PMID- 28586036
OWN - NLM
STAT- MEDLINE
DCOM- 20180326
LR  - 20181202
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 16
IP  - 1
DP  - 2017 Jul
TI  - Epigenetically silenced PTPRO functions as a prognostic marker and tumor 
      suppressor in human lung squamous cell carcinoma.
PG  - 746-754
LID - 10.3892/mmr.2017.6665 [doi]
AB  - Protein tyrosine phosphatase receptor‑type O (PTPRO), a member of the PTP family, 
      has been frequently reported as potential tumor suppressor in many types of 
      cancer. However, the exact function of PTPRO in lung squamous cell carcinoma 
      (LSCC) remains unclear. Bisulfite sequencing and methylation specific polymerase 
      chain reaction (PCR) were used to identify the methylation status of PTPRO in 
      LSCC cells, and quantitative methylation specific PCR was used to evaluate the 
      methylation levels of PTPRO in LSCC patients. Stably expressing PTPRO vectors 
      were constructed and transfected into H520 and SK‑MES‑1 cells, followed by MTT 
      and colony formation assays, and analysis of tumor weight and volume in in vivo 
      mouse xenograft models. The present study demonstrated that the CpG island of 
      PTPRO exon 1 was obviously hypermethylated in LSCC cells and tissues. The mRNA 
      expression of PTPRO could be restored by treatment with a demethylation agent. 
      Increased methylation and decreased mRNA levels of PTPRO were observed in LSCC 
      samples compared with adjacent healthy tissues, and were associated with poor 
      prognosis of patients. The mRNA expression of PTPRO was negatively correlated 
      with its methylation level in tumors. Functionally, ectopic PTPRO expression in 
      LSCC cells significantly inhibited the proliferation rates, and colony formation, 
      in comparison with control and non‑transfected cells. In vivo assays confirmed 
      the inhibitory effect of PTPRO on LSCC cell growth. In conclusion, these data 
      provided evidence that epigenetic regulation of PTPRO impairs its tumor 
      suppressor role in LSCC, and restoration of PTPRO may be a potential therapeutic 
      strategy.
FAU - Ming, Fei
AU  - Ming F
AD  - Department of Thoracic Surgery, Hubei Cancer Hospital, Wuhan, Hubei 430000, P.R. 
      China.
FAU - Sun, Qianqiang
AU  - Sun Q
AD  - Department of Thoracic Surgery, Hubei Cancer Hospital, Wuhan, Hubei 430000, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20170531
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 776B62CQ27 (Decitabine)
RN  - EC 3.1.3.48 (PTPRO protein, human)
RN  - EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 3)
RN  - M801H13NRU (Azacitidine)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Animals
MH  - Azacitidine/analogs & derivatives/pharmacology
MH  - Carcinoma, Squamous Cell/*genetics/*mortality/pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Cell Survival/genetics
MH  - CpG Islands
MH  - DNA Methylation
MH  - Decitabine
MH  - Disease Models, Animal
MH  - *Epigenesis, Genetic
MH  - Exons
MH  - Female
MH  - Gene Expression Regulation, Neoplastic/drug effects
MH  - *Gene Silencing
MH  - *Genes, Tumor Suppressor
MH  - Heterografts
MH  - Humans
MH  - Lung Neoplasms/*genetics/*mortality/pathology
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Prognosis
MH  - Receptor-Like Protein Tyrosine Phosphatases, Class 3/*genetics
PMC - PMC5482203
EDAT- 2017/06/07 06:00
MHDA- 2018/03/27 06:00
PMCR- 2017/05/31
CRDT- 2017/06/07 06:00
PHST- 2016/04/11 00:00 [received]
PHST- 2017/03/16 00:00 [accepted]
PHST- 2017/06/07 06:00 [pubmed]
PHST- 2018/03/27 06:00 [medline]
PHST- 2017/06/07 06:00 [entrez]
PHST- 2017/05/31 00:00 [pmc-release]
AID - mmr-16-01-0746 [pii]
AID - 10.3892/mmr.2017.6665 [doi]
PST - ppublish
SO  - Mol Med Rep. 2017 Jul;16(1):746-754. doi: 10.3892/mmr.2017.6665. Epub 2017 May 
      31.