Identifying genes with differential expression in gemcitabine-resistant pancreatic cancer cells using comprehensive transcriptome analysis.

Yousuke Nakai, Motoyuki Otsuka, Yujin Hoshida, Minoru Tada, Yutaka Komatsu, Takao Kawabe, Masao Omata

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Pancreatic cancer is often unresectable at diagnosis, and chemotherapy using gemcitabine is now the standard treatment for advanced pancreatic cancer. However, acquired resistance to gemcitabine resulting in therapeutic failure is often encountered. Therefore, we sought to identify genes that determine gemcitabine resistance by evaluating the relationship between gene expression profiles and gemcitabine sensitivity to provide molecular targets for overcoming gemcitabine resistance. First, the gemcitabine concentration needed for 50% growth inhibition was examined in six pancreatic cancer cell lines. By exposing MIA PaCa-2 cells to long-term gemcitabine, we established gemcitabine-resistant cells. The gene expression profiles of the six pancreatic cancer cell lines and gemcitabine-resistant cells were determined using cDNA microarray analysis. By comparing the results, 30 genes were identified as differentially expressed genes correlated with gemcitabine sensitivity. Differentially expressed genes in the parental cell lines were also examined, and six overlapping genes were identified as genes correlated with gemcitabine sensitivity in both assays. Of these genes, the down-regulated expression of TNFSF6 protein, also known as Fas ligand, was confirmed in the gemcitabine-resistant cell line. These results should provide therapeutic molecular targets for overcoming gemcitabine resistance.

Original languageEnglish (US)
Pages (from-to)1263-1267
Number of pages5
JournalOncology reports
Volume14
Issue number5
StatePublished - Nov 2005
Externally publishedYes

Fingerprint

gemcitabine
Gene Expression Profiling
Pancreatic Neoplasms
Genes
Cell Line
Transcriptome
Overlapping Genes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Identifying genes with differential expression in gemcitabine-resistant pancreatic cancer cells using comprehensive transcriptome analysis. / Nakai, Yousuke; Otsuka, Motoyuki; Hoshida, Yujin; Tada, Minoru; Komatsu, Yutaka; Kawabe, Takao; Omata, Masao.

In: Oncology reports, Vol. 14, No. 5, 11.2005, p. 1263-1267.

Research output: Contribution to journalArticle

Nakai, Yousuke ; Otsuka, Motoyuki ; Hoshida, Yujin ; Tada, Minoru ; Komatsu, Yutaka ; Kawabe, Takao ; Omata, Masao. / Identifying genes with differential expression in gemcitabine-resistant pancreatic cancer cells using comprehensive transcriptome analysis. In: Oncology reports. 2005 ; Vol. 14, No. 5. pp. 1263-1267.
@article{cd7f4679c4fc4bc6a9db8795a2097505,
title = "Identifying genes with differential expression in gemcitabine-resistant pancreatic cancer cells using comprehensive transcriptome analysis.",
abstract = "Pancreatic cancer is often unresectable at diagnosis, and chemotherapy using gemcitabine is now the standard treatment for advanced pancreatic cancer. However, acquired resistance to gemcitabine resulting in therapeutic failure is often encountered. Therefore, we sought to identify genes that determine gemcitabine resistance by evaluating the relationship between gene expression profiles and gemcitabine sensitivity to provide molecular targets for overcoming gemcitabine resistance. First, the gemcitabine concentration needed for 50{\%} growth inhibition was examined in six pancreatic cancer cell lines. By exposing MIA PaCa-2 cells to long-term gemcitabine, we established gemcitabine-resistant cells. The gene expression profiles of the six pancreatic cancer cell lines and gemcitabine-resistant cells were determined using cDNA microarray analysis. By comparing the results, 30 genes were identified as differentially expressed genes correlated with gemcitabine sensitivity. Differentially expressed genes in the parental cell lines were also examined, and six overlapping genes were identified as genes correlated with gemcitabine sensitivity in both assays. Of these genes, the down-regulated expression of TNFSF6 protein, also known as Fas ligand, was confirmed in the gemcitabine-resistant cell line. These results should provide therapeutic molecular targets for overcoming gemcitabine resistance.",
author = "Yousuke Nakai and Motoyuki Otsuka and Yujin Hoshida and Minoru Tada and Yutaka Komatsu and Takao Kawabe and Masao Omata",
year = "2005",
month = "11",
language = "English (US)",
volume = "14",
pages = "1263--1267",
journal = "Oncology Reports",
issn = "1021-335X",
publisher = "Spandidos Publications",
number = "5",

