Up-regulation of interferon-stimulated gene 15 and its conjugation machinery, UbE1L and UbcH8 expression by tumor necrosis factor-α through p38 MAPK and JNK signaling pathways in human lung carcinoma.
Furthermore, results showed that alantolactone could activate p38 MAPK pathway and suppress NF-κB pathway, which are involving in lung cancer development.
The results of this study indicated that p38 α and EGFR might play an important role in the development and growth of lung cancer and might be a potential therapeutic target for the treatment of lung cancer.
Our data show that miR-30a-3p suppressed the progression of lung cancer via regulating p38 MAPK pathway by targeting DNMT3A in A549 cells, indicating that miR-30a-3p might be a novel potential therapeutic strategy in the treatment of lung cancer.
The expression of HDAC1, uPAR and p38 MAPK are observed and analyzed in different stages of lung cancer using immunohistochemistry and Western blotting.
In contrast, inactivation of p38 in lung cancer cells leads to upregulation of the stemness proteins, thus promoting the cancer stem cell properties of these cells.
The chemotaxis of lung cancer cell lines corresponded with the activity of heme oxygenase‑1 (HO‑1), as stimulation of these cells by FSH, LH, and PRL downregulated its expression in a p38 MAPK‑dependent manner.
Curcumin downregulates p38 MAPK-dependent X-ray repair cross-complement group 1 (XRCC1) expression to enhance cisplatin-induced cytotoxicity in human lung cancer cells.
Vitamin A (retinol) downregulates the receptor for advanced glycation endproducts (RAGE) by oxidant-dependent activation of p38 MAPK and NF-kB in human lung cancer A549 cells.
Inhibition of p38 MAPK-dependent excision repair cross-complementing 1 expression decreases the DNA repair capacity to sensitize lung cancer cells to etoposide.
The authors investigated whether p38 MAPK activity contributed to the viability of cisplatin in lung cancer cell lines from never or light smokers and to ERCC1 mRNA expression.
These results demonstrate that the suppression of p16Ink4a by either the induction of Bmi-1 or the hypermethylation of p16Ink4 may be an important step in avoiding tumor surveillance by p38 MAPK during the development of lung cancer.
Overall, our study revealed for the first time that the NAG-1 protein inhibits urethane-induced tumor formation, probably mediated by the p38 MAPK pathway, and is a possible new target for lung cancer chemoprevention.
These results demonstrated that DHA can induce apoptosis of lung cancer cell line PC-14 cells and calcium and p38 play important roles in the apoptotic signalling pathways.