MicroRNA-205 Directly Regulates the Tumor Suppressor, Interleukin-24, in Human KB Oral Cancer Cells

被引:57
作者
Kim, Jae-Sung [1 ]
Yu, Sun-Kyoung [1 ]
Lee, Myoung-Hwa [1 ]
Park, Min-Gyeong [1 ]
Park, Euteum [2 ]
Kim, Su-Gwan [1 ,3 ]
Lee, Sook-Young [3 ]
Kim, Chun Sung [1 ]
Kim, Heung-Joong [1 ]
Chun, Hong Sung [2 ]
Chun, Sang-Woo [4 ]
Kim, Do Kyung [1 ,3 ]
机构
[1] Chosun Univ, Sch Dent, Oral Biol Res Inst, Kwangju 501759, South Korea
[2] Chosun Univ, Dept Biotechnol, Kwangju 501759, South Korea
[3] Chosun Univ, Reg Innovat Ctr Dent Sci & Engn, Kwangju 501759, South Korea
[4] Wonkwang Univ, Inst Wonkwang Biomaterial & Implant, Coll Dent, Dept Oral Physiol, Iksan 570749, South Korea
关键词
apoptosis; human oral cancer; interleukin-24; microRNA-205; APOPTOSIS-INDUCING CYTOKINE; BREAST-CANCER; MELANOMA PROGRESSION; CARCINOMA-CELLS; PROSTATE-CANCER; MDA-7/IL-24; EXPRESSION; MIR-205; MIRNA; PROLIFERATION;
D O I
10.1007/s10059-013-2154-7
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
MicroRNA (miRNA) is a form of small noncoding RNA that regulates the expression of genes either by inhibiting mRNA translation or by inducing its degradation. Small microRNA play important roles in regulating a large number of cellular processes, including development, proliferation and apoptosis. This study examined the biological functions of miR-205 as a tumor suppressor in KB oral cancer cells. The results showed that miR-205 expression was significantly lower in KB oral cancer cells than in human normal oral keratinocytes. Furthermore, the miR-205 over-expressed in KB oral cancer cells increased the cell cytotoxicity and induced apoptosis through the activation of caspase-3/-7. The transfection of miR-205 into KB oral cancer cells strongly induced IL-24, a well known cytokine that acts as a tumor suppressor in a range of tumor tissues. In addition, miR-205 targeted the IL-24 promoter directly to induce gene expression. Overall, miR-205 has significant therapeutic potential to turn on silenced tumor suppressor genes by targeting them with miRNA.
引用
收藏
页码:17 / 24
页数:8
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