ArticleJournal of cellular and molecular medicine2019
MICAL-L2 potentiates Cdc42-dependent EGFR stability and promotes gastric cancer cell migration.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- Prevalence and Functional Roles of Intrinsic Disorder in the [F-actin]-monooxygenase MICAL Family Members and their Interactors.Cell biochemistry and biophysics · 2026Article
- Interpretable Cancer Survival Prediction by Fusing Semantic Labelling of Cell Types and Whole Slide Images.Interdisciplinary sciences, computational life sciences · 2026Article
- Cyclized Peptide Inhibitors of the Small G Protein Cdc42 Mimic Binding of Effector Proteins.Biochemistry · 2026Article
- Molecules interacting with CasL-Like 2 enhances tumor angiogenesis and progression by activating mTOR/HIF1α/VEGF pathway in kidney renal clear cell carcinoma.Scientific reports · 2025Article
- Circular RNA CircSLC22A23 Promotes Gastric Cancer Progression by Activating HNRNPU Expression.Digestive diseases and sciences · 2024Article
- Comprehensive Analysis of MICALL2 Reveals Its Potential Roles in EGFR Stabilization and Ovarian Cancer Cell Invasion.International journal of molecular sciences · 2023Article
- Recent Advances in the Management of Clear Cell Renal Cell Carcinoma: Novel Biomarkers and Targeted Therapies.Cancers · 2023Review
- Micall2 Is Responsible for the Malignancy of Clear Cell Renal Cell Carcinoma.Yonago acta medica · 2023Article
- Prognostic impact of MICALL1 and associates with immune infiltration in liver hepatocellular carcinoma patients.Cancer biomarkers : section A of Disease markers · 2023Article
- High MICAL1 expression correlates with cancer progression and immune infiltration in renal clear cell carcinoma.BMC cancer · 2022Article
- MICALL2 as a substrate of ubiquitinase TRIM21 regulates tumorigenesis of colorectal cancer.Cell communication and signaling : CCS · 2022Article
- MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway.Cell communication and signaling : CCS · 2022Article
- Article
- Identification of MICALL2 as a Novel Prognostic Biomarker Correlating with Inflammation and T Cell Exhaustion of Kidney Renal Clear Cell Carcinoma.Journal of Cancer · 2022Article
- lncRNA DSCR8 mediates miR-137/Cdc42 to regulate gastric cancer cell proliferation, invasion, and cell cycle as a competitive endogenous RNA.Molecular therapy oncolytics · 2021Article
- miR-497 defect contributes to gastric cancer tumorigenesis and progression via regulating CDC42/ITGB1/FAK/PXN/AKT signaling.Molecular therapy. Nucleic acids · 2021Article
- MICAL2 Contributes to Gastric Cancer Cell Proliferation by Promoting YAP Dephosphorylation and Nuclear Translocation.Oxidative medicine and cellular longevity · 2021Article
- KIF15 Promotes Progression of Castration Resistant Prostate Cancer by Activating EGFR Signaling Pathway.Frontiers in oncology · 2021Article
- MICAL-L2 Is Essential for c-Myc Deubiquitination and Stability in Non-small Cell Lung Cancer Cells.Frontiers in cell and developmental biology · 2020Article
- Structural Characteristics, Binding Partners and Related Diseases of the Calponin Homology (CH) Domain.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enhanced migration potential is a common characteristic of cancer cells induced by mechanisms that are incompletely defined. The present study was designed to investigate relationship of a new discovered cytoskeleton regulator MICAL-L2 and the endogenous epidermal growth factor receptor (EGFR) signalling pathways in gastric cancer cell migration. Increased expression of MICAL-L2 in gastric cancer cells up-regulated EGFR protein level, accompanied by the increase of cell migration, whereas silencing MICAL-L2 down-regulated EGFR and inhibited cell migration. Expression of MICAL-L2 was also shown positively correlated with the activation of HSP27/cytoskeleton and HSP27/β-catenin signalling pathways that provide key mechanisms controlling cell migration. The up-regulating effect of MICAL-L2 on EGFR is mediated through a transcription-independent mechanism that involves inhibiting EGFR protein degradation in lysosome. Further analysis indicated that Cdc42 activation contributed in maintaining the effect of MICAL-L2 on EGFR stability. Furthermore analysis of clinic specimens revealed increased expression of MICAL-L2 in carcinoma tissues and a positive correlation between MICAL-L2 and EGFR expression levels. The above results indicate that MICAL-L2 potentiates gastric cell migration via inhibiting EGFR degradation in lysosome via a Cdc42-dependent manner that leads to the activation of EGFR/HSP27 signalling pathways.
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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 Socratic graph.