scholarly journals UCA1 promotes cell viability, proliferation and migration potential through UCA1/miR-204/CCND2 pathway in primary cystitis glandularis cells

2019 ◽  
Vol 114 ◽  
pp. 108872 ◽  
Author(s):  
Xu Zhou ◽  
Yu Cui ◽  
Jinbo Chen ◽  
Chao Li ◽  
Fengmin Chen ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cystitis Glandularis ◽  
Migration Potential ◽  
And Migration ◽  
Proliferation And Migration

Abstract 451: Oxygen Regulation of Human Coronary Artery Smooth Muscle Cell Proliferation and Migration

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Mingming Yang ◽  
Tomoko Kamishima ◽  
Caroline Dart ◽  
John M Quayle
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Coronary Artery ◽  
Cell Viability ◽  
Smooth Muscle Cell ◽  
Human Coronary Artery ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Introduction: Intimal thickening of blood vessels, a hallmark of several vascular diseases including atherosclerosis and a potential point of therapeutic intervention, is caused by vascular smooth muscle cell proliferation and migration. It has been suggested that oxygen availability in vessels not only regulates behavior of smooth muscle cells but also serves as a trigger that may lead to pathological responses. In this study we determined whether hypoxia elicits proliferative and migratory responses in Human Coronary Artery SMCs (HCASMCs). Methods: Proliferation of HCASMCs was assessed using a 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. SMCs were plated in 96-well plates (n=5), serum starved, and then placed under hypoxic or normoxic conditions for 2, 4 and 6 days (2D/4D/6D) before MTT was added to each well. Absorbance at the wavelength 570 nm was read on an ELISA plate reader, and percent change in cell viability was determined and normalized to control (cell viability under normoxia). Cell migration was characterized by scratch-wound assay. SMCs were seeded in 6 well plates overnight (n=3), then a ‘scratch’ on the cell monolayer was created for each well before putting into different oxygen levels for 4 hours, 12 hours and 24 hours. Images were captured at the beginning and at intervals during cell migration to close the scratch, and the degree of migration was determined by comparing the images. Results: Compared to normoxic condition, cell number changed to 118.1%±1.3% in 5% O 2 (p<0.05) and 98.2%%±1.9% in 1% O 2 after 2D; to 151.9% ±8.5% in 5% O 2 (p<0.001) and 119.4%±5.0% in 1% O 2 (p<0.05) after 4D; and to 163.0%±4.3% in 5% O 2 (p<0.001) and 120.3%±2.2% in 1% O 2 (p<0.05) after 6D. In the cell migration assay, the difference in migration rate between different groups after 4 hours was not obvious, but there was a significant difference after 12 hours (29.3%±1.3% closure in normoxia vs 39.8%±1.9% in 5% O 2 vs 40.9%±3.5% in 1% O 2 , p<0.05) and 24 hours (71.5%±4.4% in normoxia vs 87.2%±2.2% in 5% O 2 vs 87.5%±3.1% in 1% O 2 , p<0.05). Conclusion: Our studies reveal that hypoxia induces both proliferation and migration of HCASMCs.

scholarly journals Lobaplatin Inhibits Prostate Cancer Proliferation and Migration Through Regulation of BCL2 and BAX

Dose-Response ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. 155932581985098 ◽  
Author(s):  
Hongwen Cao ◽  
Yigeng Feng ◽  
Lei Chen ◽  
Chao Yu
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Cancer Proliferation ◽  
Expression Levels ◽  
And Migration ◽  
Proliferation And Migration

