PMID- 28498460
OWN - NLM
STAT- MEDLINE
DCOM- 20180301
LR  - 20220318
IS  - 1791-2431 (Electronic)
IS  - 1021-335X (Linking)
VI  - 37
IP  - 6
DP  - 2017 Jun
TI  - MCM7 amplification and overexpression promote cell proliferation, colony 
      formation and migration in esophageal squamous cell carcinoma by activating the 
      AKT1/mTOR signaling pathway.
PG  - 3590-3596
LID - 10.3892/or.2017.5614 [doi]
AB  - The roles and mechanisms of mini-chromosome maintenance complex component 7 
      (MCM7) amplification and overexpression in esophageal carcinogenesis were 
      investigated. By analyzing the TCGA datasets, we found that MCM7 was amplified in 
      approximately 12% of esophageal squamous cell carcinomas (ESCCs), and in more 
      than 4% of head and neck squamous cell carcinomas and stomach carcinomas. 
      Overexpression of MCM7 was further verified in three independent GEO datasets of 
      esophageal cancer. Knockdown of MCM7 using two siRNAs significantly inhibited 
      cell proliferation, colony formation and migration of KYSE510 and EC9706 cells 
      in vitro. Noteworthy, we further found that silencing of MCM7 suppressed the 
      phosphorylation of AKT1 and mTOR both in KYSE510 and EC9706 cells, and reduced 
      the cell cycle regulatory proteins cyclin D1, cyclin E2 and CDK2. Taken together, 
      our findings suggested that MCM7 promoted tumor cell proliferation, colony 
      formation and migration of ESCC cells via activating AKT1/mTOR signaling pathway.
FAU - Qiu, Yun-Tan
AU  - Qiu YT
AD  - Faculty of Medicine, Kunming University of Science and Technology, Kunming, 
      Yunnan 650500, P.R. China.
FAU - Wang, Wen-Jun
AU  - Wang WJ
AD  - Faculty of Medicine, Kunming University of Science and Technology, Kunming, 
      Yunnan 650500, P.R. China.
FAU - Zhang, Bing
AU  - Zhang B
AD  - Faculty of Medicine, Kunming University of Science and Technology, Kunming, 
      Yunnan 650500, P.R. China.
FAU - Mei, Li-Li
AU  - Mei LL
AD  - Faculty of Medicine, Kunming University of Science and Technology, Kunming, 
      Yunnan 650500, P.R. China.
FAU - Shi, Zhi-Zhou
AU  - Shi ZZ
AD  - Faculty of Medicine, Kunming University of Science and Technology, Kunming, 
      Yunnan 650500, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20170502
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (CCND1 protein, human)
RN  - 0 (RNA, Small Interfering)
RN  - 136601-57-5 (Cyclin D1)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (AKT1 protein, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.22 (CDK2 protein, human)
RN  - EC 2.7.11.22 (Cyclin-Dependent Kinase 2)
RN  - EC 3.6.4.12 (MCM7 protein, human)
RN  - EC 3.6.4.12 (Minichromosome Maintenance Complex Component 7)
SB  - IM
MH  - Carcinoma, Squamous Cell/*genetics
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Cyclin D1/genetics
MH  - Cyclin-Dependent Kinase 2/genetics
MH  - Esophageal Neoplasms/*genetics
MH  - Esophageal Squamous Cell Carcinoma
MH  - Gene Amplification/genetics
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Knockdown Techniques
MH  - Humans
MH  - Minichromosome Maintenance Complex Component 7/*genetics
MH  - Proto-Oncogene Proteins c-akt/*genetics
MH  - RNA, Small Interfering/genetics
MH  - Stem Cells/metabolism
MH  - TOR Serine-Threonine Kinases/*genetics
EDAT- 2017/05/13 06:00
MHDA- 2018/03/02 06:00
CRDT- 2017/05/13 06:00
PHST- 2016/10/28 00:00 [received]
PHST- 2017/04/24 00:00 [accepted]
PHST- 2017/05/13 06:00 [pubmed]
PHST- 2018/03/02 06:00 [medline]
PHST- 2017/05/13 06:00 [entrez]
AID - 10.3892/or.2017.5614 [doi]
PST - ppublish
SO  - Oncol Rep. 2017 Jun;37(6):3590-3596. doi: 10.3892/or.2017.5614. Epub 2017 May 2.