Time Course of Cell Proliferation in Rat Liver in the Early Postnatal Ontogeny and Role of Epidermal Growth Factor in Organization of Proliferative Regimen

2005 ◽  
Vol 139 (5) ◽  
pp. 622-625 ◽  
Author(s):  
V. B. Zakharov ◽  
S. N. Smirnov ◽  
S. G. Mamontov ◽  
E. T. Zakharova
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Rat Liver ◽  
Time Course ◽  
Postnatal Ontogeny ◽  
Early Postnatal Ontogeny ◽  
Epidermal Growth

scholarly journals LINC00037 Inhibits Proliferation of Renal Cell Carcinoma Cells in an Epidermal Growth Factor Receptor-Dependent Way

2018 ◽  
Vol 45 (2) ◽  
pp. 523-536 ◽  
Author(s):  
Xiaohui Gong ◽  
Xianjin Du ◽  
Yong Xu ◽  
Wenze Zheng
Keyword(s):  
Cell Cycle ◽  
Renal Cell Carcinoma ◽  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Epidermal Growth

Background/Aims: LINC00037 has previously been reported to be up-regulated in clear cell renal cell carcinoma (ccRCC), however, the underlying mechanism remained unknown. In this study, we designed to investigate the functional role of LINC00037 in ccRCC Methods: LINC00037 knockdown and re-expressing 786-O and A498 cells were established. CCK8 assay and EdU assay were performed to evaluate the proliferation rates of ccRCC cells. Flow cytometry assay was performed to detect the cell apoptosis and cell cycle. Subcutaneous injection xenotransplantation mouse model was used to observe the role of LINC00037 in tumor growth in vivo. Mass spectrometry (MS) was performed to find the interacting partner of LINC00037 and RNA immunoprecipitation (RIP) was carried out to validate their interaction. Results: We found that knockdown of LINC00037 resulted in inhibited cell proliferation with activated apoptosis and cell cycle arrest in vitro. Over-expression of LINC00037 in LINC00037 knockdown cells restored and enhanced cell proliferation. In vivo mouse model indicated reduced tumor progression by LINC00037 depletion and promoted tumor progression by LINC00037 overexpression. LINC00037 could bind to epidermal growth factor receptor (EGFR) and increase the protein level of EGFR. Conclusion: LINC00037 could inhibit proliferation of ccRCC in an epidermal growth factor receptor-dependent way.

Role of heparin-binding epidermal growth factor–like growth factor as a hepatotrophic factor in rat liver regeneration after partial hepatectomy

Hepatology ◽  
1995 ◽  
Vol 22 (5) ◽  
pp. 1584-1590 ◽  
Author(s):  
Shinichi Kiso ◽  
Sumio Kawata ◽  
Shinji Tamura ◽  
Shigeki Higashiyama ◽  
Nobuyuki Ito ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Rat Liver ◽  
Heparin Binding ◽  
Rat Liver Regeneration ◽  
Epidermal Growth

scholarly journals cAMP Regulates Cell Proliferation and Cyst Formation in Autosomal Polycystic Kidney Disease Cells

2000 ◽  
Vol 11 (7) ◽  
pp. 1179-1187 ◽  
Author(s):  
KAZUSHIGE HANAOKA ◽  
WILLIAM B. GUGGINO
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Kidney Disease ◽  
Epidermal Growth Factor ◽  
Fluid Secretion ◽  
Cyst Formation ◽  
Polycystic Kidney ◽  
Epidermal Growth ◽  
Cyst Growth

Abstract. Both epithelial cell proliferation and fluid accumulation are responsible for cyst growth in autosomal dominant polycystic kidney disease (ADPKD). It was previously reported that the cystic fibrosis transmembrane conductance regulator (CFTR) is expressed in cysts from ADPKD patients and suggested that cAMP-stimulated Cl-and fluid secretion occurs through CFTR. The purpose of this study was to investigate the role of cell proliferation in cyst formation in ADPKD and to explore further the role of fluid secretion in cyst growth. Primary cultures both of ADPKD epithelial cells and a mixed population of normal renal epithelial cells isolated from the cortex (HRCE cells) were used. This study tested whether cAMP was involved both in stimulating cell proliferation and formation of cystsin vitro.3H-Thymidine incorporation assays showed that epidermal growth factor stimulated proliferation both in ADPKD cells and HRCE cells. In addition, cAMP stimulated DNA synthesis and cell proliferation in ADPKD, but not HRCE, cells. The effects of cAMP and epidermal growth factor on cell growth in ADPKD cells were additive. cAMP also stimulated cyst enlargement and fluid secretion in ADPKD cells. By contrast, cyst formation and enlargement from HRCE cells occurred without cAMP. Fluid secretion into the cyst lumen was blocked by diphenylamine carboxylic acid (DPC) and glibenclamide in ADPKD cells but blocked only by DPC in HRCE cells. This study showed that ADPKD cells have unique characteristics ; cAMP stimulates fluid secretion and cell proliferation, indicating cAMP plays a very important role in cyst growth during the course of ADPKD.

scholarly journals The activating role of phospho-(Tyr)-calmodulin on the epidermal growth factor receptor

2015 ◽  
Vol 472 (2) ◽  
pp. 195-204 ◽  
Author(s):  
Silviya R. Stateva ◽  
Valentina Salas ◽  
Alberto Benguría ◽  
Itziar Cossío ◽  
Estefanía Anguita ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Tumour Growth ◽  
Growth Factor Receptor ◽  
Epidermal Growth

The existence of a calmodulin (CaM)/phospho-(Tyr)-CaM cycle involved in the regulation of the epidermal growth factor receptor could have important consequences for the control of cell proliferation, as its alteration could potentially result in uncontrolled tumour growth.

Sign in / Sign up

Export Citation Format

Share Document