The prognostic significance of RUNX2 and miR-10a/10b and their inter-relationship in breast cancer
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- 作者：Chih-Hao Chang ; Tan-Chi Fan ; Jyh-Cherng Yu…
- 关键词：RUNX2 ; miR ; 10a ; miR ; 10b ; Breast cancer prognosis
- 刊名：Journal of Translational Medicine
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：12
- 期：1
- 全文大小：2,683 KB
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16. Lee, RC, Ambros, V (2 - 刊物主题：Biomedicine general; Medicine/Public Health, general;
- 出版者：BioMed Central
- ISSN：1479-5876
文摘
Background The major cancer related mortality is caused by metastasis and invasion. It is important to identify genes regulating metastasis and invasion in order to curtail metastatic spread of cancer cells. Methods This study investigated the association between RUNX2 and miR-10a/miR-10b and the risk of breast cancer relapse. Expression levels of RUNX2 and miR-10a/b in108 pairs of tumor and non-tumor tissue of breast cancer were assayed by quantitative PCR analysis and evaluated for their prognostic implications. Results The median expression levels of RUNX2 and miR-10b in tumor tissue normalized using adjacent non-tumor tissue were significantly higher in relapsed patients than in relapse-free patients. Higher expression of these three genes were significantly correlated with the hazard ratio for breast cancer recurrence (RUNX2: 3.02, 95% CI--.50?~-.07; miR-10a: 2.31, 95% CI--.00?~-.32; miR-10b: 3.96, 95% CI--.21?~-2.98). The joint effect of higher expression of all three genes was associated with a hazard ratio of 12.37 (95% CI--.62?~-4.55) for relapse. In a breast cancer cell line, RUNX2 silencing reduced the expression of miR-10a/b and also impaired cell motility, while RUNX2 overexpression elicited opposite effects. Conclusions These findings indicate that higher expression of RUNX2 and miR-10a/b was associated with adverse outcome of breast cancer. Expression levels of RUNX2 and miR-10a/b individually or jointly are potential prognostic factors for predicting breast cancer recurrence. Data from in vitro studies support the notion that RUNX2 promoted cell motility by upregulating miR-10a/b.