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GWAS Study

Metformin pharmacogenomics: a genome-wide association study to identify genetic and epigenetic biomarkers involved in metformin anticancer response using human lymphoblastoid cell lines.

Niu N, Liu T, Cairns J et al.

28173075 PubMed ID
GWAS Study Type
288 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

NN
Niu N
LT
Liu T
CJ
Cairns J
LR
Ly RC
TX
Tan X
DM
Deng M
FB
Fridley BL
KK
Kalari KR
AR
Abo RP
JG
Jenkins G
BA
Batzler A
CE
Carlson EE
BP
Barman P
MS
Moran S
HH
Heyn H
EM
Esteller M
WL
Wang L
Chapter II

Abstract

Summary of the research findings

Metformin is currently considered as a promising anticancer agent in addition to its anti-diabetic effect. To better individualize metformin therapy and explore novel molecular mechanisms in cancer treatment, we conducted a pharmacogenomic study using 266 lymphoblastoid cell lines (LCLs). Metformin cytotoxicity assay was performed using the MTS assay. Genome-wide association (GWA) analyses were performed in LCLs using 1.3 million SNPs, 485k DNA methylation probes, 54k mRNA expression probe sets, and metformin cytotoxicity (IC50s). Top candidate genes were functionally validated using siRNA screening, followed by MTS assay in breast cancer cell lines. Further study of one top candidate, STUB1, was performed to elucidate the mechanisms by which STUB1 might contribute to metformin action. GWA analyses in LCLs identified 198 mRNA expression probe sets, 12 SNP loci, and 5 DNA methylation loci associated with metformin IC50 with P-values <10−4 or <10−5. Integrated SNP/methylation loci-expression-IC50 analyses found 3 SNP loci or 5 DNA methylation loci associated with metformin IC50 through trans-regulation of expression of 11 or 26 genes with P-value <10−4. Functional validation of top 61 candidate genes in 4 IPA networks indicated down regulation of 14 genes significantly altered metformin sensitivity in two breast cancer cell lines. Mechanistic studies revealed that the E3 ubiquitin ligase, STUB1, could influence metformin response by facilitating proteasome-mediated degradation of cyclin A. GWAS using a genomic data-enriched LCL model system, together with functional and mechanistic studies using cancer cell lines, help us to identify novel genetic and epigenetic biomarkers involved in metformin anticancer response.

up to 96 African American lymphoblastoid cell lines, up to 96 Han Chinese American lymphoblastoid cell lines, up to 96 European ancestry lymphoblastoid cell lines

Chapter III

Study Statistics

Key metrics and study information

288
Total Participants
GWAS
Study Type
No
Replicated
European, East Asian, African American or Afro-Caribbean
Ancestry
U.S.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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