scholarly journals Endostatin in Renal and Cardiovascular Diseases

2021 ◽  
pp. 1-14
Author(s):  
Mei Li ◽  
Zoran Popovic ◽  
Chang Chu ◽  
Bernhard K. Krämer ◽  
Berthold Hocher
Keyword(s):  
Cardiovascular Diseases ◽  
Tissue Regeneration ◽  
Endogenous Inhibitor ◽  
Physiological Processes ◽  
Current Review ◽  
Collagen Xviii ◽  
And Migration ◽  
Preclinical And Clinical Studies ◽  
The Impact ◽  
Proliferation And Migration

Endostatin, a protein derived from the cleavage of collagen XVIII by the action of proteases, is an endogenous inhibitor known for its ability to inhibit proliferation and migration of endothelial cells, angiogenesis, and tumor growth. Angiogenesis is defined as the formation of new blood vessels from pre-existing vasculature, which is crucial in many physiological processes, such as embryogenesis, tissue regeneration, and neoplasia. <b><i>Summary:</i></b> Increasing evidence shows that dysregulation of angiogenesis is crucial for the pathogenesis of renal and cardiovascular diseases. Endostatin plays a pivotal role in the regulation of angiogenesis. Recent studies have provided evidence that circulating endostatin increases significantly in patients with kidney and heart failure and may also contribute to disease progression. <b><i>Key Message:</i></b> In the current review, we summarize the latest findings on preclinical and clinical studies analyzing the impact of endostatin on renal and cardiovascular diseases.

scholarly journals Role of Anillin in Tumour: From a Prognostic Biomarker to a Novel Target

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1600
Author(s):  
Nguyen Minh Tuan ◽  
Chang Hoon Lee
Keyword(s):  
Prognostic Biomarker ◽  
Tumour Microenvironment ◽  
Vital Role ◽  
Actin Binding ◽  
Cell Proliferation And Migration ◽  
Novel Target ◽  
And Migration ◽  
The Impact ◽  
Proliferation And Migration

Anillin (ANLN), an actin-binding protein, reportedly plays a vital role in cell proliferation and migration, particularly in cytokinesis. Although there have been findings pointing to a contribution of ANLN to the development of cancer, the association of ANLN to cancer remains not fully understood. Here, we gather evidence to determine the applicability of ANLN as a prognostic tool for some types of cancer, and the impact that ANLN has on the hallmarks of cancer. We searched academic repositories including PubMed and Google Scholar to find and review studies related to cancer and ANLN. The conclusion is that ANLN could be a potent target for cancer treatment, but the roles ANLN, other than in cytokinesis and its influence on tumour microenvironment remodeling in cancer development, must be further elucidated, and specific ANLN inhibitors should be found.

scholarly journals Actin Beta-Like 2 as a New Mediator of Proliferation and Migration in Epithelial Ovarian Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Nicole Elisabeth Topalov ◽  
Doris Mayr ◽  
Clemens Scherer ◽  
Anca Chelariu-Raicu ◽  
Susanne Beyer ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Regulatory Element ◽  
Prognostic Impact ◽  
Activated T Cells ◽  
And Migration ◽  
Sirna Knockdown ◽  
The Impact ◽  
Proliferation And Migration

The impact of Actin beta-like 2 (ACTBL2), a novel described actin isoform, on epithelial ovarian cancer (EOC) biology has not been investigated so far. In this study, we analyzed the prognostic and functional significance of ACTBL2 and its regulatory element Nuclear factor of activated T-cells 5 (NFAT5). The expression of ACTBL2 and NFAT5 was examined in tissue microarrays of 156 ovarian cancer patients by immunohistochemistry. Aiming to assess the molecular impact of ACTBL2 on cellular characteristics, functional assays were executed in vitro upon siRNA knockdown of ACTBL2 and NFAT5. ACTBL2 expression was identified as an independent negative prognostic factor for overall survival of EOC patients. EOC cell lines showed a significantly increased mRNA and protein level of ACTBL2 compared to the benign control. In vitro analyses upon siRNA knockdown of ACTBL2 displayed a significantly reduced cellular viability, proliferation and migration. siRNA knockdown of NFAT5 proved a significant molecular interplay by inducing a downregulation of ACTBL2 with a thus resulting concordant alteration in cellular functions, predominantly reflected in a decreased migratory potential of EOC cells. Our results provide significant evidence on the negative prognostic impact of ACTBL2 in EOC, suggesting its crucial importance in ovarian carcinogenesis by modulating cellular motility and proliferation.

scholarly journals Injectable Human Hair Keratin–Fibrinogen Hydrogels for Engineering 3D Microenvironments to Accelerate Oral Tissue Regeneration

2021 ◽  
Vol 22 (24) ◽  
pp. 13269
Author(s):  
Hyeon Jeong Kang ◽  
Nare Ko ◽  
Seung Jun Oh ◽  
Seong Yeong An ◽  
Yu-Shik Hwang ◽  
...  
Keyword(s):  
Tissue Regeneration ◽  
Traumatic Injury ◽  
Cell Interaction ◽  
The Novel ◽  
Simple Formulation ◽  
Hair Keratin ◽  
Oral Tissue ◽  
And Migration ◽  
Uncontrolled Bleeding ◽  
Proliferation And Migration

