scholarly journals Immunocytochemical study of collagen in epidermal growth factor (EGF)-treated osteoblastic cells.

1984 ◽  
Vol 32 (11) ◽  
pp. 1231-1233 ◽  
Author(s):  
Y Osaki ◽  
M Tsunoi ◽  
Y Hakeda ◽  
K Kurisu ◽  
M Kumegawa
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Type I Collagen ◽  
Osteoblastic Cells ◽  
Type Iii Collagen ◽  
Type I ◽  
Immunocytochemical Study ◽  
Type Iii ◽  
Epidermal Growth ◽  
And Control

The alteration of collagen components in clone MC3T3-E1 cells by epidermal growth factor (EGF) was investigated immunocytochemically, using antibodies to type I and type III collagens. EGF transformed those cells that had become more slender than those of control cultures. Type I and type III collagens were observed in the same cells in both EGF-treated and control cultures. Type I collagen was decreased by EGF, whereas type III collagen appeared to be increased. However, no cells with only type III collagen were observed, suggesting that EGF influences collagen metabolism in clone MC3T3-E1 cells.

Selective Inhibition of Type I Collagen Synthesis in Osteoblastic Cells by Epidermal Growth Factor*

Endocrinology ◽  
1984 ◽  
Vol 115 (3) ◽  
pp. 867-876 ◽  
Author(s):  
RYU-ICHIRO HATA ◽  
HISAE HORI ◽  
YUTAKA NAGAI ◽  
SHIGEYASU TANAKA ◽  
MAYURI KONDO ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Collagen Synthesis ◽  
Type I Collagen ◽  
Selective Inhibition ◽  
Osteoblastic Cells ◽  
Type I ◽  
Epidermal Growth

scholarly journals Regulation of Tenascin-C, a Vascular Smooth Muscle Cell Survival Factor that Interacts with the αvβ3 Integrin to Promote Epidermal Growth Factor Receptor Phosphorylation and Growth

1997 ◽  
Vol 139 (1) ◽  
pp. 279-293 ◽  
Author(s):  
Peter Lloyd Jones ◽  
Julie Crack ◽  
Marlene Rabinovitch
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Survival ◽  
Type I Collagen ◽  
Type I ◽  
Tenascin C ◽  
Epidermal Growth ◽  
Β3 Integrin ◽  
Dependent Growth

Tenascin-C (TN-C) is induced in pulmonary vascular disease, where it colocalizes with proliferating smooth muscle cells (SMCs) and epidermal growth factor (EGF). Furthermore, cultured SMCs require TN-C for EGF-dependent growth on type I collagen. In this study, we explore the regulation and function of TN-C in SMCs. We show that a matix metalloproteinase (MMP) inhibitor (GM6001) suppresses SMC TN-C expression on native collagen, whereas denatured collagen promotes TN-C expression in a β3 integrin– dependent manner, independent of MMPs. Floating type I collagen gel also suppresses SMC MMP activity and TN-C protein synthesis and induces apoptosis, in the presence of EGF. Addition of exogenous TN-C to SMCs on floating collagen, or to SMCs treated with GM6001, restores the EGF growth response and “rescues” cells from apoptosis. The mechanism by which TN-C facilitates EGF-dependent survival and growth was then investigated. We show that TN-C interactions with αvβ3 integrins modify SMC shape, and EGF- dependent growth. These features are associated with redistribution of filamentous actin to focal adhesion complexes, which colocalize with clusters of EGF-Rs, tyrosine-phosphorylated proteins, and increased activation of EGF-Rs after addition of EGF. Cross-linking SMC β3 integrins replicates the effect of TN-C on EGF-R clustering and tyrosine phosphorylation. Together, these studies represent a functional paradigm for ECM-dependent cell survival whereby MMPs upregulate TN-C by generating β3 integrin ligands in type I collagen. In turn, αvβ3 interactions with TN-C alter SMC shape and increase EGF-R clustering and EGF-dependent growth. Conversely, suppression of MMPs downregulates TN-C and induces apoptosis.

