The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma

Young Ae Park, Jeong Won Lee, Jung Joo Choi, Hye Kyung Jeon, Youngjae Cho, Chelhun Choi, Tae Joong Kim, Nak Woo Lee, Byoung Gie Kim, Duk Soo Bae

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Objective: Increased expression of miR-200c was recently reported in endometrial carcinoma compared with normal tissues. In this study, we evaluated the role of miR-200c in cell growth and drug sensitivity in endometrial carcinoma and investigated the underlying mechanisms. Methods: The expression of miR-200c in human endometrial tissues was detected by quantitative RT-PCR. The transfection with anti-miRNA (anti-miR) or the premature form of miRNA (pre-miR) was performed to regulate the level of expression of miRNA-200c in endometrial carcinoma cells, HEC-1A and Ishikawa. To identify the target genes for miR-200c, we performed mRNA microarray after pre-miR-200c transfection in HEC-1A cells. Results: We found that miR-200c expression was increased in endometrial carcinoma compared with normal endometrial tissues. Anti-miR or pre-miR-200c could regulate cell survival, proliferation, and apoptosis and affect cytotoxicity in endometrial cancer cells. Through mRNA microarray analysis, we found that miR-200c inhibits the expression of BRD7, which was recently reported as a potential tumor suppressor gene. MiR-200c regulated the translocation of β-catenin from the cytoplasm to the nucleus via inhibition of BRD7, resulting in increased expression of its transcriptional target genes, cyclinD1 and c-myc. Conclusion: The interaction between miR-200c and BRD7 might have important roles in controlling growth of endometrial of cancer cells and suggest a novel target pathway for treatment of this cancer.

Original languageEnglish
Pages (from-to)125-133
Number of pages9
JournalGynecologic Oncology
Volume124
Issue number1
DOIs
Publication statusPublished - 2012 Jan 1

Fingerprint

Endometrial Neoplasms
MicroRNAs
Transfection
Catenins
Messenger RNA
myc Genes
Microarray Analysis
Growth
Tumor Suppressor Genes
Cell Survival
Cytoplasm
Cell Proliferation
Apoptosis
Polymerase Chain Reaction
Pharmaceutical Preparations
Genes
Neoplasms

Keywords

  • β-catenin
  • BRD7
  • Endometrial carcinoma
  • MicroRNA
  • MicroRNA-200c

ASJC Scopus subject areas

  • Oncology
  • Obstetrics and Gynaecology

Cite this

Park, Y. A., Lee, J. W., Choi, J. J., Jeon, H. K., Cho, Y., Choi, C., ... Bae, D. S. (2012). The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma. Gynecologic Oncology, 124(1), 125-133. https://doi.org/10.1016/j.ygyno.2011.09.026

The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma. / Park, Young Ae; Lee, Jeong Won; Choi, Jung Joo; Jeon, Hye Kyung; Cho, Youngjae; Choi, Chelhun; Kim, Tae Joong; Lee, Nak Woo; Kim, Byoung Gie; Bae, Duk Soo.

In: Gynecologic Oncology, Vol. 124, No. 1, 01.01.2012, p. 125-133.

Research output: Contribution to journalArticle

Park, YA, Lee, JW, Choi, JJ, Jeon, HK, Cho, Y, Choi, C, Kim, TJ, Lee, NW, Kim, BG & Bae, DS 2012, 'The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma', Gynecologic Oncology, vol. 124, no. 1, pp. 125-133. https://doi.org/10.1016/j.ygyno.2011.09.026
Park, Young Ae ; Lee, Jeong Won ; Choi, Jung Joo ; Jeon, Hye Kyung ; Cho, Youngjae ; Choi, Chelhun ; Kim, Tae Joong ; Lee, Nak Woo ; Kim, Byoung Gie ; Bae, Duk Soo. / The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma. In: Gynecologic Oncology. 2012 ; Vol. 124, No. 1. pp. 125-133.
@article{ff45344ae7d443c6aec9aa365fb08da8,
title = "The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma",
abstract = "Objective: Increased expression of miR-200c was recently reported in endometrial carcinoma compared with normal tissues. In this study, we evaluated the role of miR-200c in cell growth and drug sensitivity in endometrial carcinoma and investigated the underlying mechanisms. Methods: The expression of miR-200c in human endometrial tissues was detected by quantitative RT-PCR. The transfection with anti-miRNA (anti-miR) or the premature form of miRNA (pre-miR) was performed to regulate the level of expression of miRNA-200c in endometrial carcinoma cells, HEC-1A and Ishikawa. To identify the target genes for miR-200c, we performed mRNA microarray after pre-miR-200c transfection in HEC-1A cells. Results: We found that miR-200c expression was increased in endometrial carcinoma compared with normal endometrial tissues. Anti-miR or pre-miR-200c could regulate cell survival, proliferation, and apoptosis and affect cytotoxicity in endometrial cancer cells. Through mRNA microarray analysis, we found that miR-200c inhibits the expression of BRD7, which was recently reported as a potential tumor suppressor gene. MiR-200c regulated the translocation of β-catenin from the cytoplasm to the nucleus via inhibition of BRD7, resulting in increased expression of its transcriptional target genes, cyclinD1 and c-myc. Conclusion: The interaction between miR-200c and BRD7 might have important roles in controlling growth of endometrial of cancer cells and suggest a novel target pathway for treatment of this cancer.",
keywords = "β-catenin, BRD7, Endometrial carcinoma, MicroRNA, MicroRNA-200c",
author = "Park, {Young Ae} and Lee, {Jeong Won} and Choi, {Jung Joo} and Jeon, {Hye Kyung} and Youngjae Cho and Chelhun Choi and Kim, {Tae Joong} and Lee, {Nak Woo} and Kim, {Byoung Gie} and Bae, {Duk Soo}",
year = "2012",
month = "1",
day = "1",
doi = "10.1016/j.ygyno.2011.09.026",
language = "English",
volume = "124",
pages = "125--133",
journal = "Gynecologic Oncology",
issn = "0090-8258",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma

AU - Park, Young Ae

AU - Lee, Jeong Won

AU - Choi, Jung Joo

AU - Jeon, Hye Kyung

AU - Cho, Youngjae

AU - Choi, Chelhun

AU - Kim, Tae Joong

AU - Lee, Nak Woo

AU - Kim, Byoung Gie

AU - Bae, Duk Soo

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Objective: Increased expression of miR-200c was recently reported in endometrial carcinoma compared with normal tissues. In this study, we evaluated the role of miR-200c in cell growth and drug sensitivity in endometrial carcinoma and investigated the underlying mechanisms. Methods: The expression of miR-200c in human endometrial tissues was detected by quantitative RT-PCR. The transfection with anti-miRNA (anti-miR) or the premature form of miRNA (pre-miR) was performed to regulate the level of expression of miRNA-200c in endometrial carcinoma cells, HEC-1A and Ishikawa. To identify the target genes for miR-200c, we performed mRNA microarray after pre-miR-200c transfection in HEC-1A cells. Results: We found that miR-200c expression was increased in endometrial carcinoma compared with normal endometrial tissues. Anti-miR or pre-miR-200c could regulate cell survival, proliferation, and apoptosis and affect cytotoxicity in endometrial cancer cells. Through mRNA microarray analysis, we found that miR-200c inhibits the expression of BRD7, which was recently reported as a potential tumor suppressor gene. MiR-200c regulated the translocation of β-catenin from the cytoplasm to the nucleus via inhibition of BRD7, resulting in increased expression of its transcriptional target genes, cyclinD1 and c-myc. Conclusion: The interaction between miR-200c and BRD7 might have important roles in controlling growth of endometrial of cancer cells and suggest a novel target pathway for treatment of this cancer.

AB - Objective: Increased expression of miR-200c was recently reported in endometrial carcinoma compared with normal tissues. In this study, we evaluated the role of miR-200c in cell growth and drug sensitivity in endometrial carcinoma and investigated the underlying mechanisms. Methods: The expression of miR-200c in human endometrial tissues was detected by quantitative RT-PCR. The transfection with anti-miRNA (anti-miR) or the premature form of miRNA (pre-miR) was performed to regulate the level of expression of miRNA-200c in endometrial carcinoma cells, HEC-1A and Ishikawa. To identify the target genes for miR-200c, we performed mRNA microarray after pre-miR-200c transfection in HEC-1A cells. Results: We found that miR-200c expression was increased in endometrial carcinoma compared with normal endometrial tissues. Anti-miR or pre-miR-200c could regulate cell survival, proliferation, and apoptosis and affect cytotoxicity in endometrial cancer cells. Through mRNA microarray analysis, we found that miR-200c inhibits the expression of BRD7, which was recently reported as a potential tumor suppressor gene. MiR-200c regulated the translocation of β-catenin from the cytoplasm to the nucleus via inhibition of BRD7, resulting in increased expression of its transcriptional target genes, cyclinD1 and c-myc. Conclusion: The interaction between miR-200c and BRD7 might have important roles in controlling growth of endometrial of cancer cells and suggest a novel target pathway for treatment of this cancer.

KW - β-catenin

KW - BRD7

KW - Endometrial carcinoma

KW - MicroRNA

KW - MicroRNA-200c

UR - http://www.scopus.com/inward/record.url?scp=83055172665&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=83055172665&partnerID=8YFLogxK

U2 - 10.1016/j.ygyno.2011.09.026

DO - 10.1016/j.ygyno.2011.09.026

M3 - Article

VL - 124

SP - 125

EP - 133

JO - Gynecologic Oncology

JF - Gynecologic Oncology

SN - 0090-8258

IS - 1

ER -