Lobaplatin is a diastereometric mixture of platinum (II) complexes, which contain a 1,2-bis (aminomethyl) cyclobutane stable ligand and lactic acid. Previous studies have showed that lobaplatin plays inhibiting roles in various types of tumors. However, the role of lobaplatin in prostate cancer remains unknown. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Cell proliferation was detected by cell colony formation assay. Cell migration and invasion were determined by transwell migration and invasion assay. Cell apoptosis was detected by flow cytometry. The messenger RNA and protein expression levels were detected by quantitative real-time polymerase chain reaction and Western blot. Lobaplatin treatment inhibits cell viability, cell proliferation, cell migration, and invasion, while promotes cell apoptosis of prostate cancer cell lines DU145 and PC3. Meanwhile, lobaplatin treatment regulates apoptosis by downregulation of BCL2 expression and upregulation of BAX expression levels. Our study suggests lobaplatin inhibits prostate cancer proliferation and migration through regulation of BCL2 and BAX expression.

scholarly journals Restoration of miR‐330 expression suppresses lung cancer cell viability, proliferation, and migration

2020 ◽  
Vol 236 (1) ◽  
pp. 273-283
Author(s):  
Ali Mohammadi ◽  
Behzad Mansoori ◽  
Pascal H. G. Duijf ◽  
Elham Safarzadeh ◽  
Leila Tebbi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
Lung Cancer Cell ◽  
And Migration ◽  
Proliferation And Migration

LINC00265 promotes the viability, proliferation, and migration of bladder cancer cells via the miR-4677-3p/FGF6 axis

2021 ◽  
pp. 096032712110434
Author(s):  
Yunlai Zhi ◽  
Fanghu Sun ◽  
Chengkuan Cai ◽  
Haitao Li ◽  
Kunpeng Wang ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Viability ◽  
Messenger Rna ◽  
Binding Capacity ◽  
Quantitative Polymerase Chain Reaction ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Xenograft Tumor ◽  
And Migration ◽  
Proliferation And Migration

Background Bladder cancer (BCa) is a common genitourinary malignancy with higher incidence in males. Long intergenic non-protein coding RNA 265 (LINC00265) is identified as an oncogene in many malignancies, while its role in BCa development remains unknown. Purpose To explore the functions and mechanism of LINC00265 in BCa Research Design Reverse transcription quantitative polymerase chain reaction was performed to examine LINC00265 expression in BCa cells. Cell counting kit-8 assays, colony formation assays, TdT-mediated dUTP Nick-End Labeling assays, and Transwell assays were conducted to examine BCa cell viability, proliferation, apoptosis, and migration. Luciferase reporter assays and RNA immunoprecipitation assays were carried out to explore the binding capacity between miR-4677-3p and messenger RNA fibroblast growth factor 6 (FGF6) (or LINC00265). Xenograft tumor model was established to explore the role of LINC00265 in vivo. Results LINC00265 was highly expressed in BCa cells. LINC00265 knockdown inhibited xenograft tumor growth and BCa cell viability, proliferation and migration while enhancing cell apoptosis. Moreover, LINC00265 interacted with miR-4677-3p to upregulate the expression of FGF6. FGF6 overexpression reversed the suppressive effect of LINC00265 knockdown on malignant phenotypes of BCa cells. Conclusions LINC00265 promotes the viability, proliferation, and migration of BCa cells by binding with miR-4677-3p to upregulate FGF6 expression.

scholarly journals The Histone Demethylase KDM3B Promotes Osteo-/Odontogenic Differentiation, Cell Proliferation, and Migration Potential of Stem Cells from the Apical Papilla

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Chen Zhang ◽  
Xiao Han ◽  
Yuncun Liang ◽  
Huina Liu ◽  
Zhipeng Fan ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Histone Demethylase ◽  
Alp Activity ◽  
Cell Proliferation And Migration ◽  
Odontogenic Differentiation ◽  
Migration Potential ◽  
Apical Papilla ◽  
And Migration ◽  
Proliferation And Migration

