Protective effect of caffeic acid on paclitaxel induced anti-proliferation and apoptosis of lung cancer cells involves NF-κb pathway
Journal
International Journal of Molecular Sciences
Journal Volume
13
Journal Issue
5
Pages
6236-6245
Date Issued
2012
Author(s)
Lin, C.-L.
Abstract
Caffeic acid (CA), a natural phenolic compound, is abundant in medicinal plants. CA possesses multiple biological effects such as anti-bacterial and anti-cancer growth. CA was also reported to induce fore stomach and kidney tumors in a mouse model. Here we used two human lung cancer cell lines, A549 and H1299, to clarify the role of CA in cancer cell proliferation. The growth assay showed that CA moderately promoted the proliferation of the lung cancer cells. Furthermore, pre-treatment of CA rescues the proliferation inhibition induced by a sub-IC50 dose of paclitaxel (PTX), an anticancer drug. Western blot showed that CA up-regulated the pro-survival proteins survivin and Bcl-2, the down-stream targets of NF-κB. This is consistent with the observation that CA induced nuclear translocation of NF-κB p65. Our study suggested that the pro-survival effect of CA on PTX-treated lung cancer cells is mediated through a NF-κB signaling pathway. This may provide mechanistic insights into the chemoresistance of cancer calls. ? 2012 by the authors; licensee MDPI, Basel, Switzerland.
Subjects
Bcl-2; Caffeic acid; NF κB; Non-small cell lung cancer; Paclitaxel; Survivin
SDGs
Other Subjects
caffeic acid; immunoglobulin enhancer binding protein; paclitaxel; protein bcl 2; survivin; transcription factor RelA; antineoplastic agent; BIRC5 protein, human; caffeic acid; caffeic acid derivative; immunoglobulin enhancer binding protein; inhibitor of apoptosis protein; paclitaxel; antiproliferative activity; apoptosis; article; cancer cell culture; cancer inhibition; cancer resistance; cancer survival; cell activation; cell assay; cell proliferation; cell protection; controlled study; drug effect; human; human cell; IC 50; lung non small cell cancer; protein function; protein localization; protein targeting; signal transduction; tumor promotion; upregulation; Western blotting; apoptosis; Carcinoma, Non-Small-Cell Lung; drug effects; drug resistance; Lung Neoplasms; metabolism; tumor cell line; Bacteria (microorganisms); Antineoplastic Agents, Phytogenic; Apoptosis; Caffeic Acids; Carcinoma, Non-Small-Cell Lung; Cell Line, Tumor; Cell Proliferation; Drug Resistance, Neoplasm; Humans; Inhibitor of Apoptosis Proteins; Lung Neoplasms; NF-kappa B; Paclitaxel; Signal Transduction; Up-Regulation
Type
journal article