Senescence-Associated Gene YPEL3 Is Downregulated in Human Colon Tumors

Rebecca Tuttle; Margo Simon; David C. Hitch; J. Nicholas Maiorano; Minia Hellan; James R. Ouellette; Paula M. Termuhlen; Steven J. Berberich

doi:10.1245/s10434-011-1558-x

Senescence-Associated Gene YPEL3 Is Downregulated in Human Colon Tumors

Rebecca Tuttle
, Margo Simon
, David C. Hitch
, J. Nicholas Maiorano
, Minia Hellan
, James R. Ouellette
, Paula M. Termuhlen
, Steven J. Berberich

Research output: Contribution to journal › Article › peer-review

Abstract

<p> <h3> Background </h3></p><p> Previous work has demonstrated YPEL3 to be a growth-suppressive protein that acts through a pathway of cellular senescence. We set out to determine whether human colon tumors demonstrated downregulation of <em> YPEL3 </em> . <h3> Methods </h3></p><p> We collected colon tumor samples with matched normal control samples and analyzed them for <em> YPEL3 </em> gene expression by reverse transcriptase–polymerase chain reaction and <a href="http://link.springer.com/search?dc.title=CpG&facet-content-type=ReferenceWorkEntry&sortOrder=relevance"> CpG </a> hypermethylation of the <em> YPEL3 </em> promoter by base-specific polymerase chain reaction analysis. Colon cancer cell lines (Caco-2 and HCT116 <sup> −/− </sup> p53) were used to assess <em> YPEL3 </em> gene expression after treatment with 5-azadeoxycytidine or trichostatin A. <h3> Results </h3></p><p> Reverse transcriptase–polymerase chain reaction analysis demonstrated a decrease in <em> YPEL3 </em> expression in tumor samples when compared to their patient-matched normal tissue. We determined that DNA methylation of the <em> YPEL3 </em> promoter <a href="http://link.springer.com/search?dc.title=CpG&facet-content-type=ReferenceWorkEntry&sortOrder=relevance"> CpG </a> island does not play a role in <em> YPEL3 </em> regulation in human colon tumors or colon cancer cells lines, consistent with the inability of 5-azadeoxycytidine treatment to induce <em> YPEL3 </em> expression in colon cancer cell lines. In contrast, colon cell line results suggest that histone acetylation may play a role in <em> YPEL3 </em> regulation in colon cancer. <h3> Conclusions </h3></p><p> <em> YPEL3 </em> is preferentially downregulated in human colon adenocarcinomas. DNA hypermethylation does not appear to be the mechanism of <em> YPEL3 </em> downregulation in this subset of collected patient samples or in colon cell lines. Histone acetylation may be a relevant epigenetic modulator of <em> YPEL3 </em> in colon adenocarcinomas. Future investigation of <em> YPEL3 </em> and its role in colon cancer signaling and development may lead to increased understanding and alternative treatment options for this disease.</p>

Original language	American English
Journal	Annals of Surgical Oncology
Volume	18
DOIs	https://doi.org/10.1245/s10434-011-1558-x
State	Published - Jun 1 2011
Externally published	Yes

Keywords

Oncology
Surgery
Surgical Oncology

Disciplines

Medical Specialties
Medicine and Health Sciences
Oncology
Surgery

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@article{a608b3cbd55a418f948472f8cae4e199,

title = "Senescence-Associated Gene YPEL3 Is Downregulated in Human Colon Tumors",

abstract = " Background Previous work has demonstrated YPEL3 to be a growth-suppressive protein that acts through a pathway of cellular senescence. We set out to determine whether human colon tumors demonstrated downregulation of YPEL3 . Methods We collected colon tumor samples with matched normal control samples and analyzed them for YPEL3 gene expression by reverse transcriptase\–polymerase chain reaction and CpG hypermethylation of the YPEL3 promoter by base-specific polymerase chain reaction analysis. Colon cancer cell lines (Caco-2 and HCT116 \−/\− p53) were used to assess YPEL3 gene expression after treatment with 5-azadeoxycytidine or trichostatin A. Results Reverse transcriptase\–polymerase chain reaction analysis demonstrated a decrease in YPEL3 expression in tumor samples when compared to their patient-matched normal tissue. We determined that DNA methylation of the YPEL3 promoter CpG island does not play a role in YPEL3 regulation in human colon tumors or colon cancer cells lines, consistent with the inability of 5-azadeoxycytidine treatment to induce YPEL3 expression in colon cancer cell lines. In contrast, colon cell line results suggest that histone acetylation may play a role in YPEL3 regulation in colon cancer. Conclusions YPEL3 is preferentially downregulated in human colon adenocarcinomas. DNA hypermethylation does not appear to be the mechanism of YPEL3 downregulation in this subset of collected patient samples or in colon cell lines. Histone acetylation may be a relevant epigenetic modulator of YPEL3 in colon adenocarcinomas. Future investigation of YPEL3 and its role in colon cancer signaling and development may lead to increased understanding and alternative treatment options for this disease.",

