Abstract

Colorectal cancer is one of the most common cancers worldwide. Surgery is usually the primary treatment for colon cancers that have not spread to distant sites. However, chemotherapy may be considered after surgery to eliminate remaining cancer cells or in case the cancer has a high risk of recurrence. Oxaliplatin is often used in combination regimens such as FOLFOX, CapeOX, and FOLFOXIRI because of the cost-effectiveness of adjuvant treatment for patients and also the good tolerability profile. However, some patients show resistance to oxaliplatin which causes poor treatment outcomes. Most colon cancer studies focused on treatments and patient survival. Some studies focused on genetic associations of specific genes. However, pathway and network analyses of oxaliplatin resistance in colon cancer cells using gene expression patterns are still lacking. We performed a microarray analysis and found that endothelin-1 (EDN1), dishevelled segment polarity protein (DV1), toll-like receptor 5(TLR5), mitogen-activated protein kinase 3 (MAP2K3), phosphatidylinositol-4,5-bisphosphate 3-kinase, and catalytic subunit beta (PIK3CB) were closely related to responsiveness to oxaliplatin treatment. Furthermore, we found that the signal transduction, melanogenesis, and toll-like receptor signaling pathways might be involved in oxaliplatin-resistant colon cancer. These genes and pathways might be potential targets for improving oxaliplatin treatment in colon cancer patients.

Original languageEnglish
Pages (from-to)583-590
JournalTumor Biology
Volume37
Issue number1
DOIs
Publication statusPublished - Jan 1 2016

Fingerprint

oxaliplatin
Computational Biology
Colonic Neoplasms
Toll-Like Receptor 5
Therapeutics
Neoplasms
Mitogen-Activated Protein Kinase 3
Toll-Like Receptors
Endothelin-1
Microarray Analysis
Genes
Cost-Benefit Analysis
Colorectal Neoplasms
Signal Transduction
Catalytic Domain

Keywords

  • Bioinformatic analysis
  • Colon cancer
  • Network and pathway analysis
  • Oxaliplatin

ASJC Scopus subject areas

  • Cancer Research

Cite this

Bioinformatic analyses revealed underlying biological functions correlated with oxaliplatin responsiveness. / Klahan, Sukhontip; Huang, Chi Cheng; Chien, Shu-Chen; Wu, Mei Shin; Wong, Henry Sung Ching; Huang, Chien Yu; Chang, Wei Chiao; Wei, Po Li.

In: Tumor Biology, Vol. 37, No. 1, 01.01.2016, p. 583-590.

Research output: Contribution to journalArticle

@article{aaf958b2a12c41a49cc3899ee827020c,
title = "Bioinformatic analyses revealed underlying biological functions correlated with oxaliplatin responsiveness",
abstract = "Colorectal cancer is one of the most common cancers worldwide. Surgery is usually the primary treatment for colon cancers that have not spread to distant sites. However, chemotherapy may be considered after surgery to eliminate remaining cancer cells or in case the cancer has a high risk of recurrence. Oxaliplatin is often used in combination regimens such as FOLFOX, CapeOX, and FOLFOXIRI because of the cost-effectiveness of adjuvant treatment for patients and also the good tolerability profile. However, some patients show resistance to oxaliplatin which causes poor treatment outcomes. Most colon cancer studies focused on treatments and patient survival. Some studies focused on genetic associations of specific genes. However, pathway and network analyses of oxaliplatin resistance in colon cancer cells using gene expression patterns are still lacking. We performed a microarray analysis and found that endothelin-1 (EDN1), dishevelled segment polarity protein (DV1), toll-like receptor 5(TLR5), mitogen-activated protein kinase 3 (MAP2K3), phosphatidylinositol-4,5-bisphosphate 3-kinase, and catalytic subunit beta (PIK3CB) were closely related to responsiveness to oxaliplatin treatment. Furthermore, we found that the signal transduction, melanogenesis, and toll-like receptor signaling pathways might be involved in oxaliplatin-resistant colon cancer. These genes and pathways might be potential targets for improving oxaliplatin treatment in colon cancer patients.",
keywords = "Bioinformatic analysis, Colon cancer, Network and pathway analysis, Oxaliplatin",
author = "Sukhontip Klahan and Huang, {Chi Cheng} and Shu-Chen Chien and Wu, {Mei Shin} and Wong, {Henry Sung Ching} and Huang, {Chien Yu} and Chang, {Wei Chiao} and Wei, {Po Li}",
year = "2016",
month = "1",
day = "1",
doi = "10.1007/s13277-015-3807-2",
language = "English",
volume = "37",
pages = "583--590",
journal = "Tumor Biology",
issn = "1010-4283",
publisher = "Springer Netherlands",
number = "1",

