Saringosterol Acetate from a Popular Edible Seaweed, Hizikia Fusiformis Attenuated Proliferation of Human Lung Adenocarcinoma Epithelial Cells (A549 Cells) via Apoptosis Signaling Pathway

Hizikia fusiformis is a common, edible marine alga found in Asia. Although the anticancer activity of its extracts has previously been investigated, its active compounds have not been identified. In this study, saringosterol acetate (SA) was isolated from H. fusiformis extracts by centrifugal partition chromatography (CPC) system (two phase solvents condition: n-hexane:ethyl acetate/methanol:water = 5:3:7:1, v/v), exhibited anticancer effects in the human lung adenocarcinoma epithelial cell line, A549, by inducing apoptosis and sub-G1 phase cell cycle arrest. In addition, SA increased the expression of the pro-apoptotic proteins, Bax and cleaved caspase 3, and decreased that of the anti-apoptotic protein Bcl-xL. Although, SA did not affect the expression of p53, induces expression of Bid and caspase 8. In conclusion, we suggested that SA induces apoptosis against A549 cells via Bid and caspase 8 dependent pathway.

Download Full-text

Effects of Salinomycin on Cancer Stem Cell in Human Lung Adenocarcinoma A549 Cells

Medicinal Chemistry ◽

10.2174/157340611794859307 ◽

2011 ◽

Vol 7 (2) ◽

pp. 106-111 ◽

Cited By ~ 56

Author(s):

Yi Wang

Keyword(s):

Stem Cell ◽

Cancer Stem Cell ◽

Lung Adenocarcinoma ◽

Human Lung ◽

A549 Cells ◽

Human Lung Adenocarcinoma ◽

Lung Adenocarcinoma A549

Download Full-text

A novel compound RY10-4 induces apoptosis and inhibits invasion via inhibiting STAT3 through ERK-, p38-dependent pathways in human lung adenocarcinoma A549 cells

Chemico-Biological Interactions ◽

10.1016/j.cbi.2013.11.014 ◽

2014 ◽

Vol 209 ◽

pp. 25-34 ◽

Cited By ~ 12

Author(s):

Pingping Xue ◽

Yang Zhao ◽

Yang Liu ◽

Qianying Yuan ◽

Chaomei Xiong ◽

...

Keyword(s):

Lung Adenocarcinoma ◽

Human Lung ◽

A549 Cells ◽

Human Lung Adenocarcinoma ◽

Lung Adenocarcinoma A549

Download Full-text

Biological Evaluation of Alkyl Triphenylphosphonium Ostruthin Derivatives as Potential Anti-Inflammatory Agents Targeting the Nuclear Factor κB Signaling Pathway in Human Lung Adenocarcinoma A549 Cells

BioChem ◽

10.3390/biochem1020010 ◽

2021 ◽

Vol 1 (2) ◽

pp. 107-121

Author(s):

Nghia Trong Vo ◽

Eiichi Kusagawa ◽

Kaori Nakano ◽

Chihiro Moriwaki ◽

Yasunobu Miyake ◽

...

Keyword(s):

Lung Adenocarcinoma ◽

Signaling Pathway ◽

Human Lung ◽

A549 Cells ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Human Lung Adenocarcinoma ◽

Tnf Α ◽

Anti Inflammatory ◽

Lung Adenocarcinoma A549

Ostruthin (6-geranyl-7-hydroxycoumarin) is one of the constituents isolated from Paramignya trimera and has been classified as a simple coumarin. We recently reported the synthesis of alkyl triphenylphosphonium (TPP) derivatives from ostruthin and evaluated their anticancer activities. In the present study, we demonstrated that alkyl TPP ostruthin derivatives inhibited the up-regulation of cell-surface intercellular adhesion molecule-1 (ICAM-1) in human lung adenocarcinoma A549 cells stimulated with tumor necrosis factor-α (TNF-α) without affecting cell viability, while ostruthin itself exerted cytotoxicity against A549 cells. The heptyl TPP ostruthin derivative (termed OS8) attenuated the up-regulation of ICAM-1 mRNA expression at concentrations higher than 40 µM in TNF-α-stimulated A549 cells. OS8 inhibited TNF-α-induced nuclear factor κB (NF-κB)-responsive luciferase reporter activity at concentrations higher than 40 µM, but did not affect the translocation of the NF-κB subunit RelA in response to the TNF-α stimulation at concentrations up to 100 µM. A chromatin immunoprecipitation assay showed that OS8 at 100 µM prevented the binding of RelA to the ICAM-1 promoter. We also showed that OS8 at 100 µM inhibited the TNF-α-induced phosphorylation of RelA at Ser 536. Moreover, the TNF-α-induced phosphorylation of an inhibitor of NF-κB α and extracellular signal-regulated kinase was reduced by OS8. These results indicate that OS8 has potential as an anti-inflammatory agent that targets the NF-κB signaling pathway.

