Abstract Title:

Bisdemethoxycurcumin (BDMC) Alters Gene Expression-associated Cell Cycle, Cell Migration and Invasion and Tumor Progression in Human Lung Cancer NCI-H460 Cells.

Abstract Source:

In Vivo. 2015 11-12;29(6):711-728. PMID: 26546528

Abstract Author(s):

Chien-Chih Yu, Mei-Due Yang, Hui-Yi Lin, An-Cheng Huang, Jing-Pin Lin, Chao-Lin Kuo, Kuo-Ching Liu, Hsin-Chung Liu, Su-Tso Yang, Jing-Gung Chung

Article Affiliation:

Chien-Chih Yu

Abstract:

BACKGROUND/AIM: Lung cancer is one of the most common malignancies and a predominant cause of cancer-related death. It can metastasize in almost all organs, and currently, while new cases are increasing, treatment is still insufficient. Bisdemethoxycurcumin (BDMC), one of the components of turmeric, has been known to possess biological activities. However, the effects of BDMC on the genetic level remain unclear.

MATERIALS AND METHODS: Human lung cancer NCI-H460 cells were treated with 35μM BDMC for 24 h and cells were harvested for total RNA extraction. The purified RNA was used for cDNA synthesis, labeling, microarray hybridization, and flour-labeled cDNA on-chip hybridization. The expression Console software (Affymetrix) with default RNA parameters was used to detect and quantitate concentrations of fluorescent molecules. The key genes involved and their possible interaction pathways were analyzed by the GeneGo software.

RESULTS: Seven genes, such as CCNE2 (cyclin E), associated with cell cycle, were over 4-fold overexpressed, 22 genes, such as ERCC6L (excision repair cross-complementing rodent repair deficiency, complementation group 6-like) associated with DNA damage and repair, were from 3- to 4-fold overexpressed and 266, such as cell division cycle, S-phase associated kinase and associated with cell death, genes were from 2- to 3-fold overexpressed.

CONCLUSION: BDMC induced changes in gene expression that may reveal cytotoxic information on the genetic level while presenting novel biomarkers or targets for treatment of human lung cancer in the future.

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