ArticleOncotarget2016
TRPC1-STIM1 activation modulates transforming growth factor β-induced epithelial-to-mesenchymal transition.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 44 citations in OpenAlex.
- Magnetic Reprogramming of Macrophages Stimulates Phagocytosis of Breast Cancer Cells via a TRPC1-STING Inflammatory Axis.Smart medicine · 2026Article
- Store-operated CaAmerican journal of physiology. Lung cellular and molecular physiology · 2025Article
- Article
- Similarities and Differences between the Orai1 Variants: Orai1α and Orai1β.International journal of molecular sciences · 2022Review
- Article
- Potassium and Calcium Channel Complexes as Novel Targets for Cancer Research.Reviews of physiology, biochemistry and pharmacology · 2022Article
- Focusing on Mechanoregulation Axis in Fibrosis: Sensing, Transduction and Effecting.Frontiers in molecular biosciences · 2022Review
- TRP Channels as Molecular Targets to Relieve Endocrine-Related Diseases.Frontiers in molecular biosciences · 2022Review
- Inhibition of CaFrontiers in physiology · 2022Article
- Transient Receptor Potential Channels in the Epithelial-to-Mesenchymal Transition.International journal of molecular sciences · 2021Review
- Mechanosensitive ion channels in cell migration.Cells & development · 2021Review
- CaCancers · 2021Review
- Effects of the Tumor Environment on Ion Channels: Implication for Breast Cancer Progression.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Membrane Transporters and Channels in Melanoma.Reviews of physiology, biochemistry and pharmacology · 2021Review
- Calcium Channel Protein ORAI1 Mediates TGF-β Induced Epithelial-to-Mesenchymal Transition in Colorectal Cancer Cells.Frontiers in oncology · 2021Article
- Calcium Homeostasis: A Potential Vicious Cycle of Bone Metastasis in Breast Cancers.Frontiers in oncology · 2020Review
- A Novel Calcium-Mediated EMT Pathway Controlled by Lipids: An Opportunity for Prostate Cancer Adjuvant Therapy.Cancers · 2019Article
- Calcium-sensing stromal interaction molecule 2 upregulates nuclear factor of activated T cells 1 and transforming growth factor-β signaling to promote breast cancer metastasis.Breast cancer research : BCR · 2019Article
- The Calcium-Signaling Toolkit in Cancer: Remodeling and Targeting.Cold Spring Harbor perspectives in biology · 2019Review
- TRPV4 regulates matrix stiffness and TGFβ1-induced epithelial-mesenchymal transition.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Activation of Epithelial-to-Mesenchymal Transition (EMT) is important for tumor metastasis. Although growth factors such as TGFβ and EGF have been shown to induce EMT in breast epithelial cells, the mechanism resulting in migration is not well understood. Herein, we provide evidence that Ca2+ entry into the cell, especially upon store-depletion, plays an important role in TGFβ-induced EMT by promoting cellular migration and potentially leading to metastasis. The increased migration by TGFβ in non-cancerous cells was due to the loss of E-cadherin along with a subsequent increase in N-cadherin levels. Importantly, TGFβ-treatment increases store-mediated Ca2+ entry, which was essential for the activation of calpain leading to the loss of E-cadherin and MMP activation. Inhibition of Ca2+ entry by using Ca2+ channel blocker SKF-96365, significantly decreased Ca2+ entry, decreased TGFβ-induced calpain activation, and suppressed the loss of E-cadherin along with inhibiting cell migration. Furthermore, TRPC1 function as an endogenous Ca2+ entry channel and silencing of either TRPC1 or its activator, STIM1, significantly decreased TGFβ induced Ca2+ entry, inhibited TGFβ-mediated calpain activation and cell migration. In contrast, overexpression of TRPC1 showed increased Ca2+ entry and promoted TGFβ-mediated cell migration. Moreover, increased TRPC1 expression was observed in ductal carcinoma cells. Together these results suggest that disrupting Ca2+ influx via TRPC1/STIM1 mechanism reduces calpain activity, which could restore intercellular junction proteins thereby inhibiting EMT induced motility.
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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.