Evidence map›Paper›PMID 21876174›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Calcium store sensor stromal-interaction molecule 1-dependent signaling plays an important role in cervical cancer growth, migration, and angiogenesis.

Yih-Fung Chen, Wen-Tai Chiu, Ying-Ting Chen, Pey-Yun Lin, Huey-Jy Huang, Cheng-Yang Chou, Hsien-Chang Chang, Ming-Jer Tang, Meng-Ru Shen

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers.

0numbers the graph read from it
0cells of the map it votes in
195citing papers in PubMed
9.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

195 citing papers in PubMed, 322 citations in OpenAlex.

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  7. Store-operated calcium entry-based targets for novel cancer therapeutic development.The Journal of pharmacology and experimental therapeutics · 2025
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  11. Article
  12. Review
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  15. Review
  16. CaBiophysics reports · 2024
    Article
  17. Article
  18. STIM1 in tumor cell death: angel or devil?Cell death discovery · 2023
    Review
  19. Article
  20. Review

135 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Yih-Fung ChenDepartment of Pharmacology, National Cheng Kung University, Tainan 70101, Taiwan.
Wen-Tai Chiu
Ying-Ting Chen
Pey-Yun Lin
Huey-Jy Huang
Cheng-Yang Chou
Hsien-Chang Chang
Ming-Jer Tang
Meng-Ru Shen
Institute of Biomedical Science · GBCzech Academy of Sciences, Institute of Physiology · CZNational Cheng Kung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Store-operated Ca(2+) entry (SOCE) is the principal Ca(2+) entry mechanism in nonexcitable cells. Stromal-interaction molecule 1 (STIM1) is an endoplasmic reticulum Ca(2+) sensor that triggers SOCE activation. However, the role of STIM1 in regulating cancer progression remains controversial and its clinical relevance is unclear. Here we show that STIM1-dependent signaling is important for cervical cancer cell proliferation, migration, and angiogenesis. STIM1 overexpression in tumor tissue is noted in 71% cases of early-stage cervical cancer. In tumor tissues, the level of STIM1 expression is significantly associated with the risk of metastasis and survival. EGF-stimulated cancer cell migration requires STIM1 expression and EGF increases the interaction between STIM1 and Orai1 in juxta-membrane areas, and thus induces Ca(2+) influx. STIM1 involves the activation of Ca(2+)-regulated protease calpain, as well as Ca(2+)-regulated cytoplasmic kinase Pyk2, which regulate the focal-adhesion dynamics of migratory cervical cancer cells. Because of an increase of p21 protein levels and a decrease of Cdc25C protein levels, STIM1-silencing in cervical cancer cells significantly inhibits cell proliferation by arresting the cell cycle at the S and G2/M phases. STIM1 also regulates the production of VEGF in cervical cancer cells. Interference with STIM1 expression or blockade of SOCE activity inhibits tumor angiogenesis and growth in animal models, confirming the crucial role of STIM1-mediated Ca(2+) influx in aggravating tumor development in vivo. These results make STIM1-dependent signaling an attractive target for therapeutic intervention.

Indexed as

Cell MovementSignal TransductionAnimalsCalciumCalcium ChannelsCell CycleCell ProliferationDisease Models, AnimalEpidermal Growth FactorFemaleFocal AdhesionsHumansMembrane ProteinsMiceNeoplasm MetastasisNeoplasm ProteinsCalciumCalcium ChannelsEpidermal Growth FactorMembrane ProteinsNeoplasm ProteinsORAI1 ProteinORAI1 protein, humanSTIM1 protein, humanStromal Interaction Molecule 1

Identifiers

PMID21876174
PMCPMC3174613
OpenAlexW2077807460

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.