Traumatic injury of the oral cavity is atypical and often accompanied by uncontrolled bleeding and inflammation. Injectable hydrogels have been considered to be promising candidates for the treatment of oral injuries because of their simple formulation, minimally invasive application technique, and site-specific delivery. Fibrinogen-based hydrogels have been widely explored as effective materials for wound healing in tissue engineering due to their uniqueness. Recently, an injectable foam has taken the spotlight. However, the fibrin component of this biomaterial is relatively stiff. To address these challenges, we created keratin-conjugated fibrinogen (KRT-FIB). This study aimed to develop a novel keratin biomaterial and assess cell–biomaterial interactions. Consequently, a novel injectable KRT-FIB hydrogel was optimized through rheological measurements, and its injection performance, swelling behavior, and surface morphology were investigated. We observed an excellent cell viability, proliferation, and migration/cell–cell interaction, indicating that the novel KRT-FIB-injectable hydrogel is a promising platform for oral tissue regeneration with a high clinical applicability.

scholarly journals A study of the impact of inhibitors of DNA binding‐1 on proliferation and migration in human colon carcinoma cells

2019 ◽  
Vol 35 (4) ◽  
pp. 209-213 ◽  
Author(s):  
Xue‐Liang Wu ◽  
Li‐Kun Wang ◽  
Jun Xue ◽  
Yong‐Jun Dai ◽  
Dong‐Dong Yang ◽  
...  
Keyword(s):  
Dna Binding ◽  
Colon Carcinoma ◽  
Human Colon ◽  
Carcinoma Cells ◽  
Colon Carcinoma Cells ◽  
Human Colon Carcinoma ◽  
And Migration ◽  
The Impact ◽  
Proliferation And Migration

scholarly journals MicroRNA-488 inhibits proliferation and motility of tumor cells via downregulating FSCN1, modulated by Notch3 in breast carcinomas

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Yang Wu ◽  
Ming-Heng Yuan ◽  
Hua-Tao Wu ◽  
Wen-Jia Chen ◽  
Man-Li Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Malignant Tumors ◽  
Luciferase Assay ◽  
Breast Cancers ◽  
Breast Carcinomas ◽  
Translation Process ◽  
Physiological Processes ◽  
And Migration ◽  
Proliferation And Migration

Abstract As important modulators in multiple physiological processes, microRNAs (miRNAs) have been reported in various malignant tumors, including breast cancer. The current study investigated the function of a new tumor suppressor microRNA, miR-488, and its molecular mechanism of metastasis in breast cancers. CCK8 and transwell assays revealed that the upregulated miR-488 level significantly inhibited the proliferation and migration of breast cancer cells. As a potential downstream gene, the mRNA and protein level of FSCN1 was suppressed by increased miR-488 and vice versa. Luciferase assay showed that miR-488 directly bind to the 3′UTR of FSCN1 and suppressed the translation process of FSCN1. The promoter region of miR-488 was directly bound by Notch3 and promoted the expression of miR-488 transcriptionally. Immunohistochemistry results revealed that in patients with breast cancer, the expression of Notch3 and were negatively correlated with the FSCN1 levels significantly. Therefore, the current finding predicted miR-488 as a tumor suppressor molecule in breast cancer, and demonstrated that Notch3/miR-488/FSCN1 axis is established and involved in regulating the metastasis of breast cancers, providing novel therapeutic targets for patients with breast cancers.

scholarly journals LINC00470 accelerates the proliferation and metastasis of melanoma through promoting APEX1 expression

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Ting Huang ◽  
Yong-Jie Wang ◽  
Mi-Tao Huang ◽  
Yu Guo ◽  
Li-Chang Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Underlying Mechanism ◽  
Melanoma Cells ◽  
Normal Tissues ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Functional Investigation ◽  
The Impact ◽  
Proliferation And Migration

AbstractRecently studies found that APEX1 was abnormally expressed in melanoma, indicating that it might be involved in the development of melanoma. However, the underlying mechanism and the interaction between APEX1 and LINC00470 in melanoma are not clear. Therefore, we aimed to investigate the role of LINC00470 in the development of melanoma in this work. We discovered that LINC00470 was overexpressed in melanoma tissues and cells compared with the adjacent normal tissues and cells by qPCR. The overexpression of LINC00470 promoted the proliferation and migration of melanoma cells. The functional investigation demonstrated that LINC00470 activated the transcription factor, ZNF131, to regulate the APEX1 expression, which finally promoted cell proliferation and migration. In contrast, knockdown of LINC00470 could significantly inhibit the melanoma cell proliferation and migration, and suppress the growth of tumor in vivo. Overexpression of APEX1 could reverse the impact of the silence of LINC00470 in melanoma cells. In summary, our studies revealed that LINC00470 promoted melanoma proliferation and migration by enhancing the expression of APEX1, which indicated that LINC00470 might be a therapeutic target for the treatment of melanoma.

