scholarly journals Inhibition of Osteoblast Proliferation and Migration by Exogenous and Endogenous Formaldehyde

2019 ◽  
Author(s):  
Xu Teng ◽  
Wei Huang ◽  
Hefeng Yu ◽  
Pei Wang ◽  
Weishi Li ◽  
...  
Keyword(s):  
Cell Growth ◽  
Potential Role ◽  
Expression Patterns ◽  
Cell Counting ◽  
Rna Seq ◽  
Cell Growth And Migration ◽  
Naturally Occurring ◽  
Significant Enrichment ◽  
And Migration ◽  
Proliferation And Migration

AbstractExogenous and endogenous formaldehyde (FA) plays an important role in cell growth and migration; however, its potential role in osteoblasts remains largely unclear. Cell counting kit-8 (CCK-8) and wound healing assays revealed that FA exposure at naturally occurring concentrations inhibited the proliferation and migration of mouse preosteoblast MC3T3-E1 cells. Moreover, RNA sequencing (RNA-seq) analysis revealed that FoxO1 signaling pathway components displayed distinct expression patterns upon FA exposure, reflected through significant enrichment of cell migration. In particular, FoxO1 Sirt1 and FA-induced related protein expression which were closely with cell proliferation and migration were confirmed by western blotting. The present results indicate that the FoxO1 pathway is involved in FA-induced inhibition of cell growth and migration.

scholarly journals Inhibition of osteoblast proliferation and migration by exogenous and endogenous formaldehyde

2020 ◽  
pp. 096032712097512
Author(s):  
Xu Teng ◽  
Pei Wang ◽  
Tianshu Yang ◽  
Wei Huang ◽  
Hefeng Yu ◽  
...  
Keyword(s):  
Cell Growth ◽  
Potential Role ◽  
Expression Patterns ◽  
Cell Counting ◽  
Rna Seq ◽  
Cell Growth And Migration ◽  
Naturally Occurring ◽  
Significant Enrichment ◽  
And Migration ◽  
Proliferation And Migration

Exogenous and endogenous formaldehyde (FA) both play an important role in cell growth and migration; however, their potential role in osteoblasts remains largely unclear. Cell counting kit-8 (CCK-8) and wound-healing assays revealed that FA exposure at naturally occurring concentrations inhibited the proliferation and migration of mouse preosteoblast MC3T3-E1 cells. Moreover, RNA sequencing (RNA-seq) analysis revealed that FoxO1 signaling pathway components displayed distinct expression patterns upon FA exposure, reflected through significant enrichment of cell migration. In particular, FoxO1-, Sirt1-, and FA-induced protein expression, which was closely associated with cell proliferation and migration, was confirmed by western blotting. The results obtained indicated that the FoxO1 pathway is involved in FA-induced inhibition of cell growth and migration.

scholarly journals Down-regulated Long Noncoding RNAHOXA11-ASaffects trophoblast cell proliferation and migration by regulatingRND3andHOXA7expression in preeclampsia

2018 ◽  
Author(s):  
Yetao Xu ◽  
Dan Wu ◽  
Jie Liu ◽  
Zhonghua Ma ◽  
Bingqing Hui ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Noncoding Rna ◽  
Trophoblast Cell ◽  
Rna Seq ◽  
Biological Mechanisms ◽  
Aberrant Expression ◽  
Cell Growth And Migration ◽  
And Migration ◽  
Proliferation And Migration

