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Mol. Cells 2013; 35(1): 17-24

Published online December 3, 2012

https://doi.org/10.1007/s10059-013-2154-7

© The Korean Society for Molecular and Cellular Biology

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

Jae-Sung Kim, Sun-Kyoung Yu, Myoung-Hwa Lee, Min-Gyeong Park, Euteum Park, Su-Gwan Kim, Sook-Young Lee, Chun Sung Kim, Heung-Joong Kim, Hong Sung Chun, Sang-Woo Chun, and Do Kyung Kim

Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju, Korea, Department of Biotechnology, Regional Innovation Center for Dental Science and Engineering, Chosun University, Gwangju, Korea, 4Department of Oral Physiology, College of Dentistry, Institute of Wonkwang Biomaterial and Implant, Wonkwang University, Iksan, Korea

Received: June 4, 2012; Revised: October 31, 2012; Accepted: November 8, 2012

Abstract

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.

Keywords apoptosis, human oral cancer, interleukin-24, microRNA-205

Article

Research Article

Mol. Cells 2013; 35(1): 17-24

Published online January 31, 2013 https://doi.org/10.1007/s10059-013-2154-7

Copyright © The Korean Society for Molecular and Cellular Biology.

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

Jae-Sung Kim, Sun-Kyoung Yu, Myoung-Hwa Lee, Min-Gyeong Park, Euteum Park, Su-Gwan Kim, Sook-Young Lee, Chun Sung Kim, Heung-Joong Kim, Hong Sung Chun, Sang-Woo Chun, and Do Kyung Kim

Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju, Korea, Department of Biotechnology, Regional Innovation Center for Dental Science and Engineering, Chosun University, Gwangju, Korea, 4Department of Oral Physiology, College of Dentistry, Institute of Wonkwang Biomaterial and Implant, Wonkwang University, Iksan, Korea

Received: June 4, 2012; Revised: October 31, 2012; Accepted: November 8, 2012

Abstract

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.

Keywords: apoptosis, human oral cancer, interleukin-24, microRNA-205

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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