Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016 May;17(3):468-78.
doi: 10.1093/bib/bbv053. Epub 2015 Jul 27.

A literature mining-based approach for identification of cellular pathways associated with chemoresistance in cancer

A literature mining-based approach for identification of cellular pathways associated with chemoresistance in cancer

Jung Hun Oh et al. Brief Bioinform. 2016 May.

Abstract

Chemoresistance is a major obstacle to the successful treatment of many human cancer types. Increasing evidence has revealed that chemoresistance involves many genes and multiple complex biological mechanisms including cancer stem cells, drug efflux mechanism, autophagy and epithelial-mesenchymal transition. Many studies have been conducted to investigate the possible molecular mechanisms of chemoresistance. However, understanding of the biological mechanisms in chemoresistance still remains limited. We surveyed the literature on chemoresistance-related genes and pathways of multiple cancer types. We then used a curated pathway database to investigate significant chemoresistance-related biological pathways. In addition, to investigate the importance of chemoresistance-related markers in protein-protein interaction networks identified using the curated database, we used a gene-ranking algorithm designed based on a graph-based scoring function in our previous study. Our comprehensive survey and analysis provide a systems biology-based overview of the underlying mechanisms of chemoresistance.

Keywords: cancer; chemoresistance; chemotherapy; gene; pathway; systems biology.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Venn diagrams depicting the number of shared and unique genes (A) among breast, ovarian, and pancreatic cancers and (B) among breast, ovarian, and lung cancers using the gene list shown in Table 1 (a family of proteins was counted as 1). For both the Venn diagrams, the left-top and right-top circles indicate breast cancer and ovarian cancer, respectively. A colour version of this figure is available at BIB online: http://bib.oxfordjournals.org.
Figure 2.
Figure 2.
Connected protein–protein interaction networks constructed using (A) a MetaCore platform tool, and (B) a power graph analysis tool with a list of chemoresistance-related genes of pancreatic cancer.
Figure 2.
Figure 2.
Connected protein–protein interaction networks constructed using (A) a MetaCore platform tool, and (B) a power graph analysis tool with a list of chemoresistance-related genes of pancreatic cancer.

References

    1. Guo X, Ma N, Wang J, et al. Increased p38-MAPK is responsible for chemotherapy resistance in human gastric cancer cells. BMC Cancer 2008;8:375. - PMC - PubMed
    1. Rivera E, Gomez H. Chemotherapy resistance in metastatic breast cancer: the evolving role of ixabepilone. Breast Cancer Res 2010;12(Suppl 2):S2. - PMC - PubMed
    1. Yang JY, Chang CJ, Xia W, et al. Activation of FOXO3a is sufficient to reverse mitogen-activated protein/extracellular signal-regulated kinase kinase inhibitor chemoresistance in human cancer. Cancer Res 2010;70:4709–18. - PMC - PubMed
    1. Antoon JW, White MD, Slaughter EM, et al. Targeting NFĸB mediated breast cancer chemoresistance through selective inhibition of sphingosine kinase-2. Cancer Biol Ther 2011;11:678–89. - PMC - PubMed
    1. An Y, Ongkeko WM. ABCG2: the key to chemoresistance in cancer stem cells?. Expert Opin Drug Metab Toxicol 2009;5:1529–42. - PubMed