PMID- 31258780
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1837-9664 (Print)
IS  - 1837-9664 (Electronic)
IS  - 1837-9664 (Linking)
VI  - 10
IP  - 12
DP  - 2019
TI  - Dysregulation of MiR-519d Affects Oral Squamous Cell Carcinoma Invasion and 
      Metastasis by Targeting MMP3.
PG  - 2720-2734
LID - 10.7150/jca.31825 [doi]
AB  - MicroRNA-519d (miR-519d) has been reported to play important roles in tumor 
      development and progression in multiple cancers, either as tumor suppressor or 
      tumor promotor. However, the expression level, biological function and molecular 
      mechanisms of miR-519d in oral squamous cell carcinoma (OSCC) remain unclear. 
      Therefore, the aims of this study were to investigate the functional role of 
      miR-519d in OSCC and the possible underlying regulatory mechanism. In this study, 
      we found that miR-519d was significantly downregulated in OSCC tissues and cell 
      lines compared with normal oral mucosae and normal oral epithelial cells. 
      Importantly, downregulation of miR-519d was closely correlated with the lymph 
      node metastasis, advanced tumor stage and poor overall survival of OSCC patients. 
      Furthermore, miR-519d significantly inhibited the migration and invasion of OSCC 
      cells. Using bioinformatics and biological approaches, we showed that miR-519d 
      directly targeted matrix metalloproteinase-3 (MMP3), which might account for the 
      underlying mechanism involved in the miR-519d mediated suppression of OSCC 
      progression. What is more, miR-519d expression was inversely correlated with MMP3 
      expression in OSCC tissues, and high levels of MMP3 expression in OSCC tissues 
      were also associated with the metastasis and poor prognosis of these patients. In 
      addition, we further identified that miR-519d acted as a regulator of 
      epithelial-mesenchymal transition (EMT) in OSCC cells. Overall, the present study 
      highlighted miR-519d as a tumor suppressor in OSCC by targeting MMP3 and 
      supported biological and clinical links between miR-519d-MMP3 and OSCC, thus 
      indicating the potential therapeutic value of miR-519d for alleviating OSCC 
      metastasis.
FAU - Jin, Yu
AU  - Jin Y
AD  - Department of General Dentistry, Ninth People's Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, 200011, PR China.
AD  - Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of 
      Stomatology, National Clinical Research Center of Stomatology, 200000, PR China.
FAU - Li, Yuexiu
AU  - Li Y
AD  - Department of Stomatology, Tai'an Central Hospital, Tai'an, Shandong 271000, P.R. 
      China.
FAU - Wang, Xin
AU  - Wang X
AD  - Department of General Dentistry, Ninth People's Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, 200011, PR China.
AD  - Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of 
      Stomatology, National Clinical Research Center of Stomatology, 200000, PR China.
FAU - Yang, Ya
AU  - Yang Y
AD  - Department of General Dentistry, Ninth People's Hospital, Shanghai Jiao Tong 
      University School of Medicine, Shanghai, 200011, PR China.
AD  - Shanghai Key Laboratory of Stomatology and Shanghai Research Institute of 
      Stomatology, National Clinical Research Center of Stomatology, 200000, PR China.
LA  - eng
PT  - Journal Article
DEP - 20190602
PL  - Australia
TA  - J Cancer
JT  - Journal of Cancer
JID - 101535920
PMC - PMC6584932
OTO - NOTNLM
OT  - MMP3
OT  - epithelial-mesenchymal transition (EMT)
OT  - invasion
OT  - metastasis
OT  - miR-519d
OT  - oral squamous cell carcinoma
COIS- Competing Interests: The authors have declared that no competing interest exists.
EDAT- 2019/07/02 06:00
MHDA- 2019/07/02 06:01
PMCR- 2019/01/01
CRDT- 2019/07/02 06:00
PHST- 2018/11/27 00:00 [received]
PHST- 2019/05/05 00:00 [accepted]
PHST- 2019/07/02 06:00 [entrez]
PHST- 2019/07/02 06:00 [pubmed]
PHST- 2019/07/02 06:01 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - jcav10p2720 [pii]
AID - 10.7150/jca.31825 [doi]
PST - epublish
SO  - J Cancer. 2019 Jun 2;10(12):2720-2734. doi: 10.7150/jca.31825. eCollection 2019.