ArticleCancer science2014
Inhibition of transforming growth factor beta/SMAD signal by MiR-155 is involved in arsenic trioxide-induced anti-angiogenesis in prostate cancer.
Article in Cancer science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Riboflavin activates the Bmp4/Bmpr1α signaling to reverse arsenic-induced male reproductive toxicity: in vivo and in vitro studies.NPJ science of food · 2026Article
- Article
- miRNA-mediated resistance mechanisms in prostate cancer: implications for targeted therapy and metastatic progression.Medical oncology (Northwood, London, England) · 2025Review
- Dual role of miR-155 and exosomal miR-155 in tumor angiogenesis: implications for cancer progression and therapy.European journal of medical research · 2025Review
- EZH2-mediated downregulation of miR-155-5p contributes to prostate cancer cell malignancy through SMAD2 and TAB2.The Kaohsiung journal of medical sciences · 2025Article
- The Potential Use of Arsenic Trioxide in the Treatment of Systemic Lupus Erythematosus.International journal of molecular sciences · 2024Review
- Arsenic-induced prostate cancer: an enigma.Medical oncology (Northwood, London, England) · 2024Review
- The interaction between miRNAs and hazardous materials.Non-coding RNA research · 2023Review
- Crosstalk between Endothelial Cells and Tumor Cells: A New Era in Prostate Cancer Progression.International journal of molecular sciences · 2023Review
- Arsenic impairs stem cell differentiation via the Hippo signaling pathway.Toxicology research · 2023Article
- Review
- Combined anticancer effects of simvastatin and arsenic trioxide on prostate cancer cell lines via downregulation of the VEGF and OPN isoforms genes.Journal of cellular and molecular medicine · 2022Article
- Targeting Cell Death Mechanism Specifically in Triple Negative Breast Cancer Cell Lines.International journal of molecular sciences · 2022Article
- The role of TGF-β or BMPR2 signaling pathway-related miRNA in pulmonary arterial hypertension and systemic sclerosis.Arthritis research & therapy · 2021Review
- Anticancer mechanisms of phytochemical compounds: focusing on epigenetic targets.Environmental science and pollution research international · 2021Review
- Long-term arsenic exposure impairs differentiation in mouse embryonal stem cells.Journal of applied toxicology : JAT · 2021Article
- Review
- The Molecular Basis and Therapeutic Aspects of Cisplatin Resistance in Oral Squamous Cell Carcinoma.Frontiers in oncology · 2021Review
- Angiogenesis Inhibition in Prostate Cancer: An Update.Cancers · 2020Review
- MicroRNAs and Natural Compounds Mediated Regulation of TGF Signaling in Prostate Cancer.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer is the most common cause of cancer-related deaths in men. Current practices for treatment of prostate cancer are less than satisfactory because of metastasis and recurrence, which are primarily attributed to angiogenesis. Hence, anti-angiogenesis treatment is becoming a promising new approach for prostate cancer therapy. In addition to treating acute promyelocytic leukemia, arsenic trioxide (As2 O3 ) suppresses other solid tumors, including prostate cancer. However, the effects of As2 O3 on angiogenesis in prostate cancer cells, and the underlying molecular mechanisms remain unclear. In the present study, As2 O3 attenuated angiogenic ability through microRNA-155 (miR-155)-mediated inhibition of transforming growth factor beta (TGF-β)/SMAD signal pathway in human prostate cancer PC-3 and LNCaP cells in vitro and in vivo. Briefly, As2 O3 inhibited the activations/expressions of both TGFβ-induced and endogenous SMAD2/3. Furthermore, As2 O3 improved the expression of miR-155 via DNA-demethylation. MiR-155, which targeted the SMAD2-3'UTR, decreased the expression and function of SMAD2. Knockdown of miR-155 abolished the As2 O3 -induced inhibitions of the TGF-β/SMAD2 signaling, the vascular endothelial growth factor secretion and angiogenesis. Through understanding a novel mechanism whereby As2 O3 inhibits angiogenic potential of prostate cancer cells, our study would help in the development of As2 O3 as a potential chemopreventive agent when used alone or in combination with other current anticancer drugs.
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Registered trials
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