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Journal of Cancer Prevention

Original Article

Journal of Cancer Prevention 2015; 20(4): 268-274

Published online December 30, 2015

https://doi.org/10.15430/JCP.2015.20.4.268

© Korean Society of Cancer Prevention

The Significance of miR-34a Expression in Endometrial Carcinogenesis: Correlation With Expression of p16 and Ki-67 Proteins in Endometrial Cancers

Yoon Sung Choi, and Kyung Eun Lee

Department of Clinical Laboratory Science, College of Health Sciences, Catholic University of Pusan, Busan, Korea

Correspondence to :
Kyung Eun Lee, Department of Clinical Laboratory Science, College of Health Sciences, Catholic University of Pusan, 57 Oryundae-ro, Geumjeong-gu, Busan 46252, Korea, Tel: +82-51-510-0562, Fax: +82-51-510-0568, E-mail: kelee@cup.ac.kr, ORCID: Kyung Eun Lee, http://orcid.org/0000-0001-9543-4159

Received: October 8, 2015; Revised: October 30, 2015; Accepted: October 30, 2015

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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Background:

A microRNA, miR-34a, plays a key role in inhibiting cellular transformation and carcinogenesis by controlling cell cycle regulation and cell proliferation in various human tumors. However, miR-34a has rarely been reported in endometrial cancer research in Korea. This study was undertaken to analyze miR-34a expression in simple endometrial hyperplasia and endometrial cancer, and to evaluate the relationship between expression of miR-34a and p16 and Ki-67 proteins in endometrial cancers.

Methods:

A retrospective study was carried out on 66 formalin-fixed, paraffin-embedded tissues with simple endometrial hyperplasia (31 cases) and endometrial cancer (35 cases) patients. These were analyzed for miR-34a expression by quantitative real-time PCR, and the expression of p16 and Ki-67 proteins in endometrial cancers was evaluated by immunohistochemistry.

Results:

The miR-34a expression level was lower in endometrial cancer tissues (?0.71 ± 3.90) than in simple endometrial hyperplasia tissues (2.68 ± 8.62). The endometrial hyperplasia tissues showed underexpression of miR-34a in 13 of the 31 cases (41.9%) while the endometrial cancer tissues showed underexpression of miR-34a in 24 of 35 cases (68.6%). Thus, miR-34a was significantly underexpressed in endometrial cancer tissues when compared endometrial hyperplasia tissues (P = 0.046). Overexpression of p16 was detected in 25 (71.4%) and Ki-67 immunoreactivity was detected in 27 (77.1%) of the 35 endometrial cancers. Although not statistically significant, the frequency of p16 and Ki-67 overexpression tended to be lower in the cases with miR-34a underexpression than in cases with miR-34a overexpression.

Conclusions:

These findings suggest that underexpression of miR-34a might be involved in endometrial carcinogenesis. Further studies are needed to define the relationship between miR-34a expression and tissue specific protein expression.

Keywords: miR-34a, p16, Ki-67, Simple endometrial hyperplasia, Endometrial cancer

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