PMID- 24318902
OWN - NLM
STAT- MEDLINE
DCOM- 20140725
LR  - 20220624
IS  - 1559-131X (Electronic)
IS  - 1357-0560 (Linking)
VI  - 31
IP  - 1
DP  - 2014 Jan
TI  - MiR-139 targets CXCR4 and inhibits the proliferation and metastasis of laryngeal 
      squamous carcinoma cells.
PG  - 789
LID - 10.1007/s12032-013-0789-z [doi]
AB  - Our previous studies have showed that chemokine receptor 4 (CXCR4) was 
      over-expressed in laryngeal squamous cell carcinoma (LSCC). However, the 
      mechanism underlying aberrant CXCR4 expression remains unclear. To investigate 
      the roles played by miRNAs in CXCR4 over-expression in LSCC, putative miR-139 was 
      predicted through computational algorithms, including TargetScan, PicTar and 
      miRBase, and luciferase reporter assay was explored to confirm that whether CXCR4 
      was directly regulated by miR-139. Then, quantitative real-time PCR, 
      immunohistochemistry and in situ hybridization methods were employed to detect 
      the expression of miR-139 and CXCR4 in primary LSCC tissues, normal adjacent 
      mucosal tissues and metastatic lesions derived from 40 LSCC patients in the 
      Second Hospital, Xi'An JiaoTong University. Finally, gain- and loss-of-function 
      assays were adopted to explore the effects of miR-139 and CXCR4 on proliferation, 
      invasion and metastasis of the human LSCC cell line Hep-2 in vitro and in vivo. 
      Our results showed that miR-139 dampened CXCR4 expression, and CXCR4 was directly 
      targeted by miR-139. Additionally, the expression of miR-139 was reduced in 
      alignment with the progression of primary to metastatic LSCC. Moreover, an 
      inverse correlation was observed between miR-139 and CXCR4 protein levels in LSCC 
      specimens. Functional analyses demonstrated that ectopic expression of miR-139 
      inhibited cell proliferation, migration and metastasis of Hep-2 cells in vitro 
      and in vivo. Similar to the observations seen in restoring miR-139 expression, 
      dampening of CXCR4 expression inhibited cell growth, migration and invasion, 
      whereas miR-139 over-expression reversed the pro-metastatic effect of CXCR4. 
      Taken together, we conclude that miR-139 targets CXCR4 and inhibits proliferation 
      and metastasis of LSCC.
FAU - Luo, Hua-Nan
AU  - Luo HN
AD  - Department of Otolaryngology-Head and Neck Surgery, The Second Hospital, Xi'an 
      Jiao Tong University, Xi Wu Road #157, Xi'an, 710004, Shan'Xi Province, China.
FAU - Wang, Zheng-Hui
AU  - Wang ZH
FAU - Sheng, Ying
AU  - Sheng Y
FAU - Zhang, Qing
AU  - Zhang Q
FAU - Yan, Jing
AU  - Yan J
FAU - Hou, Jin
AU  - Hou J
FAU - Zhu, Kang
AU  - Zhu K
FAU - Cheng, Ying
AU  - Cheng Y
FAU - Xu, Ying-Long
AU  - Xu YL
FAU - Zhang, Xiang-Hong
AU  - Zhang XH
FAU - Xu, Min
AU  - Xu M
FAU - Ren, Xiao-Yong
AU  - Ren XY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131207
PL  - United States
TA  - Med Oncol
JT  - Medical oncology (Northwood, London, England)
JID - 9435512
RN  - 0 (CXCR4 protein, human)
RN  - 0 (MIRN139 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Receptors, CXCR4)
SB  - IM
MH  - Animals
MH  - Carcinoma, Squamous Cell/*metabolism
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Gene Expression Profiling
MH  - *Gene Expression Regulation, Neoplastic
MH  - HEK293 Cells
MH  - Humans
MH  - Laryngeal Neoplasms/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - MicroRNAs/*metabolism
MH  - Neoplasm Metastasis
MH  - Neoplasm Transplantation
MH  - Receptors, CXCR4/*metabolism
EDAT- 2013/12/10 06:00
MHDA- 2014/07/26 06:00
CRDT- 2013/12/10 06:00
PHST- 2013/10/21 00:00 [received]
PHST- 2013/11/24 00:00 [accepted]
PHST- 2013/12/10 06:00 [entrez]
PHST- 2013/12/10 06:00 [pubmed]
PHST- 2014/07/26 06:00 [medline]
AID - 10.1007/s12032-013-0789-z [doi]
PST - ppublish
SO  - Med Oncol. 2014 Jan;31(1):789. doi: 10.1007/s12032-013-0789-z. Epub 2013 Dec 7.