Effect of EI24 expression on the tumorigenesis of ApcMin/+ colorectal cancer mouse model

Tae Wook Nam; Song Yi Park; Jae Hoon Lee; Jae il Roh; Han Woong Lee

doi:10.1016/j.bbrc.2019.04.186

Effect of EI24 expression on the tumorigenesis of Apc^Min/+ colorectal cancer mouse model

Tae Wook Nam, Song Yi Park, Jae Hoon Lee, Jae il Roh, Han Woong Lee

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

1 Citation (Scopus)

Abstract

Etoposide-induced 2.4 kb transcript (EI24, also known as PIG8) is a p53 target gene involved in cell growth suppression and apoptosis and known to be frequently altered in human cancers. Although EI24 expression is decreased in various cancers and is associated with colorectal cancer progression and metastasis, the physiological function of EI24 in colorectal cancer is yet unclear. We generated an Ei24 conditional transgenic (Tg) mouse to study the therapeutic effects of Ei24 in vivo and evaluated whether Ei24 plays a role of a tumor suppressor using Ei24 Tg mouse crossed with Apc^Min/+ mouse, which develops multiple intestinal adenomas. The overexpression of Ei24 failed to cause any notable difference in the number of polyps, lengths of the intestine and spleen, and survival rate between Apc^Min/+ and Apc^Min/+ Ei24 Tg mice. Ei24 plays no significant role in colon cancer caused by the substitutional mutation of Apc in mice. Therefore, our result dismisses the hypothesized direct link between Apc^Min/+ mutation and Ei24 expression in colorectal cancer model.

Original language	English
Pages (from-to)	1087-1092
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	514
Issue number	4
DOIs	https://doi.org/10.1016/j.bbrc.2019.04.186
Publication status	Published - 2019 Jul 5

Bibliographical note

Funding Information:
This work was supported by grants from the National Research Foundation of Korea (NRF; 2017R1A4A1015328 and 2018R1A2A1A05022746 ). Both grants were supported in managing the mouse and gave funds for studying Ei24. The National Research Foundation of Korea was not involved in study design, data collection, data analysis, or interpretation of study results.

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

Access to Document

10.1016/j.bbrc.2019.04.186

Fingerprint Dive into the research topics of 'Effect of EI24 expression on the tumorigenesis of Apc<sup>Min/+</sup> colorectal cancer mouse model'. Together they form a unique fingerprint.

Cite this

@article{532c3eb36f7f4c5b89c359b6eaec0718,

title = "Effect of EI24 expression on the tumorigenesis of ApcMin/+ colorectal cancer mouse model",

abstract = "Etoposide-induced 2.4 kb transcript (EI24, also known as PIG8) is a p53 target gene involved in cell growth suppression and apoptosis and known to be frequently altered in human cancers. Although EI24 expression is decreased in various cancers and is associated with colorectal cancer progression and metastasis, the physiological function of EI24 in colorectal cancer is yet unclear. We generated an Ei24 conditional transgenic (Tg) mouse to study the therapeutic effects of Ei24 in vivo and evaluated whether Ei24 plays a role of a tumor suppressor using Ei24 Tg mouse crossed with ApcMin/+ mouse, which develops multiple intestinal adenomas. The overexpression of Ei24 failed to cause any notable difference in the number of polyps, lengths of the intestine and spleen, and survival rate between ApcMin/+ and ApcMin/+ Ei24 Tg mice. Ei24 plays no significant role in colon cancer caused by the substitutional mutation of Apc in mice. Therefore, our result dismisses the hypothesized direct link between ApcMin/+ mutation and Ei24 expression in colorectal cancer model.",

author = "Nam, {Tae Wook} and Park, {Song Yi} and Lee, {Jae Hoon} and Roh, {Jae il} and Lee, {Han Woong}",

note = "Funding Information: This work was supported by grants from the National Research Foundation of Korea (NRF; 2017R1A4A1015328 and 2018R1A2A1A05022746 ). Both grants were supported in managing the mouse and gave funds for studying Ei24. The National Research Foundation of Korea was not involved in study design, data collection, data analysis, or interpretation of study results. ",

year = "2019",

month = jul,

day = "5",

doi = "10.1016/j.bbrc.2019.04.186",

language = "English",

volume = "514",

pages = "1087--1092",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Academic Press Inc.",

number = "4",

}

TY - JOUR

T1 - Effect of EI24 expression on the tumorigenesis of ApcMin/+ colorectal cancer mouse model

AU - Nam, Tae Wook

AU - Park, Song Yi

AU - Lee, Jae Hoon

AU - Roh, Jae il

AU - Lee, Han Woong

N1 - Funding Information: This work was supported by grants from the National Research Foundation of Korea (NRF; 2017R1A4A1015328 and 2018R1A2A1A05022746 ). Both grants were supported in managing the mouse and gave funds for studying Ei24. The National Research Foundation of Korea was not involved in study design, data collection, data analysis, or interpretation of study results.

PY - 2019/7/5

Y1 - 2019/7/5

N2 - Etoposide-induced 2.4 kb transcript (EI24, also known as PIG8) is a p53 target gene involved in cell growth suppression and apoptosis and known to be frequently altered in human cancers. Although EI24 expression is decreased in various cancers and is associated with colorectal cancer progression and metastasis, the physiological function of EI24 in colorectal cancer is yet unclear. We generated an Ei24 conditional transgenic (Tg) mouse to study the therapeutic effects of Ei24 in vivo and evaluated whether Ei24 plays a role of a tumor suppressor using Ei24 Tg mouse crossed with ApcMin/+ mouse, which develops multiple intestinal adenomas. The overexpression of Ei24 failed to cause any notable difference in the number of polyps, lengths of the intestine and spleen, and survival rate between ApcMin/+ and ApcMin/+ Ei24 Tg mice. Ei24 plays no significant role in colon cancer caused by the substitutional mutation of Apc in mice. Therefore, our result dismisses the hypothesized direct link between ApcMin/+ mutation and Ei24 expression in colorectal cancer model.

AB - Etoposide-induced 2.4 kb transcript (EI24, also known as PIG8) is a p53 target gene involved in cell growth suppression and apoptosis and known to be frequently altered in human cancers. Although EI24 expression is decreased in various cancers and is associated with colorectal cancer progression and metastasis, the physiological function of EI24 in colorectal cancer is yet unclear. We generated an Ei24 conditional transgenic (Tg) mouse to study the therapeutic effects of Ei24 in vivo and evaluated whether Ei24 plays a role of a tumor suppressor using Ei24 Tg mouse crossed with ApcMin/+ mouse, which develops multiple intestinal adenomas. The overexpression of Ei24 failed to cause any notable difference in the number of polyps, lengths of the intestine and spleen, and survival rate between ApcMin/+ and ApcMin/+ Ei24 Tg mice. Ei24 plays no significant role in colon cancer caused by the substitutional mutation of Apc in mice. Therefore, our result dismisses the hypothesized direct link between ApcMin/+ mutation and Ei24 expression in colorectal cancer model.

UR - http://www.scopus.com/inward/record.url?scp=85065524056&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85065524056&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2019.04.186

DO - 10.1016/j.bbrc.2019.04.186

M3 - Article

C2 - 31097220

AN - SCOPUS:85065524056

VL - 514

SP - 1087

EP - 1092

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 4

ER -