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.
Highlights
Lung cancer is the worldwide leading cause of death, and non-small cell lung cancer (NSCLC)accounts for 80% of total lung cancer cases [1]
Our results demonstrated the protective effect of Caffeic acid (CA) on paclitaxel-induced cell death in lung cancer cells A549 and H1299, in which NF-κB was involved in the protective effect by CA
It has been shown that the combination of CA and anti-cancer drugs reduces the cell growth of leukemic monocyte [19] and inhibits angiogenesis of renal carcinoma cells [20]
Summary
Lung cancer is the worldwide leading cause of death, and non-small cell lung cancer (NSCLC). The anti-cancer drug, paclitaxel (PTX), does not always completely induce apoptosis of tumor cells. Tumor cells survive from apoptosis induced by PTX, and become more drug-resistant [3]. Previous studies demonstrated that CA sensitized multidrug-resistant human breast cancer cells towards doxorubicin treatment [9], and that. Onori’s work reported that CAPE induced anti-proliferation and apoptosis of cholangiocarcinoma by inhibiting nuclear factor-κB (NF-κB). In comparison to the definite anti-cancer effect of CAPE, some studies showed that CA could exert protective effects. We investigated the effect of CA on proliferation and cell death of human lung cancer cells. Our results demonstrated the protective effect of CA on paclitaxel-induced cell death in lung cancer cells A549 and H1299, in which NF-κB was involved in the protective effect by CA
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