apoptosis through P38 MAPK and JNK1/2 pathways, and therefore may prove to be an adjuvant to the treatment of non-small cell lung cancer

Negative feedback regulation of AXL by miR-34a modulates apoptosis in lung cancer cells by activating the transcription factor ELK1 via the JNK signaling pathway.

cAMP signaling increases HDAC8 protein levels by reducing JNK-mediated autophagy and ubiquitin-proteasome-dependent degradation of the HDAC8 protein in H1299 lung cancer cells.

Results indicate that cordycepin promotes caveolin-1 (CAV1)upregulation to enhance c-jun N-terminal kinase (JNK)/forkhead box O3A protein (Foxo3a) signaling pathway activation, inducing apoptosis in lung cancer cells.

High JNK expression is associated with non-small-cell lung cancer.

These data suggested that Annexin A2 induces cisplatin resistance of non-small cell lung cancer (NSCLC)via regulation of JNK/c-Jun/p53 signaling, and provided an evidence that blockade of Annexin A2 could serve as a novel therapeutic approach for overcoming drug resistance in NSCLCs

Study reports that JNK1/2 activities attenuate LKB1-deficiency-driven lung squamous cell carcinoma (LSCC) initiation and progression through repressing DeltaNp63 signaling. LSCC patients with higher JNK1/2 activities have better survival rates and activating JNK1/2 activities attenuate LSCC progression.

in lung fibroblasts from tumor necrosis factor receptor 1-deficient mice the ability of hydrogen peroxide to activate c-jun N-terminal kinase was inhibited