Sodium 4-phenylbutyrate induces apoptosis of human lung carcinoma cells through activating JNK pathway

Journal of Cellular Biochemistry
Xing ZhangQiang Yu

Abstract

Sodium 4-phenylbutyrate (PB) has been used in the therapy of urea cycle defects for many years. Recently, it has been shown to cause cellular differentiation, growth arrest, and apoptosis in certain malignancies. We have analyzed the effects of PB on human lung carcinoma cells. PB has distinct patterns of effects on different lung carcinoma cells, inducing apoptosis in NCI-H460 and NCI-H1792 cells, causing G1 arrest in A549 and SK-LU-1 cells, but having no effect on a non-transformed bronchial epithelial cell line HBE4-E6/E7. We investigated the role of MAP kinase family members, extracellular signal-regulated kinase (ERK), JNK, and p38 mitogen-activated protein kinase (MAPK), as well as other important cell survival signaling molecules in PB-induced apoptosis. We observed activation of JNK and ERK by PB in the lung cancer cells. JNK was activated only in the two apoptotic cells, whereas ERK was activated in both the apoptotic and the growth-arrested cells, demonstrating a correlation between apoptosis and activation of JNK in response to PB. Both JNK inhibitor and JNK RNA interference (RNAi) inhibited PB-induced apoptosis, whereas MEK inhibitor did not, supporting that apoptosis induced by PB is through activation of JNK. De n...Continue Reading

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Citations

Jun 1, 2011·Cancer Management and Research·Nadine Martinet, Philippe Bertrand
Jun 8, 2013·Toxicology and Applied Pharmacology·Midori IsomuraShigeru Ohta
Aug 12, 2015·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Magdalena KusaczukMarzanna Cechowska-Pasko
Jul 7, 2016·International Journal of Experimental Pathology·Milan Holecek, Melita Vodenicarovova
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Sep 21, 2017·Chemical Research in Toxicology·Maha S Al-Keilani, Nour A Al-Sawalha

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