AbstractThe long noncoding RNAHOXA11-ASreveals abnormal expression in numerous human diseases. However, its function and biological mechanisms remain unclear in Preeclampsia (PE). In this study, we report thatHOXA11-ASwas significantly downregulated in preeclampsic placental tissues and could contribute to the occurrence and development of Preeclampsia. Silencing ofHOXA11-ASexpression could significantly suppress trophoblast cell growth and migration, whereasHOXA11-ASoverexpression facilitated cell growth in HTR-8/SVneo, JEG3 and JAR cell lines. RNA-seq analysis also indicated thatHOXA11-ASsilencing preferentially regulated numerous genes associated with cell proliferation and cell migration. Mechanistic analyses showed thatHOXA11-AScould recruit Ezh2 and Lsd1 protein, and regulateRND3mRNA expression in nucleus. In cytoplasm,HOXA11-ASmodulateHOXA7expression by sponged miR-15b-5p, thus affecting trophoblast cell proliferation. Together, these resulting data confirm that aberrant expression ofHOXA11-ASis involved in the occurrence and development of Preeclampsia, and may act as a prospective diagnosis and therapeutic target in PE.

scholarly journals The Potential Role of Cycloastragenol in Promoting Diabetic Wound Repair In Vitro

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Cao ◽  
Li Xu ◽  
Xiaohong Yang ◽  
Yuan Dong ◽  
Hongbin Luo ◽  
...  
Keyword(s):  
Wound Healing ◽  
Wound Repair ◽  
Cell Counting ◽  
Migration Ability ◽  
Cell Growth And Migration ◽  
Cell Based Therapy ◽  
And Migration ◽  
Proliferation And Migration

Background. Refractory wound healing is a severe complication of diabetes with a significant socioeconomic burden. Whereas current therapies are insufficient to accelerate repair, stem cell-based therapy is increasingly recognized as an alternative that improves healing outcomes. The aim of the present study is to explore the role of cycloastragenol (CAG), a naturally occurring compound in Astragali Radix, in ameliorating refractory cutaneous wound healing in vitro, which may provide a new insight into therapeutic strategy for diabetic wounds. Methods. Human epidermal stem cells (EpSCs) obtained from nine patients were exposed to CAG, with or without DKK1 (a Wnt signaling inhibitor). A lentiviral short hairpin RNA (shRNA) system was used to establish the telomerase reverse transcriptase (TERT) and β-catenin knockdown cell line. Cell counting kit-8, scratch wound healing, and transwell migration assay were used to determine the effects of CAG in cell growth and migration. The activation of TERT, β-catenin, and c-Myc was determined using real-time qPCR and western blot analysis. Chromatin immunoprecipitation (ChIP) was performed to evaluate the associations among CAG, TERT, and Wnt/β-catenin signals. Results. CAG not only promoted the proliferation and migration ability of EpSCs but also increased the expression levels of TERT, β-catenin, c-Myc. These effects of CAG were most pronounced at a dose of 0.3 μM. Notably, the CAG-promoted proliferative and migratory abilities of EpSCs were abrogated in TERT and β-catenin-silenced cells. In addition, the ChIP results strongly suggested that CAG-modulated TERT was closely associated with the activation of Wnt/β-catenin signaling. Conclusion. Our data indicate that CAG is a TERT activator of EpSCs and is associated with their proliferation and migration, a role it may play through the activation of Wnt/β-catenin signaling.

miR-338-5p inhibits cell growth and migration via inhibition of the METTL3/m6A/c-Myc pathway in lung cancer

2020 ◽  
Author(s):  
Hongyu Wu ◽  
Fangjuan Li ◽  
Ren Zhu
Keyword(s):  
Lung Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Lung Cancer Cells ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Cell Growth And Migration ◽  
Public Health Burden ◽  
And Migration