}

TY - JOUR

T1 - Identifying genes with differential expression in gemcitabine-resistant pancreatic cancer cells using comprehensive transcriptome analysis.

AU - Nakai, Yousuke

AU - Otsuka, Motoyuki

AU - Hoshida, Yujin

AU - Tada, Minoru

AU - Komatsu, Yutaka

AU - Kawabe, Takao

AU - Omata, Masao

PY - 2005/11

Y1 - 2005/11

N2 - Pancreatic cancer is often unresectable at diagnosis, and chemotherapy using gemcitabine is now the standard treatment for advanced pancreatic cancer. However, acquired resistance to gemcitabine resulting in therapeutic failure is often encountered. Therefore, we sought to identify genes that determine gemcitabine resistance by evaluating the relationship between gene expression profiles and gemcitabine sensitivity to provide molecular targets for overcoming gemcitabine resistance. First, the gemcitabine concentration needed for 50% growth inhibition was examined in six pancreatic cancer cell lines. By exposing MIA PaCa-2 cells to long-term gemcitabine, we established gemcitabine-resistant cells. The gene expression profiles of the six pancreatic cancer cell lines and gemcitabine-resistant cells were determined using cDNA microarray analysis. By comparing the results, 30 genes were identified as differentially expressed genes correlated with gemcitabine sensitivity. Differentially expressed genes in the parental cell lines were also examined, and six overlapping genes were identified as genes correlated with gemcitabine sensitivity in both assays. Of these genes, the down-regulated expression of TNFSF6 protein, also known as Fas ligand, was confirmed in the gemcitabine-resistant cell line. These results should provide therapeutic molecular targets for overcoming gemcitabine resistance.

AB - Pancreatic cancer is often unresectable at diagnosis, and chemotherapy using gemcitabine is now the standard treatment for advanced pancreatic cancer. However, acquired resistance to gemcitabine resulting in therapeutic failure is often encountered. Therefore, we sought to identify genes that determine gemcitabine resistance by evaluating the relationship between gene expression profiles and gemcitabine sensitivity to provide molecular targets for overcoming gemcitabine resistance. First, the gemcitabine concentration needed for 50% growth inhibition was examined in six pancreatic cancer cell lines. By exposing MIA PaCa-2 cells to long-term gemcitabine, we established gemcitabine-resistant cells. The gene expression profiles of the six pancreatic cancer cell lines and gemcitabine-resistant cells were determined using cDNA microarray analysis. By comparing the results, 30 genes were identified as differentially expressed genes correlated with gemcitabine sensitivity. Differentially expressed genes in the parental cell lines were also examined, and six overlapping genes were identified as genes correlated with gemcitabine sensitivity in both assays. Of these genes, the down-regulated expression of TNFSF6 protein, also known as Fas ligand, was confirmed in the gemcitabine-resistant cell line. These results should provide therapeutic molecular targets for overcoming gemcitabine resistance.

UR - http://www.scopus.com/inward/record.url?scp=27744503070&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=27744503070&partnerID=8YFLogxK

M3 - Article

C2 - 16211294

AN - SCOPUS:27744503070

VL - 14

SP - 1263

EP - 1267

JO - Oncology Reports

JF - Oncology Reports

SN - 1021-335X

IS - 5

ER -