HCCR-1-Interacting Molecule "Deleted in Polyposis 1" Plays a Tumor-Suppressor Role in Colon Carcinogenesis

Seung Min Shin, Yeun Jun Chung, Seong Tack Oh, Hae Myung Jeon, Lae Jeong Hwang, Hong Namkoong, Hyun Kee Kim, Goang Won Cho, Soo Young Hur, Tae Eung Kim, Youn Soo Lee, Yong Gyu Park, Je Sang Ko, Jin Woo Kim

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background & Aims: Human cervical cancer oncogene (HCCR-1) has appeared to act as a negative regulator of p53 and contributes to tumorigenesis of various organs including the colon. We identified the HCCR-1 binding protein deleted in polyposis 1 (DP1) and accessed the role of HCCR-1 and DP1 in colon tumorigenesis. Methods: Yeast 2-hybrid was used to identify HCCR-1 interacting proteins. Various molecular biological approaches were used to examine the expression profile of HCCR-1 and DP1, subcellular localization, epitope mapping, the biological role of DP1, and the serum HCCR-1 level. Loss of heterozygosity frequency around DP1 also was examined. Results: We identified that HCCR-1 interacted with DP1. These 2 proteins colocalized in mitochondria but the expression of HCCR-1 showed negative correlation with that of DP1 in colorectal cancer (CRC). DP1 played a tumor-suppressor role in colon tumorigenesis (ie, DP1-transfected RKO cells showed growth inhibition, apoptosis, decreased telomerase activity, and up-regulation of p53). These phenomena were reversed when HCCR-1 was overexpressed. Loss of heterozygosity around the DP1 gene was observed frequently (50%) in CRCs. We examined the use of serum HCCR-1 in CRC patients. The sensitivity of HCCR-1 (76.0%) for detecting CRC was proven to be much higher than that of CA19-9 (32.0%). Conclusions: DP1 plays a tumor-suppressor role in CRC. DP1 and HCCR-1 are supposed to regulate each other negatively by interaction, but further study is required to get better insight into the biological significance of the interaction.

Original languageEnglish
Pages (from-to)2074-2086
Number of pages13
JournalGastroenterology
Volume130
Issue number7
DOIs
Publication statusPublished - 2006 Jul 1

Fingerprint

Colorectal Neoplasms
Colon
Carcinogenesis
Loss of Heterozygosity
Neoplasms
Epitope Mapping
Telomerase
Serum
Oncogenes
Uterine Cervical Neoplasms
Carrier Proteins
Mitochondria
Proteins
Up-Regulation
Yeasts
Apoptosis
Growth
Genes

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Shin, S. M., Chung, Y. J., Oh, S. T., Jeon, H. M., Hwang, L. J., Namkoong, H., ... Kim, J. W. (2006). HCCR-1-Interacting Molecule "Deleted in Polyposis 1" Plays a Tumor-Suppressor Role in Colon Carcinogenesis. Gastroenterology, 130(7), 2074-2086. https://doi.org/10.1053/j.gastro.2006.03.055

HCCR-1-Interacting Molecule "Deleted in Polyposis 1" Plays a Tumor-Suppressor Role in Colon Carcinogenesis. / Shin, Seung Min; Chung, Yeun Jun; Oh, Seong Tack; Jeon, Hae Myung; Hwang, Lae Jeong; Namkoong, Hong; Kim, Hyun Kee; Cho, Goang Won; Hur, Soo Young; Kim, Tae Eung; Lee, Youn Soo; Park, Yong Gyu; Ko, Je Sang; Kim, Jin Woo.

In: Gastroenterology, Vol. 130, No. 7, 01.07.2006, p. 2074-2086.

