%0 Journal Article %1 PerezRiesgo:2017:Int-J-Mol-Sci:28448473 %A Pérez-Riesgo, E %A Gutiérrez, L G %A Ubierna, D %A Acedo, A %A Moyer, M P %A Núñez, L %A Villalobos, C %D 2017 %J Int J Mol Sci %K cancer-research clustering rna-seq shouldread %N 5 %R 10.3390/ijms18050922 %T Transcriptomic Analysis of Calcium Remodeling in Colorectal Cancer %U https://www.ncbi.nlm.nih.gov/pubmed/28448473 %V 18 %X Colorectal cancer (CRC) cells undergo the remodeling of intracellular Ca2+ homeostasis, which contributes to cancer hallmarks such as enhanced proliferation, invasion and survival. Ca2+ remodeling includes critical changes in store-operated Ca2+ entry (SOCE) and Ca2+ store content. Some changes have been investigated at the molecular level. However, since nearly 100 genes are involved in intracellular Ca2+ transport, a comprehensive view of Ca2+ remodeling in CRC is lacking. We have used Next Generation Sequencing (NGS) to investigate differences in expression of 77 selected gene transcripts involved in intracellular Ca2+ transport in CRC. To this end, mRNA from normal human colonic NCM460 cells and human colon cancer HT29 cells was isolated and used as a template for transcriptomic sequencing and expression analysis using Ion Torrent technology. After data transformation and filtering, exploratory analysis revealed that both cell types were well segregated. In addition, differential gene expression using R and bioconductor packages show significant differences in expression of selected voltage-operated Ca2+ channels and store-operated Ca2+ entry players, transient receptor potential (TRP) channels, Ca2+ release channels, Ca2+ pumps, Na⁺/Ca2+ exchanger isoforms and genes involved in mitochondrial Ca2+ transport. These data provide the first comprehensive transcriptomic analysis of Ca2+ remodeling in CRC.

@article{PerezRiesgo:2017:Int-J-Mol-Sci:28448473, abstract = {Colorectal cancer (CRC) cells undergo the remodeling of intracellular Ca2+ homeostasis, which contributes to cancer hallmarks such as enhanced proliferation, invasion and survival. Ca2+ remodeling includes critical changes in store-operated Ca2+ entry (SOCE) and Ca2+ store content. Some changes have been investigated at the molecular level. However, since nearly 100 genes are involved in intracellular Ca2+ transport, a comprehensive view of Ca2+ remodeling in CRC is lacking. We have used Next Generation Sequencing (NGS) to investigate differences in expression of 77 selected gene transcripts involved in intracellular Ca2+ transport in CRC. To this end, mRNA from normal human colonic NCM460 cells and human colon cancer HT29 cells was isolated and used as a template for transcriptomic sequencing and expression analysis using Ion Torrent technology. After data transformation and filtering, exploratory analysis revealed that both cell types were well segregated. In addition, differential gene expression using R and bioconductor packages show significant differences in expression of selected voltage-operated Ca2+ channels and store-operated Ca2+ entry players, transient receptor potential (TRP) channels, Ca2+ release channels, Ca2+ pumps, Na⁺/Ca2+ exchanger isoforms and genes involved in mitochondrial Ca2+ transport. These data provide the first comprehensive transcriptomic analysis of Ca2+ remodeling in CRC.}, added-at = {2019-04-24T22:52:07.000+0200}, author = {P{\'e}rez-Riesgo, E and Guti{\'e}rrez, L G and Ubierna, D and Acedo, A and Moyer, M P and N{\'u}{\~n}ez, L and Villalobos, C}, biburl = {https://www.bibsonomy.org/bibtex/2863fec589a058ea518eb1c01f0288a7b/marcsaric}, description = {Transcriptomic Analysis of Calcium Remodeling in Colorectal Cancer. - PubMed - NCBI}, doi = {10.3390/ijms18050922}, interhash = {0868855d4b529a114736f5a3de769557}, intrahash = {863fec589a058ea518eb1c01f0288a7b}, journal = {Int J Mol Sci}, keywords = {cancer-research clustering rna-seq shouldread}, month = apr, number = 5, pmid = {28448473}, timestamp = {2019-04-24T22:52:07.000+0200}, title = {Transcriptomic Analysis of Calcium Remodeling in Colorectal Cancer}, url = {https://www.ncbi.nlm.nih.gov/pubmed/28448473}, volume = 18, year = 2017 }