Abstract Lung cancer is a common type of cancer that causes a very large public health burden worldwide. Achieving a better understanding of the molecular mechanism underlying the progression of lung cancer is of benefit for the diagnosis, prognosis, and treatment of lung cancer. Here, we first identified dramatically decreased expression of miR-338-5p in lung cancer tissues and cells using quantitative polymerase chain reaction (qPCR) analysis. We then revealed that miR-338-5p inhibited the cell growth and migration of lung cancer cells using cell counting kit 8 (CCK8), EdU, and Transwell analysis. Furthermore, we demonstrated that miR-338-5p inhibited METTL3 expression by qPCR, western blot analysis, and luciferase reporter assay, while upregulation of METTL3 alleviated the role of miR-338-5p in lung cancer cells. We also showed that METTL3 promoted c-Myc expression by increasing the m6A modification of c-Myc, and overexpression of c-Myc restored the inhibition of cell growth and migration of lung cancer cells induced by METTL3 silencing. Ultimately, this research illustrated that modification of the miR-338-5p/METTL3/c-Myc pathway affected cellular progression in lung cancer cells. Collectively, our study revealed the underlying mechanism of miR-338-5p in lung cancer, providing a novel regulatory pathway in lung cancer. There is potential for this pathway to serve as a diagnostic, prognostic, and therapeutic biomarker for lung cancer.

scholarly journals Hypoxia Induced HMMR Promotes the NSCLC Progression

2021 ◽  
Author(s):  
Duan Lin can ◽  
Jiang Xiu lin ◽  
Tan Lin ◽  
Yuan Yi xiao ◽  
Wang Juan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Poor Prognosis ◽  
High Expression ◽  
Related Gene ◽  
Cell Growth And Migration ◽  
Immune Infiltration ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Hyaluronan mediated motility receptor (also known as RHAMM) is another one of few defined hyaluronan receptors, play pivotal roles in cell growth. However, the functionof HMMR in lung adenocarcinoma remain unclear.Methods: HMMR expression was analyzed emoloyed the public databases, the prognosis of HMMR was analysis by prognoscan, KMplot and GEPIA databases. The GO and KEGG pathway was analysis by the DAVID and GSEA software. The correlation between the HMMR expression was analysis by the TIMER databases, the gene and protein networks was analysis by Genemania and STRING databases, the DNA methylation was analysis by the MethSurv and UALCAN databases. The expression of HMMR was analysis by IHC and qPCR, the function of HMMR on cell proliferation and migration was examine by the cell growth curve, clone information, transwell and wound healing assay.Results: in this study, we find that HMMR was elevated in LUAD and it’s highly expression associated with the poor prognosis and lymph node metastasis. Furthermore, the expression of HMMR was induced by hypoxia in LUAD. HMMR expression level not only positively correlation with the different immune cells, but also positively correlation with the expression of immune checkpoints related gene. Finally, depletion of HMMR significantly represses the cell growth and migration of NSCLC. We also found that the HOXB7/TMPO-AS1/Let-7b-5p axis mediated high expression of HMMR in NSCLC, depletion of TMPO-AS1 and over-expression the Let-7b-5p would result in decreased the expression of HMMR in NSCLC cells, the TMPO-AS1 was positively with the HMMR and negatively related to the Let-7b-5p in NSCLC. Overall, this study emphasized the significance of HOXB7/TMPO-AS1/Let-7b-5p axis mediated high expression of HMMR in cancer progression and Immune infiltration of LUAD.Conclusions: we demonstrated HMMR was elevated in LUAD and positively relation to poor prognosis. We find the hypoxia microenvironment and DNA hypomethylation able to up-regulation of the HMMR expression. Additionally, HMMR expression was positive with the diverse immune cell and immune regulator related gene in LUAD. Finally, we found that depletion of HMMR was inhibits the cell proliferation and migration ability of NSCLC cells. These findings suggest that HMMR could be served as a biomarker for prognosis and immune infiltration in LUAD.

scholarly journals Long Noncoding RNA GATA3-AS1 Promotes Cell Proliferation and Metastasis in Hepatocellular Carcinoma by Suppression of PTEN, CDKN1A, and TP53

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Xuee Luo ◽  
Ning Zhou ◽  
Le Wang ◽  
Qinghua Zeng ◽  
Hongying Tang
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Counting ◽  
Cell Growth And Migration ◽  
Expression Levels ◽  
Normal Tissues ◽  
Proliferation And Metastasis ◽  
And Migration ◽  
Cell Proliferation And Metastasis