Research output: Contribution to journalArticle

Shin, SM, Chung, YJ, Oh, ST, Jeon, HM, Hwang, LJ, Namkoong, H, Kim, HK, Cho, GW, Hur, SY, Kim, TE, Lee, YS, Park, YG, Ko, JS & Kim, JW 2006, 'HCCR-1-Interacting Molecule "Deleted in Polyposis 1" Plays a Tumor-Suppressor Role in Colon Carcinogenesis', Gastroenterology, vol. 130, no. 7, pp. 2074-2086. https://doi.org/10.1053/j.gastro.2006.03.055
Shin, Seung Min ; Chung, Yeun Jun ; Oh, Seong Tack ; Jeon, Hae Myung ; Hwang, Lae Jeong ; Namkoong, Hong ; Kim, Hyun Kee ; Cho, Goang Won ; Hur, Soo Young ; Kim, Tae Eung ; Lee, Youn Soo ; Park, Yong Gyu ; Ko, Je Sang ; Kim, Jin Woo. / HCCR-1-Interacting Molecule "Deleted in Polyposis 1" Plays a Tumor-Suppressor Role in Colon Carcinogenesis. In: Gastroenterology. 2006 ; Vol. 130, No. 7. pp. 2074-2086.
@article{c66d0e57e1b647bd820a791880bc1e8a,
title = "HCCR-1-Interacting Molecule {"}Deleted in Polyposis 1{"} Plays a Tumor-Suppressor Role in Colon Carcinogenesis",
abstract = "Background & Aims: Human cervical cancer oncogene (HCCR-1) has appeared to act as a negative regulator of p53 and contributes to tumorigenesis of various organs including the colon. We identified the HCCR-1 binding protein deleted in polyposis 1 (DP1) and accessed the role of HCCR-1 and DP1 in colon tumorigenesis. Methods: Yeast 2-hybrid was used to identify HCCR-1 interacting proteins. Various molecular biological approaches were used to examine the expression profile of HCCR-1 and DP1, subcellular localization, epitope mapping, the biological role of DP1, and the serum HCCR-1 level. Loss of heterozygosity frequency around DP1 also was examined. Results: We identified that HCCR-1 interacted with DP1. These 2 proteins colocalized in mitochondria but the expression of HCCR-1 showed negative correlation with that of DP1 in colorectal cancer (CRC). DP1 played a tumor-suppressor role in colon tumorigenesis (ie, DP1-transfected RKO cells showed growth inhibition, apoptosis, decreased telomerase activity, and up-regulation of p53). These phenomena were reversed when HCCR-1 was overexpressed. Loss of heterozygosity around the DP1 gene was observed frequently (50{\%}) in CRCs. We examined the use of serum HCCR-1 in CRC patients. The sensitivity of HCCR-1 (76.0{\%}) for detecting CRC was proven to be much higher than that of CA19-9 (32.0{\%}). Conclusions: DP1 plays a tumor-suppressor role in CRC. DP1 and HCCR-1 are supposed to regulate each other negatively by interaction, but further study is required to get better insight into the biological significance of the interaction.",
author = "Shin, {Seung Min} and Chung, {Yeun Jun} and Oh, {Seong Tack} and Jeon, {Hae Myung} and Hwang, {Lae Jeong} and Hong Namkoong and Kim, {Hyun Kee} and Cho, {Goang Won} and Hur, {Soo Young} and Kim, {Tae Eung} and Lee, {Youn Soo} and Park, {Yong Gyu} and Ko, {Je Sang} and Kim, {Jin Woo}",
year = "2006",
month = "7",
day = "1",
doi = "10.1053/j.gastro.2006.03.055",
language = "English",
volume = "130",
pages = "2074--2086",
journal = "Gastroenterology",
issn = "0016-5085",
publisher = "W.B. Saunders Ltd",
number = "7",

}

TY - JOUR

T1 - HCCR-1-Interacting Molecule "Deleted in Polyposis 1" Plays a Tumor-Suppressor Role in Colon Carcinogenesis

