Oncotarget

Research Papers:

Up-regulation of miR-187 modulates the advances of oral carcinoma by targeting BARX2 tumor suppressor

Shu-Chun Lin, Shou-Yen Kao, Jennifer Chen-Yu Chang, Ying-Chieh Liu, En-Hao Yu, Ssu-Hsueh Tseng, Chung-Ji Liu and Kuo-Wei Chang _

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Oncotarget. 2016; 7:61355-61365. https://doi.org/10.18632/oncotarget.11349

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Abstract

Shu-Chun Lin1,3, Shou-Yen Kao1,3, Jennifer Chen-Yu Chang1, Ying-Chieh Liu1, En-Hao Yu2, Ssu-Hsueh Tseng1, Chung-Ji Liu2,4, Kuo-Wei Chang1,3

1Institute of Oral Biology, National Yang-Ming University, Taipei, Taiwan

2Department of Dentistry, School of Dentistry, National Yang-Ming University, Taipei, Taiwan

3Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan

4Department of Dentistry, MacKay Memorial Hospital, Taipei, Taiwan

Correspondence to:

Kuo-Wei Chang, email: [email protected]

Chung-Ji Liu, email: [email protected]

Keywords: BARX2, carcinoma, invasion, metastasis, miR-187

Received: March 02, 2016     Accepted: August 09, 2016     Published: August 17, 2016

ABSTRACT

Oral squamous cell carcinoma (OSCC) is one of the most common cancers worldwide. Aberrations in miRNA regulation are known to play important roles in OSCC pathogenesis. miR-187 was shown to be up-regulated in head and neck malignancies in our previous screening. This study further investigated the oncogenic potential, clinical implications, and targets of miR-187 in OSCC. We observed that miR-187 increased oncogenicity, particularly migration, of OSCC cells. miR-187 expression increased the xenografic tumorigenicity and metastasis in mice. In addition, metastatic human OSCC had higher miR-187 expression than did non-metastatic tumors. Through vigorous screening, we confirmed BarH-like Homeobox 2 (BARX2) gene as an miR-187 target. BARX2 expression suppressed the migration, invasion, anchorage-independent colony formation, and orthotopic tumorigenesis of OSCC cells. The migratory phenotype and neck metastasis induced by miR-187 was rescued by BARX2 expression. BARX2 expression was down-regulated in the vast majority of OSCC, and this down-regulation was particularly conspicuous in tumors with advanced nodal metastasis. In addition, plasma miR-187 was significantly higher in OSCC patients than in normal individuals. This study highlights the roles of miR-187-BARX2 in driving the carcinogenesis of OSCC. The results suggest that miR-187 is a potential serological marker for OSCC and that targeting of miR-187 might prove effective in attenuating nodal metastasis.


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