CEMIP

Last update 08 May 2025

Basic Info

Synonyms

cell migration inducing hyaluronidase 1, Cell migration-inducing and hyaluronan-binding protein, CEMIP

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Introduction

Mediates depolymerization of hyaluronic acid (HA) via the cell membrane-associated clathrin-coated pit endocytic pathway. Binds to hyaluronic acid. Hydrolyzes high molecular weight hyaluronic acid to produce an intermediate-sized product, a process that may occur through rapid vesicle endocytosis and recycling without intracytoplasmic accumulation or digestion in lysosomes. Involved in hyaluronan catabolism in the dermis of the skin and arthritic synovium. Positively regulates epithelial-mesenchymal transition (EMT), and hence tumor cell growth, invasion and cancer dissemination. In collaboration with HSPA5/BIP, promotes cancer cell migration in a calcium and PKC-dependent manner. May be involved in hearing.

100 Clinical Results associated with CEMIP

100 Translational Medicine associated with CEMIP

0 Patents (Medical) associated with CEMIP

242

Literatures (Medical) associated with CEMIP

01 May 2025·Pathology - Research and Practice

MARCH8 ubiquitinates and degrades CEMIP to induce colorectal cancer cell ferroptosis through inactivating PI3K/AKT pathway

Article

Author: Wang, Maonan ; Yang, Bo ; Liu, Lintao ; Zhang, Cheng

BACKGROUNDCell migration-inducing and hyaluronan-binding protein (CEMIP) is found to act as an oncogene in colorectal cancer (CRC) progression, but the underlying molecular mechanisms need to be further elucidated.METHODSThe mRNA and protein levels of CEMIP and membrane-associated ring-CH-type finger 8 (MARCH8) were examined by qRT-PCR and western blot. Cell functions were detected by CCK8 assay, colony formation assay and transwell assay. The levels of ROS, Fe^2 +, GSH, and MDA were examined to evaluate cell ferroptosis. The interaction between MARCH8 and CEMIP was assessed by Co-IP assay and ubiquitination assay. The protein levels of ferroptosis-related markers (ACSL4, GPX4 and FTH1) and PI3K/AKT-related markers were tested using western bolt. The anti-tumor effect of MARCH8 was further confirmed by constructing xenograft tumor models.RESULTSCEMIP expression was higher in CRC tissues and cells. CEMIP knockdown could suppress CRC cell proliferation, migration, invasion, and enhance ferroptosis. MARCH8 ubiquitinated CEMIP to decrease its expression, thus inhibiting CRC cell proliferation, metastasis and inducing ferroptosis. And CEMIP overexpression could abolish the anti-proliferation, anti-metastasis and pro-ferroptosis effect of MARCH8. Also, MARCH8 overexpression repressed the activity of PI3K/AKT pathway, and CEMIP upregulation partially reversed this effect. In vivo experiments suggested that MARCH8 reduced CRC tumorigenesis by inducing ferroptosis.CONCLUSIONMARCH8 promoted CRC cell ferroptosis via inhibiting PI3K/AKT pathway by enhancing the ubiquitination and degradation of CEMIP.

01 May 2025·Acta Pharmacologica Sinica

Deletion of smooth muscle ZFP36 promotes neointimal hyperplasia in mice

Article

Author: Kovarik, Pavel ; Wang, Lei ; Wu, Zhi-Nan ; Xiong, Xiao ; Lu, Hui-Xia ; Cao, Guang-Qing ; Ji, Xiao-Ping ; Zhang, Yan-Ling ; Liu, Yan ; Tian, Mi ; He, Li-Fan ; Zhang, Wencheng

