title: Diallyl disulfide inhibits the proliferation of HT-29 human colon cancer cells by inducing differentially expressed genes.
abstract: Diallyl disulfide (DADS), a sulfur compound derived from garlic, has been shown to have protective effects against colon carcinogenesis in several studies performed in rodent models. However, its molecular mechanism of action remains unclear. This study was designed to confirm the anti-proliferative activity of DADS and to screen for differentially expressed genes induced by DADS in human colon cancer cells with the aim of exploring its possible anticancer mechanisms. The anti-proliferative capability of DADS in the HT-29 human colon cancer cells was analyzed by MTT assays and flow cytometry. The differences in gene expression between DADS-treated (experimental group) and untreated (control group) HT-29 cells were identified using two-directional suppression subtractive hybridization (SSH). Semi-quantitative reverse transcription polymerase chain reaction (semi-RT-PCR) was selected to confirm the results obtained by SSH. Based on the results, a dose- and time-dependent growth inhibition was observed in the DADS-treated HT-29 cells. Forty-nine known genes and a new gene were found to be involved in the anti-proliferative effects of DADS by SSH analysis, and two cDNA libraries, DHDG and DHUG, containing both up- and down-regulated genes in colon tumor cells, were constructed. These genes were related to transduction, cell proliferation/growth/apoptosis and secreted/extracellular matrix proteins. Semi-RT-PCR results showed an expression pattern consistent with that of the SSH analysis. In conclusion, DADS showed anti-proliferative effects on colon cancer HT-29 cells, and DHDG and DHUG genes were found to be involved in this process. Further studies on the identification and description of these genes may allow a better understanding of the protective roles of DADS in colon carcinogenesis.
authors.affiliation: Cancer Research Institute, University of South China, Hengyang, Hunan 421001, PR China.
authors.forename: You-Sheng
authors.initials: YS
authors.lastname: Huang
authors.forename: Na
authors.initials: N
authors.lastname: Xie
authors.forename: Qi
authors.initials: Q
authors.lastname: Su
authors.forename: Jian
authors.initials: J
authors.lastname: Su
authors.forename: Chen
authors.initials: C
authors.lastname: Huang
authors.forename: Qian-Jin
authors.initials: QJ
authors.lastname: Liao
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology*; D002453:Cell Cycle / Q000187:drug effects / Q000235:genetics; D016923:Cell Death / Q000187:drug effects / Q000235:genetics; D049109:Cell Proliferation / Q000187:drug effects; D003110:Colonic Neoplasms / Q000235:genetics* / Q000473:pathology*; D004220:Disulfides / Q000494:pharmacology*; D015536:Down-Regulation / Q000187:drug effects / Q000235:genetics; D004354:Drug Screening Assays, Antitumor; D005434:Flow Cytometry; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D019073:HT29 Cells; D006801:Humans; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D015854:Up-Regulation / Q000187:drug effects / Q000235:genetics
chemical_list: D000498:Allyl Compounds; D004220:Disulfides; D012333:RNA, Messenger; C028009:diallyl disulfide