}

TY - JOUR

T1 - Bioinformatic analyses revealed underlying biological functions correlated with oxaliplatin responsiveness

AU - Klahan, Sukhontip

AU - Huang, Chi Cheng

AU - Chien, Shu-Chen

AU - Wu, Mei Shin

AU - Wong, Henry Sung Ching

AU - Huang, Chien Yu

AU - Chang, Wei Chiao

AU - Wei, Po Li

PY - 2016/1/1

Y1 - 2016/1/1

N2 - Colorectal cancer is one of the most common cancers worldwide. Surgery is usually the primary treatment for colon cancers that have not spread to distant sites. However, chemotherapy may be considered after surgery to eliminate remaining cancer cells or in case the cancer has a high risk of recurrence. Oxaliplatin is often used in combination regimens such as FOLFOX, CapeOX, and FOLFOXIRI because of the cost-effectiveness of adjuvant treatment for patients and also the good tolerability profile. However, some patients show resistance to oxaliplatin which causes poor treatment outcomes. Most colon cancer studies focused on treatments and patient survival. Some studies focused on genetic associations of specific genes. However, pathway and network analyses of oxaliplatin resistance in colon cancer cells using gene expression patterns are still lacking. We performed a microarray analysis and found that endothelin-1 (EDN1), dishevelled segment polarity protein (DV1), toll-like receptor 5(TLR5), mitogen-activated protein kinase 3 (MAP2K3), phosphatidylinositol-4,5-bisphosphate 3-kinase, and catalytic subunit beta (PIK3CB) were closely related to responsiveness to oxaliplatin treatment. Furthermore, we found that the signal transduction, melanogenesis, and toll-like receptor signaling pathways might be involved in oxaliplatin-resistant colon cancer. These genes and pathways might be potential targets for improving oxaliplatin treatment in colon cancer patients.

AB - Colorectal cancer is one of the most common cancers worldwide. Surgery is usually the primary treatment for colon cancers that have not spread to distant sites. However, chemotherapy may be considered after surgery to eliminate remaining cancer cells or in case the cancer has a high risk of recurrence. Oxaliplatin is often used in combination regimens such as FOLFOX, CapeOX, and FOLFOXIRI because of the cost-effectiveness of adjuvant treatment for patients and also the good tolerability profile. However, some patients show resistance to oxaliplatin which causes poor treatment outcomes. Most colon cancer studies focused on treatments and patient survival. Some studies focused on genetic associations of specific genes. However, pathway and network analyses of oxaliplatin resistance in colon cancer cells using gene expression patterns are still lacking. We performed a microarray analysis and found that endothelin-1 (EDN1), dishevelled segment polarity protein (DV1), toll-like receptor 5(TLR5), mitogen-activated protein kinase 3 (MAP2K3), phosphatidylinositol-4,5-bisphosphate 3-kinase, and catalytic subunit beta (PIK3CB) were closely related to responsiveness to oxaliplatin treatment. Furthermore, we found that the signal transduction, melanogenesis, and toll-like receptor signaling pathways might be involved in oxaliplatin-resistant colon cancer. These genes and pathways might be potential targets for improving oxaliplatin treatment in colon cancer patients.

KW - Bioinformatic analysis

KW - Colon cancer

KW - Network and pathway analysis

KW - Oxaliplatin

UR - http://www.scopus.com/inward/record.url?scp=84938634198&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84938634198&partnerID=8YFLogxK

U2 - 10.1007/s13277-015-3807-2

DO - 10.1007/s13277-015-3807-2

M3 - Article

C2 - 26232912

AN - SCOPUS:84938634198

VL - 37

SP - 583

EP - 590

JO - Tumor Biology

JF - Tumor Biology

SN - 1010-4283

IS - 1

ER -