PMID- 30182381
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20210109
IS  - 1365-2184 (Electronic)
IS  - 0960-7722 (Print)
IS  - 0960-7722 (Linking)
VI  - 51
IP  - 6
DP  - 2018 Dec
TI  - CDR1as is overexpressed in laryngeal squamous cell carcinoma to promote the 
      tumour's progression via miR-7 signals.
PG  - e12521
LID - 10.1111/cpr.12521 [doi]
LID - e12521
AB  - OBJECTIVES: To investigate the roles played by the circular RNA (circRNA) 
      molecule ciRS-7 (CDR1as) and tumour suppressor miRNA-7 (miR-7) in laryngeal 
      squamous cell carcinoma (LSCC). METHODS: Specimens of LSCC tissue (n = 30) and 
      corresponding relative normal tissue (n = 30) were collected to determine their 
      levels and clinical significance of CDR1as/mir-7 expression. The CDR1as and miR-7 
      were overexpressed in LSCC cells to investigate its function and mechanism in 
      vitro and in vivo. RESULTS: Patients with high TNM stages, poorly differentiated 
      tumours, lymph node metastases and poor prognosis had high CDR1as levels but low 
      miR-7 levels. CDR1 expression was negatively associated with miR-7 expression in 
      LSCC. Overexpression of CDR1as in vitro enhanced cell vitality, and promoted the 
      proliferation, migration, and invasion of two LSCC cell lines (Hep2 and 
      AMC-HN-8.) However, these effects could be abrogated by knockdown of CDR1as or 
      the forced expression of miR-7. Mechanistically, overexpressed CDR1 molecules 
      functioned as miR-7 sponges and upregulated the key targets of miR-7, CCNE1, and 
      PIK3CD in Hep2 and AMC-HN-8 cells. In vivo studies demonstrated the tumourigenic 
      role of CDR1as. Overexpression of CDR1as alone promoted tumour growth and 
      increased expression of the proliferation indices ki-67, CCNE1, and PIK3CD. 
      Although the tumour suppressor miR-7 effectively inhibited the tumour growth, 
      this effect could be counteracted by co-treatment with CDR1as in vivo. 
      CONCLUSION: CDR1as is an oncogene that promotes LSCC progression by regulating 
      miR-7 signals.
CI  - (c) 2018 John Wiley & Sons Ltd.
FAU - Zhang, Jianzhong
AU  - Zhang J
AD  - Department of Otolaryngology-Head and Neck Surgery, The First Affiliated Hospital 
      of Zhengzhou University, Zhengzhou City, Henan Province, China.
AD  - Department of Otolaryngology-Head and Neck Surgery, The Fifth Affiliated Hospital 
      of the Medical University of Guangzhou, Guangzhou, China.
FAU - Hu, Huayong
AU  - Hu H
AD  - Department of Otolaryngology-Head and Neck Surgery, The Fifth Affiliated Hospital 
      of the Medical University of Guangzhou, Guangzhou, China.
FAU - Zhao, Yaoxin
AU  - Zhao Y
AD  - Department of Otolaryngology-Head and Neck Surgery, The Fifth Affiliated Hospital 
      of the Medical University of Guangzhou, Guangzhou, China.
FAU - Zhao, Yulin
AU  - Zhao Y
AUID- ORCID: 0000-0002-7410-3761
AD  - Department of Otolaryngology-Head and Neck Surgery, The First Affiliated Hospital 
      of Zhengzhou University, Zhengzhou City, Henan Province, China.
LA  - eng
PT  - Journal Article
DEP - 20180904
PL  - England
TA  - Cell Prolif
JT  - Cell proliferation
JID - 9105195
RN  - 0 (Autoantigens)
RN  - 0 (CDR1 protein, human)
RN  - 0 (MIRN7 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Nerve Tissue Proteins)
SB  - IM
MH  - Autoantigens/*genetics/metabolism
MH  - Cell Line, Tumor
MH  - Cell Proliferation/genetics
MH  - Gene Expression Regulation, Neoplastic/*genetics
MH  - Genes, Tumor Suppressor/physiology
MH  - Humans
MH  - Laryngeal Neoplasms/*genetics
MH  - MicroRNAs/*genetics
MH  - Nerve Tissue Proteins/*genetics/metabolism
MH  - Squamous Cell Carcinoma of Head and Neck/genetics
MH  - Up-Regulation
PMC - PMC6528957
OTO - NOTNLM
OT  - CCNE1
OT  - CDR1as
OT  - PIK3CD
OT  - laryngeal squamous cell carcinoma
OT  - miR-7
COIS- No competing financial interests exist.
EDAT- 2018/09/06 06:00
MHDA- 2018/12/12 06:00
PMCR- 2018/09/04
CRDT- 2018/09/06 06:00
PHST- 2018/02/08 00:00 [received]
PHST- 2018/07/15 00:00 [revised]
PHST- 2018/07/27 00:00 [accepted]
PHST- 2018/09/06 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2018/09/06 06:00 [entrez]
PHST- 2018/09/04 00:00 [pmc-release]
AID - CPR12521 [pii]
AID - 10.1111/cpr.12521 [doi]
PST - ppublish
SO  - Cell Prolif. 2018 Dec;51(6):e12521. doi: 10.1111/cpr.12521. Epub 2018 Sep 4.