Gliomas are a type of heterogeneous primary
central nervous system tumor, which arise from the glial cells; these types of
tumor generally respond poorly to surgery, radiation and conventional
chemotherapy.
Tumor necrosis factor‑α (TNF‑α) has been suggested to produce an antitumor effect by binding to specific receptors on the
tumor cell membrane to induce apoptosis. TNF‑α is known to activate a number of signaling pathways, including extracellular signal‑regulated
protein kinase, c‑Jun N‑terminal
kinase (JNK), p38 mitogen‑activated
protein kinase (p38MAPK), nuclear factor‑κB and
caspase cascades, depending on the cell type. However, the involvement of p38MAPK signaling in TNF‑α‑induced apoptosis in
glioma cells remains unclear. In the current study, the role of p38MAPK in TNF‑α‑induced apoptosis in rat
glioma C6 cells was investigated. TNF‑α was observed to induce cell apoptosis and the phosphorylation of p38MAPK in C6 cells. In addition, the inhibition of p38MAPK markedly reduced TNF‑α‑induced apoptosis, while JNK inhibition did not affect apoptosis. Furthermore, p38MAPK transfection altered the cell cycle of
glioma cells and increased the rate of apoptosis. It also led to an increase in the level of soluble TNF‑α in the culture supernatant and membrane
TNF receptor I levels in
tumor cells. In conclusion, the results of the current study demonstrated that the activation of p38MAPK mediates TNF‑α‑induced apoptosis in
glioma C6 cells, suggesting p38MAPK as a potential target for
glioma therapy.