scholarly journals Prolonged survival in hepatocarcinoma patients with increased regucalcin gene expression: HepG2 cell proliferation is suppressed by overexpression of regucalcin in vitro

2016 ◽  
Vol 49 (4) ◽  
pp. 1686-1694 ◽  
Author(s):  
Masayoshi Yamaguchi ◽  
Satoru Osuka ◽  
M. Neale Weitzmann ◽  
Bassel F. El-Rayes ◽  
Mamoru Shoji ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Hepg2 Cell ◽  
Prolonged Survival ◽  
Regucalcin Gene

scholarly journals Icariin promotes cell proliferation and regulates gene expression in human neural stem cells in vitro

2016 ◽  
Vol 14 (2) ◽  
pp. 1316-1322 ◽  
Author(s):  
Pan Yang ◽  
Yun-Qian Guan ◽  
Ya-Li Li ◽  
Li Zhang ◽  
Lan Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Cell Proliferation ◽  
Neural Stem Cells ◽  
Human Neural Stem Cells

scholarly journals Elevated S100A9 expression in chronic rhinosinusitis coincides with elevated MMP production and proliferation in vitro

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Marina Boruk ◽  
Christopher Railwah ◽  
Alnardo Lora ◽  
Sridesh Nath ◽  
Derek Wu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Plasma Concentrations ◽  
Nasal Tissue ◽  
Elevated Expression ◽  
Proliferation In Vitro ◽  
S100a9 Expression

Abstract Chronic rhinosinusitis (CRS) is a common condition associated with inflammation and tissue remodeling of the nose and paranasal sinuses, frequently occurring with nasal polyps and allergies. Here we investigate inflammation and the protease profile in nasal tissues and plasma from control non-CRS patients and CRS patients. Gene expression for several cytokines, proteases, and antiproteases was quantified in nasal tissue from non-CRS and CRS subjects with nasal polyps. Elevated expression of S100A9, IL1A, MMP3, MMP7, MMP11, MMP25, MMP28, and CTSK was observed in tissue from CRS subjects with nasal polyps compared to control tissue. Tissue protein analysis confirmed elevated levels of these targets compared to controls, and increased MMP3 and MMP7 observed in CRS subjects with nasal polyps compared to CRS subjects without polyps. Plasma concentrations of MMP3 and MMP7 were elevated in the CRS groups compared to controls. The nasal cell line, CCL-30, was exposed to S100A9 protein, resulting in increased MMP3, MMP7, and CTSK gene expression and elevated proliferation. Silencing MMP3 significantly reduced S100A9-mediated cell proliferation. Therefore, the elevated expression of S100A9 and MMPs are observed in CRS nasal tissue and S100A9 stimulated MMP3 responses to contribute to elevated nasal cell proliferation.

Adrenomedullin and its receptors expression in renal tumors

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 10568-10568
Author(s):  
J. Deville ◽  
S. Salas ◽  
C. Bartoli ◽  
C. Dupuis ◽  
F. Duffaud ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Collecting Duct ◽  
Significant Inhibition ◽  
Renal Tumors ◽  
Strong Positive Correlation ◽  
Proliferation Assay ◽  
Fuhrman Grade ◽  
Cell Proliferation Assay

10568 Background: Adrenomedullin (AM) is a 52 amino acid peptide that has an important role on tumor cell proliferation and neoangiogenesis through its receptors CRLR/RAMP2 and CRLR/RAMP3. AM gene expression is stimulated by Hypoxia Inductible Factor-1 (HIF- 1) and 60–80% of the human conventional renal carcinomas (cRCC) display mutations in the tumor suppressor protein von Hippel-Lindau, which leads to constitutively elevated HIF-1. Methods: Tumors and non-malignant kidney tissues were obtained from patients who underwent unilateral nephrectomy. We studied VEGFA, AM and its receptors expression by quantitative RT-PCR in 62 frozen renal tumors including: 40 cRCC; 5 cRCC metastasis; 5 chromophobe carcinomas; 5 Papillary carcinomas; 2 oncocytomas; 2 collecting duct carcinomas; 2 normal adjacent renal tissue; 1 unclassified renal tumor. AM and AM-receptors expression was studied in 42 paraffin-embedded renal tumors by immunohistochemistry using rabbit anti-AM, anti-CRLR, anti-RAMP2 and anti-RAMP3 polyclonal antibodies. Effects of these anti AM or anti AM- receptors antibodies on cell proliferation were examined in vitro on BIZ cell line (cRCC cells). Results: VEGFA, AM and AM-receptors genes were overexpressed in cRCC compared to other renal tumors (Except AM gene in chromophobe carcinoma). Their expressions were independent of classical prognostic factors (such as Fuhrman Grade and pT status). In cRCC, there was a strong positive correlation between VEGF-A gene expression and AM (r=0.7; p=0.01) and AM-receptors genes expressions (RAMP2 r=0.61; p= 0.01 and RAMP3 r=0.58; p= 0.01). Immunohistochemistry confirmed a tumor expression of CRLR, RAMP2 and AM in more than 80% cRCC. RAMP3 was expressed by inflammatory cells but not by tumoral cells. The cell proliferation assay showed a significant inhibition of BIZ cell proliferation by AM antibody or AM-receptors antibodies. Conclusion: AM and its receptor CRLR/RAMP2 are overexpressed in cRCC. In vitro cell proliferation assay results support that AM inhibition may suppress cRCC growth, independently of potential antiangiogenic effects. Further studies on animal models are needed but AM pathway may be a potential therapeutic target in cRCC. No significant financial relationships to disclose.