Understanding the regulation mechanisms of mesenchymal stem cells (MSCs) can assist in tissue regeneration. The histone demethylase (KDM) family has a crucial role in differentiation and cell proliferation of MSCs, while the function of KDM3B in MSCs is not well understood. In this study, we used the stem cells from the apical papilla (SCAPs) to test whether KDM3B could regulate the function of MSCs. By an alkaline phosphatase (ALP) activity assay, Alizarin red staining, real-time RT-PCR, and western blot analysis, we found that KDM3B enhanced the ALP activity and mineralization of SCAPs and promoted the expression of runt-related transcription factor 2 (RUNX2), osterix (OSX), dentin sialophosphoprotein (DSPP), and osteocalcin (OCN). Additionally, the CFSE, CCK-8, and flow cytometry assays revealed that KDM3B improved cell proliferation by accelerating cell cycle transition from the G1 to S phase. Scratch and transwell migration assays displayed that KDM3B promoted the migration potential of SCAPs. Mechanically, microarray results displayed that 98 genes were upregulated, including STAT1, CCND1, and FGF5, and 48 genes were downregulated after KDM3B overexpression. Besides, we found that the Toll-like receptor and JAK-STAT signaling pathway may be involved in the regulating function of KDM3B in SCAPs. In brief, we discovered that KDM3B promoted the osteo-/odontogenic differentiation, cell proliferation, and migration potential of SCAPs and provided a novel target and theoretical basis for regenerative medicine.

scholarly journals KCNQ1OT1 promotes the proliferation and migration of psoriatic keratinocytes by regulating miR-183-3p/GAB1

2021 ◽  
Vol 49 (5) ◽  
pp. 125-130
Author(s):  
Ting Liu ◽  
Xi Duan ◽  
Jia He ◽  
Chuan Yang
Keyword(s):  
Cell Viability ◽  
Cell Model ◽  
Growth Factor Receptor ◽  
Keratinocyte Proliferation ◽  
Tnf Α ◽  
Keratinocyte Cell Line Hacat ◽  
Gated Channel ◽  
And Migration ◽  
Proliferation And Migration

Background: Differentially expressed lncRNAs have been reported to be involved in keratinocyte proliferation and migration, and participate in the development of psoriasis. Potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (KCNQ1OT1) was implicated in the pathogenesis of various diseases, including cancer, sepsis, diabetic cardiomyopathy, and atherosclerosis. The influence of KCNQ1OT1 on proliferation and migration of psoriatic keratinocytes was unfolded in this study. Methods: Human keratinocyte cell line (HaCaT) was incubated with TNF-α to establish in vitro cell model of psoriasis. Cell viability and migration were assessed by MTT and wound healing, respectively. Target miRNA of KCNQ1OT1 was identified by luciferase activity and RNA immunoprecipitation (RIP) assays. Results: KCNQ1OT1 was up-regulated in TNF-α-induced HaCaT, and knockdown of KCNQ1OT1 reduced cell viability and suppressed migration of TNF-α-induced HaCaT. KCNQ1OT1 bind to miR-183-3p and negatively regulated expression of miR-183-3p. Over-expression of GAB1 (growth factor receptor binding 2-associated binding protein 1) counteracted with the suppressive effects of KCNQ1OT1 silence on cell viability and migration of TNF-α-induced HaCaT. Conclusion: Silence of KCNQ1OT1 suppressed proliferation and migration of TNF-α-induced HaCaT through regulation of miR-183-3p/GAB1, providing potential strategy for psoriasis.

scholarly journals MANF Produced by MRL Mouse-Derived Mesenchymal Stem Cells Is Pro-regenerative and Protects From Osteoarthritis

2021 ◽  
Vol 9 ◽  
Author(s):  
Gautier Tejedor ◽  
Patricia Luz-Crawford ◽  
Audrey Barthelaix ◽  
Karine Toupet ◽  
Sébastien Roudières ◽  
...  
Keyword(s):  
Shotgun Proteomics ◽  
Key Factors ◽  
Major Step ◽  
Differentiation Potential ◽  
Scratch Wound ◽  
Migration Potential ◽  
And Migration ◽  
Interfering Rna ◽  
Mrl Mouse ◽  
Proliferation And Migration