Platelet-derived growth factor (PDGF-BB) released from the injured intima induces the proliferation and migration of vascular smooth muscle cells (VSMCs), which is the key mechanism of neointimal hyperplasia. Zinc finger 36 (ZFP36), a widespread RNA-binding protein, is important for pathological processes in many diseases. In this study we investigated the role of ZFP36 in VSMCs proliferation, migration and neointimal hyperplasia in mice. We generated smooth muscle-specific Zfp36 knockout (Zfp36^SMKO) mice, and established restenosis mouse models by ligation of left carotid artery in Zfp36^SMKO mice. We showed that the expression levels of ZFP36 were significantly decreased in human atherosclerotic coronary arteries and murine injured carotid arteries compared with controls. Compared to control Zfp36^fl/fl mice, Zfp36^SMKO mice displayed accelerated neointimal hyperplasia. In cultured mouse VSMCs, PDGF-BB (20 ng/mL) significantly downregulated ZFP36 expression through KLF4 binding site in Zfp36 promoter. We revealed that ZFP36 could bind to the mRNA of cell migration-inducing protein (CEMIP) and promoted its degradation in VSMCs, thereby reducing the expression of CEMIP protein. Knockdown of Cemip inhibited VSMCs proliferation and migration induced by Zfp36 knockout, thereby suppressing neointimal hyperplasia in Zfp36^SMKO mice. We conclude that vascular smooth muscle ZFP36 has a protective effect against neointimal hyperplasia by reducing CEMIP expression. ZFP36 is downregulated by vascular injury and PDGF-BB treatment, which promotes VSMCs proliferation and migration and neointima formation. The results suggest that targeting ZFP36 may represent a novel therapeutic strategy for preventing or treating neointimal hyperplasia and related cardiovascular diseases.

07 Mar 2025·Cureus

Extracellular Vesicle-Associated Angiopoietin-2 and Cell Migration-Inducing Protein in Lung Cancer Progression and Brain Metastases

Article

Author: Balasa, Adrian F ; Suciu, Bogdan A ; Tamas, Flaviu ; Tamas, Corina I

BACKGROUNDAngiopoietin-2 (ANGPT2) and cell migration-inducing protein (CEMIP) are key regulators of angiogenesis, extracellular matrix remodeling, and metastatic progression in various cancers, including lung cancer (LC). The presence of these biomarkers in extracellular vesicles (EVs) may offer valuable insights into the molecular mechanisms underlying LC progression and metastasis. Extracellular vesicles play a critical role in LC by enhancing intercellular communication and supporting processes such as angiogenesis, immune evasion, and metastasis, transferring key molecules like vascular endothelial growth factor (VEGF) and pro-angiogenic microRNAs (miRNAs).METHODSThis study aimed to investigate the presence and quantification of ANGPT2 and CEMIP in the cargo of EVs isolated from plasma samples obtained from the peripheral venous blood of patients with localized lung cancer (LLC group), lung cancer with brain metastases (LCM group), and healthy controls (HC group). EVs were isolated using the density gradient ultracentrifugation method, and their characterization was performed through scanning and transmission electron microscopy as well as flow cytometry. Western blot analysis was used to identify ANGPT2 and CEMIP in EV cargo, and band intensity from western blot images was quantified using specialized software.RESULTSThe expression of ANGPT2 and CEMIP in EV cargo was significantly higher in the oncologic groups (LLC and LCM combined) compared to the HC group. Notably, EV CEMIP levels were, on average, 59% higher in patients with brain metastases than in those with localized lung cancer. Following surgical resection, postoperative EV ANGPT2 and EV CEMIP levels decreased by 36% and 8.5%, respectively, in the LLC group, and by 40% and 4.6%, respectively, in the LCM group.CONCLUSIONThese findings emphasize the potential of ANGPT2 and CEMIP as biomarkers for LC progression and prognosis. To our knowledge, no previous study has evaluated the presence and quantification of ANGPT2 and CEMIP in EV cargo from lung cancer patients. To further validate their role in cancer progression, functional studies should explore the mechanistic effects of EV-associated ANGPT2 and CEMIP on angiogenesis, immune modulation, cell migration, extracellular matrix remodeling, and tumor progression in lung cancer models.

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