ArticleJournal of cellular and molecular medicine2018
MICAL1 facilitates breast cancer cell proliferation via ROS-sensitive ERK/cyclin D pathway.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 87 citations in OpenAlex.
- Trem2-MICAL1-P-ERK Axis in Macrophages Confers Protection AgainstPathogens (Basel, Switzerland) · 2025Article
- BMSCs-targeting piezoelectric stimulation and immunomodulatory dual-functional hydrogel for promoting diabetic bone regeneration.Materials today. Bio · 2025Article
- MICAL1 Mediates TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Metastasis of Hepatocellular Carcinoma by Activating Smad2/3.Cell biochemistry and biophysics · 2025Article
- The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025Review
- Elucidating the role of MICAL1 in pan-cancer using integrated bioinformatics and experimental approaches.Cell adhesion & migration · 2024Article
- MICAL1 promotes the proliferation in acute myeloid leukemia and is associated with clinical prognosis and immune infiltration.Discover oncology · 2024Article
- ANGPTL4 regulates ovarian cancer progression by activating the ERK1/2 pathway.Cancer cell international · 2024Article
- Chemical biology approaches to uncovering nuclear ROS control.Current opinion in chemical biology · 2023Review
- MICAL-mediated oxidation of actin and its effects on cytoskeletal and cellular dynamics.Frontiers in cell and developmental biology · 2023Review
- Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species.Frontiers in pharmacology · 2023Review
- Prognostic impact of MICALL1 and associates with immune infiltration in liver hepatocellular carcinoma patients.Cancer biomarkers : section A of Disease markers · 2023Article
- Adaptive and non-adaptive gene expression responses in prostate cancer during androgen deprivation.PloS one · 2023Article
- Single-Cell Transcriptome Analysis of H5N1-HA-Stimulated Alpaca PBMCs.Biomolecules · 2022Article
- High MICAL1 expression correlates with cancer progression and immune infiltration in renal clear cell carcinoma.BMC cancer · 2022Article
- Bisphenol AF Promoted the Growth of Uterus and Activated Estrogen Signaling Related Targets in Various Tissues of Nude Mice with SK-BR-3 Xenograft Tumor.International journal of environmental research and public health · 2022Article
- MICAL1 facilitates pancreatic cancer proliferation, migration, and invasion by activating WNT/β-catenin pathway.Journal of translational medicine · 2022Article
- The Janus-faced role of TRPM2-S in retroperitoneal liposarcoma via increasing ROS levels.Cell communication and signaling : CCS · 2022Article
- mTOR pathway gene mutations predict response to immune checkpoint inhibitors in multiple cancers.Journal of translational medicine · 2022Article
- A chemical probe for BAG1 targets androgen receptor-positive prostate cancer through oxidative stress signaling pathway.iScience · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Molecule interacting with CasL 1 (MICAL1) is a multidomain flavoprotein mono-oxygenase that strongly involves in cytoskeleton dynamics and cell oxidoreduction metabolism. Recently, results from our laboratory have shown that MICAL1 modulates reactive oxygen species (ROS) production, and the latter then activates phosphatidyl inositol 3-kinase (PI3K)/protein kinase B (Akt) signalling pathway which regulates breast cancer cell invasion. Herein, we performed this study to assess the involvement of MICAL1 in breast cancer cell proliferation and to explore the potential molecular mechanism. We noticed that depletion of MICAL1 markedly reduced cell proliferation in breast cancer cell line MCF-7 and T47D. This effect of MICAL1 on proliferation was independent of wnt/β-catenin and NF-κB pathways. Interestingly, depletion of MICAL1 significantly inhibited ROS production, decreased p-ERK expression and unfavourable for proliferative phenotype of breast cancer cells. Likewise, MICAL1 overexpression increased p-ERK level as well as p-ERK nucleus translocation. Moreover, we investigated the effect of MICAL1 on cell cycle-related proteins. MICAL1 positively regulated CDK4 and cyclin D expression, but not CDK2, CDK6, cyclin A and cyclin E. In addition, more expression of CDK4 and cyclin D by MICAL1 overexpression was blocked by PI3K/Akt inhibitor LY294002. LY294002 treatment also attenuated the increase in the p-ERK level in MICAL1-overexpressed breast cancer cells. Together, our results suggest that MICAL1 exhibits its effect on proliferation via maintaining cyclin D expression through ROS-sensitive PI3K/Akt/ERK signalling in breast cancer cells.
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