Effects of Phthalates on the Human Corneal Endothelial Cell Line B4G12

2012 ◽  
Vol 31 (4) ◽  
pp. 364-371 ◽  
Author(s):  
Tanja Krüger ◽  
Yi Cao ◽  
Søren K. Kjærgaard ◽  
Lisbeth E. Knudsen ◽  
Eva C. Bonefeld-Jørgensen
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Cell Line ◽  
Corneal Endothelial Cell ◽  
Industrial Chemicals ◽  
Cell Secretion ◽  
Endothelial Cell Line ◽  
Butyl Phthalate

Phthalates are industrial chemicals used in many cosmetics. We evaluated an in vitro model for eye irritancy testing using the human corneal endothelial cell line B4G12. Cell proliferation and toxicity were assessed after exposing to di- n-butyl phthalate (DBP), benzyl butyl phthalate (BBP), di-2-ethylhexyl phthalate (DEHP), diisodecyl phthalate (DIDP), di- n-octyl phthalate (DnOP), and di-isononyl phthalate (DINP). Gene expression and secretion of inflammatory cytokines were evaluated after exposure to DBP. Decreased cell proliferation was observed for the phthalates DBP, BBP, and DEHP, and cell toxicity was observed for DBP and BBP. Upon DBP exposure at nontoxic concentrations, a significant increased gene expression and cytokine cell secretion were observed for interleukin-1β (IL-1β) and IL-8, and also an increased IL-6 secretion was observed. In conclusion, the human corneal endothelial cell line B4G12 may be a potential model for inflammatory eye irritancy testing of phthalates.

scholarly journals TMEM176B Regulates AKT/mTOR Signaling and Tumor Growth in Triple-Negative Breast Cancer

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3430
Author(s):  
Chifei Kang ◽  
Ran Rostoker ◽  
Sarit Ben-Shumel ◽  
Rola Rashed ◽  
James Andrew Duty ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Signaling Pathways ◽  
Cancer Cell ◽  
And Migration ◽  
Proliferation And Migration

TMEM176B is a member of the membrane spanning 4-domains (MS4) family of transmembrane proteins, and a putative ion channel that is expressed in immune cells and certain cancers. We aimed to understand the role of TMEM176B in cancer cell signaling, gene expression, cell proliferation, and migration in vitro, as well as tumor growth in vivo. We generated breast cancer cell lines with overexpressed and silenced TMEM176B, and a therapeutic antibody targeting TMEM176B. Proliferation and migration assays were performed in vitro, and tumor growth was evaluated in vivo. We performed gene expression and Western blot analyses to identify the most differentially regulated genes and signaling pathways in cells with TMEM176B overexpression and silencing. Silencing TMEM176B or inhibiting it with a therapeutic antibody impaired cell proliferation, while overexpression increased proliferation in vitro. Syngeneic and xenograft tumor studies revealed the attenuated growth of tumors with TMEM176B gene silencing compared with controls. We found that the AKT/mTOR signaling pathway was activated or repressed in cells overexpressing or silenced for TMEM176B, respectively. Overall, our results suggest that TMEM176B expression in breast cancer cells regulates key signaling pathways and genes that contribute to cancer cell growth and progression, and is a potential target for therapeutic antibodies.

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