AU - Shin, Seung Min

AU - Chung, Yeun Jun

AU - Oh, Seong Tack

AU - Jeon, Hae Myung

AU - Hwang, Lae Jeong

AU - Namkoong, Hong

AU - Kim, Hyun Kee

AU - Cho, Goang Won

AU - Hur, Soo Young

AU - Kim, Tae Eung

AU - Lee, Youn Soo

AU - Park, Yong Gyu

AU - Ko, Je Sang

AU - Kim, Jin Woo

PY - 2006/7/1

Y1 - 2006/7/1

N2 - Background & Aims: Human cervical cancer oncogene (HCCR-1) has appeared to act as a negative regulator of p53 and contributes to tumorigenesis of various organs including the colon. We identified the HCCR-1 binding protein deleted in polyposis 1 (DP1) and accessed the role of HCCR-1 and DP1 in colon tumorigenesis. Methods: Yeast 2-hybrid was used to identify HCCR-1 interacting proteins. Various molecular biological approaches were used to examine the expression profile of HCCR-1 and DP1, subcellular localization, epitope mapping, the biological role of DP1, and the serum HCCR-1 level. Loss of heterozygosity frequency around DP1 also was examined. Results: We identified that HCCR-1 interacted with DP1. These 2 proteins colocalized in mitochondria but the expression of HCCR-1 showed negative correlation with that of DP1 in colorectal cancer (CRC). DP1 played a tumor-suppressor role in colon tumorigenesis (ie, DP1-transfected RKO cells showed growth inhibition, apoptosis, decreased telomerase activity, and up-regulation of p53). These phenomena were reversed when HCCR-1 was overexpressed. Loss of heterozygosity around the DP1 gene was observed frequently (50%) in CRCs. We examined the use of serum HCCR-1 in CRC patients. The sensitivity of HCCR-1 (76.0%) for detecting CRC was proven to be much higher than that of CA19-9 (32.0%). Conclusions: DP1 plays a tumor-suppressor role in CRC. DP1 and HCCR-1 are supposed to regulate each other negatively by interaction, but further study is required to get better insight into the biological significance of the interaction.

AB - Background & Aims: Human cervical cancer oncogene (HCCR-1) has appeared to act as a negative regulator of p53 and contributes to tumorigenesis of various organs including the colon. We identified the HCCR-1 binding protein deleted in polyposis 1 (DP1) and accessed the role of HCCR-1 and DP1 in colon tumorigenesis. Methods: Yeast 2-hybrid was used to identify HCCR-1 interacting proteins. Various molecular biological approaches were used to examine the expression profile of HCCR-1 and DP1, subcellular localization, epitope mapping, the biological role of DP1, and the serum HCCR-1 level. Loss of heterozygosity frequency around DP1 also was examined. Results: We identified that HCCR-1 interacted with DP1. These 2 proteins colocalized in mitochondria but the expression of HCCR-1 showed negative correlation with that of DP1 in colorectal cancer (CRC). DP1 played a tumor-suppressor role in colon tumorigenesis (ie, DP1-transfected RKO cells showed growth inhibition, apoptosis, decreased telomerase activity, and up-regulation of p53). These phenomena were reversed when HCCR-1 was overexpressed. Loss of heterozygosity around the DP1 gene was observed frequently (50%) in CRCs. We examined the use of serum HCCR-1 in CRC patients. The sensitivity of HCCR-1 (76.0%) for detecting CRC was proven to be much higher than that of CA19-9 (32.0%). Conclusions: DP1 plays a tumor-suppressor role in CRC. DP1 and HCCR-1 are supposed to regulate each other negatively by interaction, but further study is required to get better insight into the biological significance of the interaction.

UR - http://www.scopus.com/inward/record.url?scp=33744523165&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33744523165&partnerID=8YFLogxK

U2 - 10.1053/j.gastro.2006.03.055

DO - 10.1053/j.gastro.2006.03.055

M3 - Article

C2 - 16762630

AN - SCOPUS:33744523165

VL - 130

SP - 2074

EP - 2086

JO - Gastroenterology

JF - Gastroenterology

SN - 0016-5085

IS - 7

ER -