ArticleOncotarget2017
Inhibition of TRPC6 reduces non-small cell lung cancer cell proliferation and invasion.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 35 citations in OpenAlex.
- Inhibition of TRPC6 channel suppresses bladder cancer proliferation by disrupting store-operated calcium entry.Scientific reports · 2026Article
- Transient Receptor Potential Canonical 6 (TRPC6) Channel in the Pathogenesis of Diseases: A Jack of Many Trades.Inflammation · 2023Review
- Ion channels in lung cancer: biological and clinical relevance.Frontiers in pharmacology · 2023Review
- A549 in-silico 1.0: A first computational model to simulate cell cycle dependent ion current modulation in the human lung adenocarcinoma.PLoS computational biology · 2021Article
- Mechanosensitive ion channels in cell migration.Cells & development · 2021Review
- Deciphering the Role of CaCancers · 2021Review
- Overview of CaExploration of targeted anti-tumor therapy · 2021Review
- Mechanism of transmembrane and coiled-coil domain 1 in the regulation of proliferation and migration of A549 cells.Oncology letters · 2020Article
- Transient Receptor Potential Canonical (TRPC) Channels as Modulators of Migration and Invasion.International journal of molecular sciences · 2020Review
- TRPV4 Overexpression Promotes Metastasis Through Epithelial-Mesenchymal Transition in Gastric Cancer and Correlates with Poor Prognosis.OncoTargets and therapy · 2020Article
- Ion Channel Targeting with Antibodies and Antibody Fragments for Cancer Diagnosis.Antibodies (Basel, Switzerland) · 2019Review
- Review
- The Role of TRP Channels in the Metastatic Cascade.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Phospholipid Phosphatase 4 promotes proliferation and tumorigenesis, and activates CaMolecular cancer · 2017Article
- Review
- Therapeutic effects of SKF-96365 on murine allergic rhinitis induced by OVA.International journal of immunopathology and pharmacologyArticle
- Mechanosensitive Ion Channels: TRPV4 and P2X7 in Disseminating Cancer Cells.Cancer journal (Sudbury, Mass.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent studies indicate that the transient receptor potential canonical 6 (TRPC6) channel is highly expressed in several types of cancer cells. However, it remains unclear whether TRPC6 contributes to the malignancy of human non-small cell lung cancer (NSCLC). We used a human NSCLC A549 cell line as a model and found that pharmacological blockade or molecular knockdown of TRPC6 channel inhibited A549 cell proliferation by arresting cell cycle at the S-G2M phase and caused a significant portion of cells detached and rounded-up, but did not induce any types of cell death. Western blot and cell cycle analysis show that the detached round cells at the S-G2M phase expressed more TRPC6 than the still attached polygon cells at the G1 phase. Patch-clamp data also show that TRPC whole-cell currents in the detached cells were significantly higher than in the still attached cells. Inhibition of Ca2+-permeable TRPC6 channels significantly reduced intracellular Ca2+ in A549 cells. Interestingly, either blockade or knockdown of TRPC6 strongly reduced the invasion of this NSCLC cell line and decreased the expression of an adherent protein, fibronectin, and a tight junction protein, zonula occluden protein-1 (ZO-1). These data suggest that TRPC6-mediated elevation of intracellular Ca2+ stimulates NSCLC cell proliferation by promoting cell cycle progression and that inhibition of TRPC6 attenuates cell proliferation and invasion. Therefore, further in vivo studies may lead to a consideration of using a specific TRPC6 blocker as a complement to treat NSCLC.
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What OpenQuestion holds
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.