ArticlePloS one2014
Store-operated Ca2+ entry (SOCE) regulates melanoma proliferation and cell migration.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
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.
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.
Who cites it
98 citing papers in PubMed, 148 citations in OpenAlex.
- Inhibition of TRPC6 channel suppresses bladder cancer proliferation by disrupting store-operated calcium entry.Scientific reports · 2026Article
- Orai1- and STIM1-mediated calcium signaling controls PD-L1 expression and modulates antitumor immunity in oral cancer.The journal of physiological sciences : JPS · 2026Article
- Crosstalk between calcium and reactive oxygen species signaling in cancer revisited.Cell calcium · 2025Review
- Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming.Cancer science · 2024Article
- EP4-induced mitochondrial localization and cell migration mediated by CALML6 in human oral squamous cell carcinoma.Communications biology · 2024Article
- Wound Repair and CaCells · 2024Review
- Physiological functions of calcium signaling via Orai1 in cancer.The journal of physiological sciences : JPS · 2023Review
- Purinergic Activation of Store-Operated Calcium Entry (SOCE) Regulates Cell Migration in Metastatic Ovarian Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Blockade of store-operated calcium entry sensitizes breast cancer cells to cisplatin therapy via modulating inflammatory response.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Genetics and RNA Regulation of Uveal Melanoma.Cancers · 2023Review
- CRAC and SK Channels: Their Molecular Mechanisms Associated with Cancer Cell Development.Cancers · 2022Review
- Suppression of CaThe EMBO journal · 2022Article
- Blockage of Orai1-Nucleolin interaction meditated calcium influx attenuates breast cancer cells growth.Oncogenesis · 2022Article
- The Regulatory Roles of Mitochondrial Calcium and the Mitochondrial Calcium Uniporter in Tumor Cells.International journal of molecular sciences · 2022Review
- Science CommuniCaCells · 2022Review
- Review
- The Role of Calcium Signaling in Melanoma.International journal of molecular sciences · 2022Review
- Suppressing Effect of NaInternational journal of molecular sciences · 2022Article
- Store-operated calcium entry via ORAI1 regulates doxorubicin-induced apoptosis and prevents cardiotoxicity in cardiac fibroblasts.PloS one · 2022Article
- The Role of Heat Shock Protein 27 in Carcinogenesis and Treatment of Colorectal Cancer.Current pharmaceutical design · 2022Review
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Store-operated Ca(2+) entry (SOCE) is a major mechanism of Ca(2) (+) import from extracellular to intracellular space, involving detection of Ca(2+) store depletion in endoplasmic reticulum (ER) by stromal interaction molecule (STIM) proteins, which then translocate to plasma membrane and activate Orai Ca(2+) channels there. We found that STIM1 and Orai1 isoforms were abundantly expressed in human melanoma tissues and multiple melanoma/melanocyte cell lines. We confirmed that these cell lines exhibited SOCE, which was inhibited by knockdown of STIM1 or Orai1, or by a pharmacological SOCE inhibitor. Inhibition of SOCE suppressed melanoma cell proliferation and migration/metastasis. Induction of SOCE was associated with activation of extracellular-signal-regulated kinase (ERK), and was inhibited by inhibitors of calmodulin kinase II (CaMKII) or Raf-1, suggesting that SOCE-mediated cellular functions are controlled via the CaMKII/Raf-1/ERK signaling pathway. Our findings indicate that SOCE contributes to melanoma progression, and therefore may be a new potential target for treatment of melanoma, irrespective of whether or not Braf mutation is present.
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Registered trials
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.