Skip to content
naulon
Not checkedNot checked for notices yet.

Galangin and TRAIL cooperate to suppress A549 lung cancer proliferation via apoptosis and p38 MAPK activation

Wenjing Zhang, Qilai Huang, Zichun Hua

Acta Pharmaceutica Sinica B · 2012

doi:10.1016/j.apsb.2012.10.009 (opens in a new tab)

We email you when a new notice or a question about this paper appears.

Abstract

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is a promising antitumor therapy against lung cancer which is currently undergoing a phase III clinical trial in China. Unfortunately some cancer patients in the clinical trial displayed resistance to TRAIL treatment. In investigating ways to overcome this resistance, we evaluated the inhibitory effect of galangin on TRAIL resistant A549 human lung adenocarcinoma cells. Here we report that, in comparison with the single agents, the combination of galangin and TRAIL markedly suppressed proliferation of A549 cells and induced apoptosis as shown by DAPI and JC-1 staining. The combination of galangin and TRAIL induced PARP cleavage, activation of caspase-8 and p38 MAPK (mitogen-activated protein kinases). These findings indicate that the combination of galangin and TRAIL may constitute a promising strategy for the treatment of lung cancer.

Abstract licence: CC BY-NC-ND

Reads

Read by people on this page

None yet.

Checked or read by AI through naulon

None yet.

A person counts once a day per paper. We keep no cookie and no address: a reader is a hash that changes every day. Any month under five reads shows no number.

Are you an author?

Is this your paper?

Claim it to add your note and be paid when agents cite it. Free.