PMID- 23136087
OWN - NLM
STAT- MEDLINE
DCOM- 20130131
LR  - 20211021
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 33
IP  - 6
DP  - 2012 Dec
TI  - Tumor suppressor TSLC1 is implicated in cell proliferation, invasion and 
      apoptosis in laryngeal squamous cell carcinoma by regulating Akt signaling 
      pathway.
PG  - 2007-17
LID - 10.1007/s13277-012-0460-x [doi]
AB  - Overwhelming evidence has demonstrated that TSLC1 (tumor suppressor in lung 
      cancer 1), a novel tumor suppressor, is crucially implicated in various 
      biological processes including progression, proliferation and apoptosis during 
      tumorigenesis. However, the exact functions and molecular details of TSLC1 in 
      laryngeal cancer remain ill-defined. Here, the expression of TSLC1 in laryngeal 
      squamous cell carcinoma (LSCC) tissues and cells was detected, and the biological 
      roles of TSLC1 in LSCC cells were investigated. The results showed that 
      expressions of TSLC1 mRNA and protein were significantly reduced in LSCC tissues 
      with low expression in 18 of 85 (21.18 %) and 16 of 85 (18.82 %), respectively. 
      Additionally, statistical analysis revealed a significant correlation of TSLC1 
      expression with TNM staging and lymph node metastases (P < 0.05), but not related 
      to age, gender and tumor differentiation (P > 0.05). Elevation of TSLC1 level 
      inhibited cell proliferation, reduced cell invasion in vitro and induced cell 
      apoptosis in Hep-2 cells, most importantly, TSLC1 upregulation decreased the 
      level of pAkt, but not changed the level of total Akt in Hep-2 cells. Stepwise 
      investigations demonstrated that overexpression of TSLC1 in Hep-2 cells increased 
      caspase-3 activity and expressions of bax and p21 proteins but decreased the 
      levels of bcl-2, MMP-2 and MMP-9 proteins. These data suggest that TSLC1 may 
      exert essential roles in the progression and development of LSCC, and thus TSLC1 
      may be a potential molecular target for LSCC treatment.
FAU - Lu, Baocai
AU  - Lu B
AD  - Department of Otorhinolaryngology, First Affiliated Hospital of Xinxiang Medical 
      College, No 88 JianKang Road, Weihui, Henan 453100, China. lu_baocai@126.com
FAU - Di, Wenyu
AU  - Di W
FAU - Wang, Huimin
AU  - Wang H
FAU - Ma, Huimin
AU  - Ma H
FAU - Li, Jinsong
AU  - Li J
FAU - Zhang, Qunmei
AU  - Zhang Q
LA  - eng
PT  - Journal Article
DEP - 20120718
PL  - Netherlands
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental 
      Biology and Medicine
JID - 8409922
RN  - 0 (CADM1 protein, human)
RN  - 0 (Cell Adhesion Molecule-1)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Immunoglobulins)
RN  - 0 (RNA, Messenger)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - *Apoptosis
MH  - Blotting, Western
MH  - Carcinoma, Squamous Cell/genetics/metabolism/*pathology
MH  - Cell Adhesion
MH  - Cell Adhesion Molecule-1
MH  - Cell Adhesion Molecules/genetics/*metabolism
MH  - *Cell Movement
MH  - *Cell Proliferation
MH  - Female
MH  - Flow Cytometry
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - Immunoglobulins/genetics/*metabolism
MH  - In Situ Hybridization
MH  - Laryngeal Neoplasms/genetics/metabolism/*pathology
MH  - Lymphatic Metastasis
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Invasiveness
MH  - Neoplasm Staging
MH  - Proto-Oncogene Proteins c-akt/genetics/*metabolism
MH  - RNA, Messenger/genetics
MH  - Real-Time Polymerase Chain Reaction
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction
MH  - Tumor Cells, Cultured
EDAT- 2012/11/09 06:00
MHDA- 2013/02/01 06:00
CRDT- 2012/11/09 06:00
PHST- 2012/06/19 00:00 [received]
PHST- 2012/07/04 00:00 [accepted]
PHST- 2012/11/09 06:00 [entrez]
PHST- 2012/11/09 06:00 [pubmed]
PHST- 2013/02/01 06:00 [medline]
AID - 10.1007/s13277-012-0460-x [doi]
PST - ppublish
SO  - Tumour Biol. 2012 Dec;33(6):2007-17. doi: 10.1007/s13277-012-0460-x. Epub 2012 
      Jul 18.