The super healer Murphy Roths Large (MRL) mouse represents the “holy grail” of mammalian regenerative model to decipher the key mechanisms that underlies regeneration in mammals. At a time when mesenchymal stem cell (MSC)-based therapy represents the most promising approach to treat degenerative diseases such as osteoarthritis (OA), identification of key factors responsible for the regenerative potential of MSC derived from MRL mouse would be a major step forward for regenerative medicine. In the present study, we assessed and compared MSC derived from MRL (MRL MSC) and C57BL/6 (BL6 MSC) mice. First, we compare the phenotype and the differentiation potential of MRL and BL6 MSC and did not observe any difference. Then, we evaluated the proliferation and migration potential of the cells and found that while MRL MSC proliferate at a slower rate than BL6 MSC, they migrate at a significantly higher rate. This higher migration potential is mediated, in part, by MRL MSC-secreted products since MRL MSC conditioned medium that contains a complex of released factors significantly increased the migration potential of BL6 MSC. A comparative analysis of the secretome by quantitative shotgun proteomics and Western blotting revealed that MRL MSC produce and release higher levels of mesencephalic astrocyte-derived neurotrophic factor (MANF) as compared to MSC derived from BL6, BALB/c, and DBA1 mice. MANF knockdown in MRL MSC using a specific small interfering RNA (siRNA) reduced both MRL MSC migration potential in scratch wound assay and their regenerative potential in the ear punch model in BL6 mice. Finally, injection of MRL MSC silenced for MANF did not protect mice from OA development. In conclusion, our results evidence that the enhanced regenerative potential and protection from OA of MRL mice might be, in part, attributed to their MSC, an effective reservoir of MANF.

scholarly journals Evaluation of antifibrotic effect of pirfenidone on human nasal mucosal fibroblast cell culture

2018 ◽  
Vol 73 (1) ◽  
pp. 23-29
Author(s):  
E. L. At'kova ◽  
N. N. Krahoveckij ◽  
V. D. Yartsev ◽  
A. M. Subbot ◽  
A. N. Gabashvili ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Fibroblast Cell ◽  
Efficacy And Safety ◽  
Cell Toxicity ◽  
Antifibrotic Effect ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Background: One of the main reasons of failure in surgical treatment of primary acquired nasolacrimal duct obstruction is excessive postoperative scarring of the dacryostomy. Despite the variety of procedures designed to prevent this, conflicting evidence of their efficacy and safety provide incentive for further research of antifibrotic therapeutics for adjunctive use in dacryocystorhinostomy.Aims: To evaluate the antifibrotic effect of pirfenidone on human nasal mucosal fibroblast cell culture.Materials and methods: Human nasal mucosal fibroblast cell cultures were established using samples obtained from 3 consecutive patients undergoing endonasal endoscopic dacryocystorhinostomy. Cell viability following treatment with pirfenidone was evaluated using MTS-assay. Induced inhibition of cell proliferation and migration was determined using scratch wound assay.Results: In this study pirfenidone exhibited a significant dose-dependent inhibiting effect on fibroblast proliferation with insignificant cell toxicity. Cell viability following 48 hours of incubation with various pirfenidone concentrations did not drop below 80%. The recovery of the fibroblast monolayer assessed after 24 hours of incubation was 84.88 and 8.26% in the control group, at a drug concentration of 0.15 mg/ml. Cell proliferation and migration was severely inhibited in cell culture specimens treated with pirfenidone compared to controls. The difference between groups was statistically significant (p=0,001).Conclusions: In our study pirfenidone demonstrated a pronounced antifibrotic effect. It is unlikely that inhibition of proliferation and migration of human nasal mucosal fibroblasts is mediated by cell toxicity of this medication as it was evaluated as low. Nonetheless an in vitro analysis is insufficient to judge pirfenidone’s efficacy and safety in preventing cicatrix formation following dacrycystorhinostomy. 

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