Increased miR-449a expression in colorectal carcinoma tissues is inversely correlated with serum carcinoembryonic antigen

被引:26
作者
Chen, Shaohua [1 ]
Dai, Yuqiao [2 ]
Zhang, Xuemei [3 ]
Jin, Daozhong [4 ]
Li, Xiaorong [1 ]
Zhang, Yi [1 ]
机构
[1] Cent S Univ, Xiangya Hosp 3, Dept Gen Surg, Changsha 410013, Hunan, Peoples R China
[2] Univ Missouri Kansas, Sch Pharm, Div Pharmacol & Toxicol, Kansas City, KS 64108 USA
[3] Cent S Univ, Dept Gastroenterol, Xiangya Hosp 3, Changsha 410013, Hunan, Peoples R China
[4] Univ Missouri Kansas, Sch Med, Dept Basic Med Sci, Kansas City, KS 64108 USA
关键词
miR-449a; colorectal carcinoma; carcinoembryonic antigen; TUMOR-SUPPRESSOR; GROWTH ARREST; CANCER; TARGETS; PROLIFERATION; MICRORNA;
D O I
10.3892/ol.2013.1737
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Previously, microRNA-449a (miR-449a) has been shown to be involved in various types of cancer. However, its role in colorectal carcinoma remains unknown. The present study found that miR-449a expression was significantly increased in cultured colorectal carcinoma cells and cancer tissues obtained from 24 patients diagnosed with colorectal carcinoma, compared with the normal colorectal cells and the adjacent non-tumor tissues. The miR-449a expression in carcinoma tissues revealed an inverse correlation with the levels of serum carcinoembryonic antigen (CEA; R-2=0.88). The increased expression of miR-449a appeared in the patients who exhibited normal serum levels of CEA (<5 ng/ml), but not in those with elevated CEA levels (>5 ng/ml). miR-449a expression increased at an early TNM stage (stage II) and did not change significantly at stages III and IV. These results suggested that miR-449a is involved in the development of colorectal carcinoma and may be a potential prognosis indicator.
引用
收藏
页码:568 / 572
页数:5
相关论文
共 21 条
[1]  
Boras Z, 2012, COLLEGIUM ANTROPOL, V36, P1355
[2]  
Boyle P, 2008, WORLD CANC REPORT 20, P374
[3]   Histone Deacetylases Activate Hepatocyte Growth Factor Signaling by Repressing MicroRNA-449 in Hepatocellular Carcinoma Cells [J].
Buurman, Reena ;
Guerlevik, Engin ;
Schaeffer, Vera ;
Eilers, Marlies ;
Sandbothe, Maria ;
Kreipe, Hans ;
Wilkens, Ludwig ;
Schlegelberger, Brigitte ;
Kuehnel, Florian ;
Skawran, Britta .
GASTROENTEROLOGY, 2012, 143 (03) :811-+
[4]   MicroRNA-449a acts as a tumor suppressor in human bladder cancer through the regulation of pocket proteins [J].
Chen, Hong ;
Lin, Yi-Wei ;
Mao, Ye-Qing ;
Wu, Jian ;
Liu, Yun-Fu ;
Zheng, Xiang-Yi ;
Xie, Li-Ping .
CANCER LETTERS, 2012, 320 (01) :40-47
[5]   MicroRNA and colorectal cancer [J].
Corte, Helene ;
Manceau, Gilles ;
Blons, Helene ;
Laurent-Puig, Pierre .
DIGESTIVE AND LIVER DISEASE, 2012, 44 (03) :195-200
[6]   MicroRNAs in Human Cancer [J].
Farazi, Thalia A. ;
Hoell, Jessica I. ;
Morozov, Pavel ;
Tuschl, Thomas .
MICRORNA CANCER REGULATION: ADVANCED CONCEPTS, BIOINFORMATICS AND SYSTEMS BIOLOGY TOOLS, 2013, 774 :1-20
[7]   The noncoding RNA, miR-126, suppresses the growth of neoplastic cells by targeting phosphatidylinositol 3-kinase signaling and is frequently lost in colon cancers [J].
Guo, Chunguang ;
Sah, Jerome F. ;
Beard, Lydia ;
Willson, James K. V. ;
Markowitz, Sanford D. ;
Guda, Kishore .
GENES CHROMOSOMES & CANCER, 2008, 47 (11) :939-946
[8]   Combining microRNA-449a/b with a HDAC inhibitor has a synergistic effect on growth arrest in lung cancer [J].
Jeon, Hyo Sung ;
Lee, Soo Young ;
Lee, Eun Jin ;
Yun, Seong Cheol ;
Cha, Eun Jung ;
Choi, Eugene ;
Na, Moon Jun ;
Park, Jae Yong ;
Kang, Jaeku ;
Son, Ji Woong .
LUNG CANCER, 2012, 76 (02) :171-176
[9]   miR-449 inhibits cell proliferation and is down-regulated in gastric cancer [J].
Kheir, Tony Bou ;
Futoma-Kazmierczak, Ewa ;
Jacobsen, Anders ;
Krogh, Anders ;
Bardram, Linda ;
Hother, Christoffer ;
Gronbaek, Kirsten ;
Federspiel, Birgitte ;
Lund, Anders H. ;
Friis-Hansen, Lennart .
MOLECULAR CANCER, 2011, 10
[10]   Reference Genes for Real-Time PCR Quantification of MicroRNAs and Messenger RNAs in Rat Models of Hepatotoxicity [J].
Lardizabal, Maria N. ;
Nocito, Ana L. ;
Daniele, Stella M. ;
Ornella, Leonardo A. ;
Palatnik, Javier F. ;
Veggi, Luis M. .
PLOS ONE, 2012, 7 (05)