keywords = "Oncology, Surgery, Surgical Oncology",

author = "Rebecca Tuttle and Margo Simon and Hitch, \{David C.\} and Maiorano, \{J. Nicholas\} and Minia Hellan and Ouellette, \{James R.\} and Termuhlen, \{Paula M.\} and Berberich, \{Steven J.\}",

year = "2011",

month = jun,

day = "1",

doi = "10.1245/s10434-011-1558-x",

language = "American English",

volume = "18",

journal = "Annals of Surgical Oncology",

}

TY - JOUR

T1 - Senescence-Associated Gene YPEL3 Is Downregulated in Human Colon Tumors

AU - Tuttle, Rebecca

AU - Simon, Margo

AU - Hitch, David C.

AU - Maiorano, J. Nicholas

AU - Hellan, Minia

AU - Ouellette, James R.

AU - Termuhlen, Paula M.

AU - Berberich, Steven J.

PY - 2011/6/1

Y1 - 2011/6/1

N2 - Background Previous work has demonstrated YPEL3 to be a growth-suppressive protein that acts through a pathway of cellular senescence. We set out to determine whether human colon tumors demonstrated downregulation of YPEL3 . Methods We collected colon tumor samples with matched normal control samples and analyzed them for YPEL3 gene expression by reverse transcriptase–polymerase chain reaction and CpG hypermethylation of the YPEL3 promoter by base-specific polymerase chain reaction analysis. Colon cancer cell lines (Caco-2 and HCT116 −/− p53) were used to assess YPEL3 gene expression after treatment with 5-azadeoxycytidine or trichostatin A. Results Reverse transcriptase–polymerase chain reaction analysis demonstrated a decrease in YPEL3 expression in tumor samples when compared to their patient-matched normal tissue. We determined that DNA methylation of the YPEL3 promoter CpG island does not play a role in YPEL3 regulation in human colon tumors or colon cancer cells lines, consistent with the inability of 5-azadeoxycytidine treatment to induce YPEL3 expression in colon cancer cell lines. In contrast, colon cell line results suggest that histone acetylation may play a role in YPEL3 regulation in colon cancer. Conclusions YPEL3 is preferentially downregulated in human colon adenocarcinomas. DNA hypermethylation does not appear to be the mechanism of YPEL3 downregulation in this subset of collected patient samples or in colon cell lines. Histone acetylation may be a relevant epigenetic modulator of YPEL3 in colon adenocarcinomas. Future investigation of YPEL3 and its role in colon cancer signaling and development may lead to increased understanding and alternative treatment options for this disease.

AB - Background Previous work has demonstrated YPEL3 to be a growth-suppressive protein that acts through a pathway of cellular senescence. We set out to determine whether human colon tumors demonstrated downregulation of YPEL3 . Methods We collected colon tumor samples with matched normal control samples and analyzed them for YPEL3 gene expression by reverse transcriptase–polymerase chain reaction and CpG hypermethylation of the YPEL3 promoter by base-specific polymerase chain reaction analysis. Colon cancer cell lines (Caco-2 and HCT116 −/− p53) were used to assess YPEL3 gene expression after treatment with 5-azadeoxycytidine or trichostatin A. Results Reverse transcriptase–polymerase chain reaction analysis demonstrated a decrease in YPEL3 expression in tumor samples when compared to their patient-matched normal tissue. We determined that DNA methylation of the YPEL3 promoter CpG island does not play a role in YPEL3 regulation in human colon tumors or colon cancer cells lines, consistent with the inability of 5-azadeoxycytidine treatment to induce YPEL3 expression in colon cancer cell lines. In contrast, colon cell line results suggest that histone acetylation may play a role in YPEL3 regulation in colon cancer. Conclusions YPEL3 is preferentially downregulated in human colon adenocarcinomas. DNA hypermethylation does not appear to be the mechanism of YPEL3 downregulation in this subset of collected patient samples or in colon cell lines. Histone acetylation may be a relevant epigenetic modulator of YPEL3 in colon adenocarcinomas. Future investigation of YPEL3 and its role in colon cancer signaling and development may lead to increased understanding and alternative treatment options for this disease.

KW - Oncology

KW - Surgery

KW - Surgical Oncology

UR - https://corescholar.libraries.wright.edu/surg/344

U2 - 10.1245/s10434-011-1558-x

DO - 10.1245/s10434-011-1558-x

M3 - Article

VL - 18

JO - Annals of Surgical Oncology

JF - Annals of Surgical Oncology

ER -

Senescence-Associated Gene YPEL3 Is Downregulated in Human Colon Tumors

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