Background. Long noncoding RNAs (lncRNAs) have been known to play important roles in the progression of various types of human cancer. LncRNA GATA3 antisense RNA 1, GATA3-AS1, has been reported to be associated with T-cell development and differentiation. However, the expression pattern and function of GATA3-AS1 in hepatocellular carcinoma (HCC) remain unknown. Methods. Real-time quantitative PCR (RT-qPCR) assay was conducted to detect GATA3-AS1 expression levels in 80 cases of pairs HCC tissues and matched normal tissues. Chi-squared (χ2) test was used to analyze the correlation between GATA3-AS1 expression and clinicopathologic variables. Survival curves were plotted using the Kaplan–Meier method and were compared via the log-rank test. The cell counting kit-8 (CCK-8) and wound scratch assays were applied to detect the effect of GATA3-AS1 knockdown and overexpression on cell growth and migration of HCC. RT-qPCR was performed for the detection of the phosphatase and tensin homolog (PTEN), cyclin-dependent kinase inhibitor 1A (CDKN1A), and tumor protein p53 (TP53) expression in HCC cells after GATA3-AS1 knockdown and overexpression. Results. GATA3-AS1 was significantly upregulated in HCC tissues compared with matched normal tissues. The high expression of GATA3-AS1 was significantly correlated with larger tumor size, advanced TNM stage, and more lymph node metastasis. High GATA3-AS1 expression was markedly correlated with shorter overall survival times of HCC patients. Furthermore, knockdown of GATA3-AS1 obviously inhibited Hep3B and HCCLM3 cell growth and migration, whereas overexpression of GATA3-AS1 had the opposite effects. In addition, GATA3-AS1 knockdown resulted in upregulated expression levels of tumor-suppressive genes, PTEN, CDKN1A, and TP53, in Hep3B and HCCLM3 cells, while restoration of GATA3-AS1 decreased PTEN, CDKN1A, and TP53 expression levels. Conclusion. Our data suggested that GATA3-AS1 promotes cell proliferation and metastasis of HCC by suppression of PTEN, CDKN1A, and TP53.

scholarly journals Hypoxia-induced HMMR Promotes Cell Proliferation, Migration and Immune Infiltrates in Lung Adenocarcinoma

2021 ◽  
Author(s):  
Duan Lin can ◽  
Jiang Xiu lin ◽  
Tan Lin ◽  
Yuan Yi xiao ◽  
Wang Juan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Related Gene ◽  
Cell Growth And Migration ◽  
Immune Infiltration ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract BackgroundHyaluronan mediated motility receptor (also known as RHAMM) is another one of few defined hyaluronan receptors, play pivotal roles in cell growth. However, the relationships between HMMR and prognosis and tumor-infiltrating lymphocytes in lung adenocarcinoma remain unclear.MethodsHMMR expression was analyzed emoloyed the TIMER, GEPIA, UALCAN, CCLE databases, the prognosis of HMMR was analysis by prognoscan, KMplot and GEPIA databases. The GO and KEGG pathway was analysis by the DAVID and GSEA software. The correlation between the HMMR expression was analysis by the TIMER databases, the gene and protein networks was analysis by Genemania and STRING databases, the DNA methylation was analysis by the MethSurv and UALCAN databases, the gene mutation of HMMR was analysis by the cBioportal and COSMIC databases. The expression of HMMR was analysis by IHC and qPCR, the function of HMMR on cell proliferation and migration was examine by the cell growth curve, clone information, transwell and wound healing assay.ResultsIn this study, we find that HMMR was elevated in LUAD and it’s highly expression associated with the poor prognosis and lymph node metastasis. Furthermore, the expression of HMMR was induced by hypoxia in LUAD. HMMR expression level not only positively correlation with the different immune cells, but also positively correlation with the expression of immune checkpoints related gene, for instance, CD279, CD274, CTLA4, LAG3, PDCD1LG2, TIGIT and HAVCR2. Finally, depletion of HMMR significantly represses the cell growth and migration of NSCLC. Overall, this study emphasized the significance of HMMR in cancer progression and Immune infiltration of LUAD.ConclusionsWe demonstrated HMMR was elevated in LUAD and positively relation to poor prognosis. We find the hypoxia microenvironment and DNA hypomethylation able to up-regulation of the HMMR expression. Additionally, HMMR expression was positive with the diverse immune cell and immune regulator related gene in LUAD. Finally, we found that depletion of HMMR was inhibits the cell proliferation and migration ability of NSCLC cells. These findings suggest that HMMR could be served as a biomarker for prognosis and immune infiltration in LUAD.