Download Full-text

Regulation of ABCG2 by nuclear factor kappa B affects the sensitivity of human lung adenocarcinoma A549 cells to arsenic trioxide

Environmental Toxicology and Pharmacology ◽

10.1016/j.etap.2017.12.011 ◽

2018 ◽

Vol 57 ◽

pp. 141-150 ◽

Cited By ~ 4

Author(s):

Xuejun Jiang ◽

Chengzhi Chen ◽

Shiyan Gu ◽

Zunzhen Zhang

Keyword(s):

Lung Adenocarcinoma ◽

Arsenic Trioxide ◽

Nuclear Factor Kappa B ◽

Human Lung ◽

A549 Cells ◽

Nuclear Factor ◽

Human Lung Adenocarcinoma ◽

Nuclear Factor Kappa ◽

Lung Adenocarcinoma A549

Download Full-text

Emodin Inhibits ATP-Induced Proliferation and Migration by Suppressing P2Y Receptors in Human Lung Adenocarcinoma Cells

Cellular Physiology and Biochemistry ◽

10.1159/000485495 ◽

2017 ◽

Vol 44 (4) ◽

pp. 1337-1351 ◽

Cited By ~ 12

Author(s):

Xia Wang ◽

Long Li ◽

Ruijuan Guan ◽

Danian Zhu ◽

Nana Song ◽

...

Keyword(s):

Cell Proliferation ◽

Lung Adenocarcinoma ◽

Human Lung ◽

A549 Cells ◽

P2y Receptors ◽

Mesenchymal Transition ◽

Human Lung Adenocarcinoma ◽

Adenocarcinoma Cells ◽

Human Lung Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells

Background/Aims: Extracellular ATP performs multiple important functions via activation of P2 receptors on the cell surface. P2Y receptors play critical roles in ATP evoked response in human lung adenocarcinoma cells (A549 cells). Emodin is an anthraquinone derivative originally isolated from Chinese rhubarb, possesses anticancer properties. In this study we examined the inhibiting effects of emodin on proliferation, migration and epithelial-mesenchymal transition (EMT) by suppressing P2Y receptors-dependent Ca2+ increase and nuclear factor-κB (NF-KB) signaling in A549 cells. Methods: A549 cells were pretreated with emodin before stimulation with ATP for the indicated time. Then, intracellular Ca2+ concentration ([Ca2+]i) was measured by Fluo-8/AM staining. Cell proliferation and cell cycle progression were tested by CCK8 assay and flow cytometry In addition, wound healing and western blot were performed to determine cell migration and related protein levels (Bcl-2, Bax, claudin-1, NF-κB). Results: Emodin blunted ATP/UTP-induced increase of [Ca2+]i and cell proliferation concentration-dependently Meanwhile, it decreased ATP-induced cells accumulation in the S phase. Furthermore, emodin altered protein abundance of Bcl-2, Bax and claudin-1 and attenuated EMT caused by ATP. Such ATP-induced cellular reactions were also inhibited by a nonselective P2Y receptors antagonist, suramin, in a similar way to emodin. Besides, emodin could inhibit activation of NF-κB, thus suppressed ATP-induced proliferation, migration and EMT. Conclusion: Our results demonstrated that emodin inhibits ATP-induced proliferation, migration, EMT by suppressing P2Y receptors-mediated [Ca2+]i increase and NF-κB signaling in A549 cells.

Download Full-text