PMID- 23022228
OWN - NLM
STAT- MEDLINE
DCOM- 20130125
LR  - 20161125
IS  - 1873-2968 (Electronic)
IS  - 0006-2952 (Linking)
VI  - 84
IP  - 12
DP  - 2012 Dec 15
TI  - Knockdown of stromal interaction molecule 1 (STIM1) suppresses store-operated 
      calcium entry, cell proliferation and tumorigenicity in human epidermoid 
      carcinoma A431 cells.
PG  - 1592-603
LID - S0006-2952(12)00652-1 [pii]
LID - 10.1016/j.bcp.2012.09.021 [doi]
AB  - Store-operated calcium (Ca(2+)) entry (SOCE) is important for cellular activities 
      such as gene transcription, cell cycle progression and proliferation in most 
      non-excitable cells. Stromal interaction molecule 1 (STIM1), a newly identified 
      Ca(2+)-sensing protein, monitors the depletion of endoplasmic reticulum (ER) 
      Ca(2+) stores and activates store-operated Ca(2+) channels at the plasma membrane 
      to induce SOCE. To investigate the possible roles of STIM1 in tumor growth in 
      relation to SOCE, we established STIM1 knockdown (KD) clones of human epidermoid 
      carcinoma A431 cells by RNA interference. Thapsigargin, an inhibitor of ER 
      Ca(2+)-ATPase, -induced and phospholipase C-coupled receptor agonist-induced 
      SOCEs were reduced in two STIM1 KD clones compared to a negative control clone. 
      Re-expression of a KD-resistant full-length STIM1, but not a Ca(2+) 
      release-activated Ca(2+) channel activation domain (CAD)-deleted STIM1 mutant, in 
      the KD clone restored the amplitude of SOCE, suggesting the specificity of the 
      STIM1 knockdown. The cell growth of the STIM1 KD clones was slower than that of 
      the negative control clone. DNA synthesis assessed by BrdU incorporation, as well 
      as EGF-stimulated EGF receptor activation, decreased in the STIM1 KD clones. 
      Xenograft growth of the STIM1 KD clones was significantly retarded compared with 
      that of the negative control. Cell migration was attenuated in the STIM1 KD clone 
      and the STIM1 silencing effect was reversed by transient re-expression of the 
      full-length STIM1 but not CAD-deletion mutant. These results indicate that STIM1 
      plays an important role in SOCE, cell-growth and tumorigenicity in human 
      epidermoid carcinoma A431cells, suggesting the potential use of STIM1-targeting 
      agents for treating epidermoid carcinoma.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Yoshida, Junko
AU  - Yoshida J
AD  - Departments of Pharmacology, School of Medicine, Kanazawa Medical University, 
      Uchinada, Ishikawa 920-0293, Japan. yayuyo@kanazawa-med.ac.jp
FAU - Iwabuchi, Kuniyoshi
AU  - Iwabuchi K
FAU - Matsui, Tadashi
AU  - Matsui T
FAU - Ishibashi, Takaharu
AU  - Ishibashi T
FAU - Masuoka, Takayoshi
AU  - Masuoka T
FAU - Nishio, Matomo
AU  - Nishio M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120926
PL  - England
TA  - Biochem Pharmacol
JT  - Biochemical pharmacology
JID - 0101032
RN  - 0 (DNA Primers)
RN  - 0 (Membrane Proteins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (STIM1 protein, human)
RN  - 0 (Stromal Interaction Molecule 1)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Base Sequence
MH  - Calcium/*metabolism
MH  - Carcinoma, Squamous Cell/metabolism/*pathology
MH  - Cell Line, Tumor
MH  - *Cell Proliferation
MH  - *Cell Transformation, Neoplastic
MH  - DNA Primers
MH  - *Gene Knockdown Techniques
MH  - Humans
MH  - Membrane Proteins/genetics/*physiology
MH  - Neoplasm Proteins/genetics/*physiology
MH  - Stromal Interaction Molecule 1
EDAT- 2012/10/02 06:00
MHDA- 2013/01/26 06:00
CRDT- 2012/10/02 06:00
PHST- 2012/07/31 00:00 [received]
PHST- 2012/09/18 00:00 [revised]
PHST- 2012/09/19 00:00 [accepted]
PHST- 2012/10/02 06:00 [entrez]
PHST- 2012/10/02 06:00 [pubmed]
PHST- 2013/01/26 06:00 [medline]
AID - S0006-2952(12)00652-1 [pii]
AID - 10.1016/j.bcp.2012.09.021 [doi]
PST - ppublish
SO  - Biochem Pharmacol. 2012 Dec 15;84(12):1592-603. doi: 10.1016/j.bcp.2012.09.021. 
      Epub 2012 Sep 26.