Linked Life Data

18449891

Source:http://linkedlifedata.com/resource/pubmed/id/18449891

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-6-2
pubmed:abstractText
microRNAs are endogenous small noncoding RNAs that regulate gene expression negatively at posttranscriptional level. This latest addition to the complex gene regulatory circuitry revolutionizes our way to understanding physiological and pathological processes in the human body. Here we investigated the possible role of microRNAs in the development of multidrug resistance (MDR) in gastric cancer cells. microRNA expression profiling revealed a limited set of microRNAs with altered expression in multidrug- resistant gastric cancer cell line SGC7901/VCR compared to its parental SGC7901 cell line. Among the downregulated microRNAs are miR-15b and miR-16, members of miR-15/16 family, whose expression was further validated by qRT-PCR. In vitro drug sensitivity assay demonstrated that overexpression of miR-15b or miR-16 sensitized SGC7901/VCR cells to anticancer drugs whereas inhibition of them using antisense oligonucleotides conferred SGC7901 cells MDR. The downregulation of miR-15b and miR-16 in SGC7901/VCR cells was concurrent with the upregulation of Bcl-2 protein. Enforced mir-15b or miR-16 expression reduced Bcl-2 protein level and the luciferase activity of a BCL2 3' untranslated region-based reporter construct in SGC7901/VCR cells, suggesting that BCL2 is a direct target of miR-15b and miR-16. Moreover, overexpression of miR-15b or miR-16 could sensitize SGC7901/VCR cells to VCR-induced apoptosis. Taken together, our findings suggest that miR-15b and miR-16 could play a role in the development of MDR in gastric cancer cells at least in part by modulation of apoptosis via targeting BCL2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1097-0215
pubmed:author
pubmed:copyrightInfo
(c) 2008 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
123
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
372-9
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed-meshheading:18449891-Antineoplastic Agents, pubmed-meshheading:18449891-Apoptosis, pubmed-meshheading:18449891-Blotting, Western, pubmed-meshheading:18449891-Cell Line, Tumor, pubmed-meshheading:18449891-Cisplatin, pubmed-meshheading:18449891-Down-Regulation, pubmed-meshheading:18449891-Doxorubicin, pubmed-meshheading:18449891-Drug Resistance, Multiple, pubmed-meshheading:18449891-Drug Resistance, Neoplasm, pubmed-meshheading:18449891-Etoposide, pubmed-meshheading:18449891-Fluorouracil, pubmed-meshheading:18449891-Gene Expression Regulation, Neoplastic, pubmed-meshheading:18449891-Genes, bcl-2, pubmed-meshheading:18449891-Humans, pubmed-meshheading:18449891-MicroRNAs, pubmed-meshheading:18449891-Microarray Analysis, pubmed-meshheading:18449891-Mitomycin, pubmed-meshheading:18449891-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:18449891-Reproducibility of Results, pubmed-meshheading:18449891-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18449891-Stomach Neoplasms, pubmed-meshheading:18449891-Up-Regulation, pubmed-meshheading:18449891-Vincristine
pubmed:year
2008
pubmed:articleTitle
miR-15b and miR-16 modulate multidrug resistance by targeting BCL2 in human gastric cancer cells.
pubmed:affiliation
State Key Laboratory of Cancer Biology and Institute of Digestive Diseases, Xijing Hospital, Fourth Military Medical University, Xi'an, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't