ArticleCell communication and signaling : CCS2022
MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 17 citations in OpenAlex.
- MICAL2 as a key effector of β-catenin signaling driving melanoma progression and therapeutic resistance.Cell death and differentiation · 2026Article
- Unraveling the dual roles of MICAL2 in skeletal muscle physiology and fusion negative rhabdomyosarcoma tumor progression.Cell death & disease · 2026Article
- SIRT6 cooperates with KDM5C to transcriptionally silence MICAL2 and inhibit tumorigenesis in pancreatic cancer.Cell communication and signaling : CCS · 2026Article
- LINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma.Oncogene · 2026Article
- A Short Report on Melanocyte/Melanoma Culture, Senescence, and Reproducibility.Pigment cell & melanoma research · 2026Article
- A ceRNA Network Mediates Salinity Adaptation Via miR-novel-3-LNC_015168-SLC17A9 Axis in Sea Cucumber.Marine biotechnology (New York, N.Y.) · 2026Article
- LncRNANon-coding RNA research · 2025Article
- The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential.Human cell · 2025Review
- Molecule interacting with CasL-2 enhances tumor progression and alters radiosensitivity in cervical cancer.Journal of translational medicine · 2025Article
- Potential biomarkers in early detection of gastric cancer.Frontiers in pharmacology · 2025Review
- Characteristics of early gastric tumors with different differentiation and predictors of long-term outcomes after endoscopic submucosal dissection.World journal of gastroenterology · 2024Article
- MICAL2 implies immunosuppressive features and acts as an independent and adverse prognostic biomarker in pancreatic cancer.Scientific reports · 2024Article
- Exploring the nexus between MYH9 and tumors: novel insights and new therapeutic opportunities.Frontiers in cell and developmental biology · 2024Review
- Downregulation of MAL2 inhibits breast cancer progression through regulating β-catenin/c-Myc axis.Cancer cell international · 2023Article
- Prognostic impact of MICALL1 and associates with immune infiltration in liver hepatocellular carcinoma patients.Cancer biomarkers : section A of Disease markers · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric cancer is a common and lethal human malignancy worldwide and cancer cell metastasis is the leading cause of cancer-related mortality. MICAL2, a flavoprotein monooxygenase, is an important regulator of epithelial-to-mesenchymal transition. The aim of this study was to explore the effects of MICAL2 on gastric cancer cell migration and determine the underlying molecular mechanisms.
methodsCell migration was examined by wound healing and transwell assays. Changes in E-cadherin/β-catenin signaling were determined by qPCR and analysis of cytoplasmic and nuclear protein fractions. E-cadherin/β-catenin binding was determined by co-immunoprecipitation assays. Cdc42 activity was examined by pulldown assay.
resultsMICAL2 was highly expressed in gastric cancer tissues. The knockdown of MICAL2 significantly attenuated migratory ability and β-catenin nuclear translocation in gastric cancer cells while LiCl treatment, an inhibitor of GSK3β, reversed these MICAL2 knockdown-induced effects. Meanwhile, E-cadherin expression was markedly enhanced in MICAL2-depleted cells. MICAL2 knockdown led to a significant attenuation of E-cadherin ubiquitination and degradation in a Cdc42-dependent manner, then enhanced E-cadherin/β-catenin binding, and reduced β-catenin nuclear translocation.
conclusionsTogether, our results indicated that MICAL2 promotes E-cadherin ubiquitination and degradation, leading to enhanced β-catenin signaling via the disruption of the E-cadherin/β-catenin complex and, consequently, the promotion of gastric cell migration. Video Abstract.
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