Epidermal growth factor affects the synthesis and degradation of type I collagen in cultured human dermal fibroblasts

2006 ◽  
Vol 25 (4) ◽  
pp. 202-212 ◽  
Author(s):  
Yoshihiro Mimura ◽  
Hironobu Ihn ◽  
Masatoshi Jinnin ◽  
Yoshihide Asano ◽  
Kenichi Yamane ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Type I Collagen ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Epidermal Growth ◽  
Synthesis And Degradation

Recent Advances on Epidermal Growth Factor Receptor as a Molecular Target for Breast Cancer Therapeutics

2020 ◽  
Vol 21 ◽  
Author(s):  
Swathi R. Shetty ◽  
Ragini Yeeravalli ◽  
Tanya Bera ◽  
Amitava Das
Keyword(s):  
Breast Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Tyrosine Kinase ◽  
Critical Role ◽  
Growth Factor Receptor ◽  
Type I ◽  
Egfr Inhibition ◽  
Epidermal Growth

: Epidermal growth factor receptor (EGFR), a type-I transmembrane protein with intrinsic tyrosine kinase activity is activated by peptide growth factors such as EGF, epigen, amphiregulin, etc. EGFR plays a vital role in regulating cell growth, migration, and differentiation in various tissue-specific cancers. It has been reported to be overexpressed in lung, head, and neck, colon, brain, pancreatic, and breast cancer that trigger tumor progression and drug resistance. EGFR overexpression alters the signaling pathway and induces cell division, invasion, and cell survival. Our prior studies demonstrated that EGFR inhibition modulates chemosensitivity in breast cancer stem cells thereby serving as a potential drug target for breast cancer mitigation. Tyrosine kinase inhibitors (Lapatinib, Neratinib) and monoclonal antibodies (Trastuzumab) targeting EGFR have been developed and approved by the US FDA for clinical use against breast cancer. This review highlights the critical role of EGFR in breast cancer progression and enumerates the various approaches being undertaken to inhibit aggressive breast cancers by suppressing the downstream pathways. Further, the mechanisms of action of potential molecules at various stages of drug development as well as clinically approved drugs for breast cancer treatment are illustrated.

scholarly journals Stimulation of prostaglandin E2 synthesis in cloned osteoblastic cells of mouse (MC3T3-E1) by epidermal growth factor.

1986 ◽  
Vol 261 (33) ◽  
pp. 15410-15415
Author(s):  
K Yokota ◽  
M Kusaka ◽  
T Ohshima ◽  
S Yamamoto ◽  
N Kurihara ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Prostaglandin E2 ◽  
Osteoblastic Cells ◽  
Epidermal Growth ◽  
Stimulation Of

Change in phenotype in long-term cultures of a clonal rat bone cell line: switch to the synthesis of α1 (I)-trimer collagen

1984 ◽  
Vol 62 (6) ◽  
pp. 462-469 ◽  
Author(s):  
Hardy Limeback ◽  
Kichibee Otsuka ◽  
Kam-Ling Yao ◽  
Jane E. Aubin ◽  
Jaro Sodek
Keyword(s):  
Collagen Synthesis ◽  
Type I Collagen ◽  
Bone Cell ◽  
Detectable Effect ◽  
Prostaglandin E ◽  
Intracellular Camp ◽  
Type Iii Collagen ◽  
Type I ◽  
Type Iii ◽  
Type V

A number of bone cell clones isolated from rat calvaria have been maintained in culture for more than 3 years. Several of these clones have undergone dramatic changes in phenotype. One of these clones, RGB 2.2, was observed originally to have a fibroblastic morphology in culture and to respond to parathyroid hormone (PTH), but not prostaglandin E2 (PGE2), with an increase in intracellular cAMP. Throughout several passages in early subcultures, these cells synthesized mostly type I collagen, with small amounts of type III and type V collagens. Whereas PTH had no detectable effect on collagen synthesis, PGE2 decreased the amount of total cell layer collagen, with the greatest effect on type III collagen, while increasing the proportion of type V collagen. Subsequent studies on these cells during 3 years in culture have indicated changes in their phenotype including a progressive change in morphology to a more cuboidal shape and a change in collagen synthesis, the cells producing large amounts of the "embryonic" collagen, α1(I) trimer. The reason(s) for the change in collagen expression is unknown, but may be the result of a change in which gene(s) is being expressed.

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