scholarly journals Atheroprotective Effects and Molecular Mechanism of Berberine

2021 ◽  
Vol 8 ◽  
Author(s):  
Lu Xing ◽  
Xin Zhou ◽  
Ai-Hong Li ◽  
Hui-Jin Li ◽  
Chun-Xia He ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Cardiovascular Diseases ◽  
Gut Microbiota ◽  
Molecular Mechanism ◽  
Foam Cell ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
Beneficial Effects ◽  
And Migration ◽  
Proliferation And Migration

Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide. Atherosclerosis is the main pathological basis of cardiovascular diseases and it is closely associated with hyperlipidemia, endothelial injury, macrophage-derived foam cells formation, proliferation and migration of vascular smooth muscle cells (VSMCs), platelet aggregation, and altered gut microbiota. Various symptomatic treatments, that are currently used to inhibit atherosclerosis, need to be administered in long term and their adverse effects cannot be ignored. Berberine (BBR) has beneficial effects on atherosclerosis through regulating multiple aspects of its progression. This review highlights the recent advances in understanding the anti-atherosclerosis mechanism of BBR. BBR alleviated atherosclerosis by attenuation of dyslipidemia, correction of endothelial dysfunction, inhibition of macrophage inflammation and foam cell formation, activation of macrophage autophagy, regulation of the proliferation and migration of VSMCs, attenuation of platelet aggregation, and modulation of gut microbiota. This review would provide a modern scientific perspective to further understanding the molecular mechanism of BBR attenuating atherosclerosis and supply new ideas for atherosclerosis management.

scholarly journals Astrogliosis Releases Pro-Oncogenic Chitinase 3-Like 1 Causing MAPK Signaling in Glioblastoma

Cancers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1437 ◽  
Author(s):  
Julian Wurm ◽  
Simon P. Behringer ◽  
Vidhya M. Ravi ◽  
Kevin Joseph ◽  
Nicolas Neidert ◽  
...  
Keyword(s):  
Mapk Signaling ◽  
Reactive Astrocytes ◽  
Mesenchymal Phenotype ◽  
Cellular Environment ◽  
Culture Model ◽  
Mitogen Activated Protein ◽  
And Migration ◽  
The Impact ◽  
Proliferation And Migration

Although reactive astrocytes constitute a major component of the cellular environment in glioblastoma, their function and crosstalk to other components of the environment is still poorly understood. Gene expression analysis of purified astrocytes from both the tumor core and non-infiltrated cortex reveals a tumor-related up-regulation of Chitinase 3-like 1 (CHI3L1), a cytokine which is related to inflammation, extracellular tissue remodeling, and fibrosis. Further, we established and validated a co-culture model to investigate the impact of reactive astrocytes within the tumor microenvironment. Here we show that reactive astrocytes promote a subtype-shift of glioblastoma towards the mesenchymal phenotype, driving mitogen-activated protein kinases (MAPK) signaling as well as increased proliferation and migration. In addition, we demonstrate that MAPK signaling is directly caused by a CHI3L1-IL13RA2 co-binding, which leads to increased downstream MAPK and AKT signaling. This novel microenvironmental crosstalk highlights the crucial role of non-neoplastic cells in malignant brain tumors and opens up new perspectives for targeted therapies in glioblastoma.

scholarly journals Effects mediated by the α7 nicotinic acetylcholine receptor on cell proliferation and migration in rat adipose-derived stem cells

2020 ◽  
Vol 64 (s2) ◽  
Author(s):  
Marta Pernarella ◽  
Roberta Piovesana ◽  
Carlo Matera ◽  
Alessandro Faroni ◽  
Mario Fiore ◽  
...  
Keyword(s):  
Stem Cells ◽  
Nicotinic Receptors ◽  
Adipose Derived Stem Cells ◽  
Α7 Nicotinic Acetylcholine Receptor ◽  
Differentiation Potential ◽  
Physiological Processes ◽  
Α7 Nachr ◽  
And Migration ◽  
Proliferation And Migration

Adipose-derived stem cells (ASCs) are an attractive source for regenerative medicine as they can be easily isolated, rapidly expandable in culture and show excellent in vitro differentiation potential. Acetylcholine (ACh), one of the main neurotransmitters in central and peripheral nervous systems, plays key roles in the control of several physiological processes also in non-neural tissues. As demonstrated in our previous studies, ACh can contribute to the rat ASCs physiology, negatively modulating ASCs proliferation and migration via M2 muscarinic receptor (mAChR) activation. In the present work we show that rat ASCs also express α7 nicotinic receptors (nAChRs). In particular, we have investigated the effects mediated by the selective activation of α7 nAChRs, which causes a reduction of ASC proliferation without affecting cell survival and morphology, and significantly promotes cell migration via upregulation of the CXCR4 expression. Interestingly, the activation of the α7 nAChR also upregulates the expression of M2 mAChR protein, indicating a cooperation between muscarinic and nicotinic receptors in the inhibition of ASC proliferation.  

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