Knockout of Ajuba Attenuates the Growth and Migration of Hepatocellular Carcinoma Cells

2020 ◽  
Vol 160 (11-12) ◽  
pp. 650-658
Author(s):  
Yichen Le ◽  
Yi He ◽  
Meirong Bai ◽  
Ying Wang ◽  
Jiaxue Wu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Cancer Progression ◽  
Normal Liver ◽  
Cell Growth And Migration ◽  
And Migration ◽  
Hcc Cells

Ajuba has been found to be mutated or aberrantly regulated in several human cancers and plays important roles in cancer progression via different signaling pathways. However, little is known about the role of Ajuba in hepatocellular carcinoma (HCC). Here, we found an upregulation of Ajuba expression in HCC tissues compared with normal liver tissues, while a poor prognosis was observed in HCC patients with high Ajuba expression. Knockout of Ajuba in HCC cells inhibited cell growth in vitro and in vivo, suppressed cell migration, and enhanced the cell apoptosis under stress. Moreover, re-expression of Ajuba in Ajuba-deficient cells could restore the phenotype of Ajuba-deficient cells. In conclusion, these results indicate that Ajuba is upregulated in HCC and promotes cell growth and migration of HCC cells, suggesting that Ajuba could possibly be a new target for HCC diagnosis and treatment.

scholarly journals Cyclooxygenase Inhibition Alters Proliferative, Migratory, and Invasive Properties of Human Glioblastoma Cells In Vitro

2021 ◽  
Vol 22 (9) ◽  
pp. 4297
Author(s):  
Matthew Thomas Ferreira ◽  
Juliano Andreoli Miyake ◽  
Renata Nascimento Gomes ◽  
Fábio Feitoza ◽  
Pollyana Bulgarelli Stevannato ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Biology ◽  
Gelatin Zymography ◽  
Viable Cell ◽  
Cell Counting ◽  
Gelatinolytic Activity ◽  
Ep4 Receptor ◽  
And Migration ◽  
Proliferation And Migration

Prostaglandin E2 (PGE2) is known to increase glioblastoma (GBM) cell proliferation and migration while cyclooxygenase (COX) inhibition decreases proliferation and migration. The present study investigated the effects of COX inhibitors and PGE2 receptor antagonists on GBM cell biology. Cells were grown with inhibitors and dose response, viable cell counting, flow cytometry, cell migration, gene expression, Western blotting, and gelatin zymography studies were performed. The stimulatory effects of PGE2 and the inhibitory effects of ibuprofen (IBP) were confirmed in GBM cells. The EP2 and EP4 receptors were identified as important mediators of the actions of PGE2 in GBM cells. The concomitant inhibition of EP2 and EP4 caused a significant decrease in cell migration which was not reverted by exogenous PGE2. In T98G cells exogenous PGE2 increased latent MMP2 gelatinolytic activity. The inhibition of COX1 or COX2 caused significant alterations in MMP2 expression and gelatinolytic activity in GBM cells. These findings provide further evidence for the importance of PGE2 signalling through the EP2 and the EP4 receptor in the control of GBM cell biology. They also support the hypothesis that a relationship exists between COX1 and MMP2 in GBM cells which merits further investigation as a novel therapeutic target for drug development.

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