Role of G protein-coupled estrogen receptor-1, matrix metalloproteinases 2 and 9, and heparin binding epidermal growth factor-like growth factor in estradiol-17β-stimulated bovine satellite cell proliferation

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.

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The Role of miR-206 in the Epidermal Growth Factor (EGF) Induced Repression of Estrogen Receptor-α (ERα) Signaling and a Luminal Phenotype in MCF-7 Breast Cancer Cells

Molecular Endocrinology ◽

10.1210/me.2009-0062 ◽

2009 ◽

Vol 23 (8) ◽

pp. 1215-1230 ◽

Cited By ~ 71

Author(s):

Brian D. Adams ◽

Danielle M. Cowee ◽

Bruce A. White

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Estrogen Receptor Α ◽

Epidermal Growth ◽

Mcf 7

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Role of membrane-anchored heparin-binding epidermal growth factor-like growth factor and CD9 on macrophages

Biochemical Journal ◽

10.1042/bj3280923 ◽

1997 ◽

Vol 328 (3) ◽

pp. 923-928 ◽

Cited By ~ 22

Author(s):

Noriyuki OUCHI ◽

Shinji KIHARA ◽

Shizuya YAMASHITA ◽

Shigeki HIGASHIYAMA ◽

Tsutomu NAKAGAWA ◽

...

Keyword(s):

Growth Factor ◽

Epidermal Growth Factor ◽

Surface Marker ◽

Heparin Binding ◽

Atherosclerotic Lesions ◽

Growth Activity ◽

Epidermal Growth ◽

Egf Family ◽

Formalin Fixed

Heparin-binding epidermal-growth-factor-like growth factor (HB-EGF) is a potent mitogen for smooth-muscle cells (SMCs) belonging to the EGF family. We have previously determined that HB-EGF is expressed in macrophages and SMCs of human atherosclerotic lesions and that its membrane-anchored precursor, proHB-EGF, also has a juxtacrine mitogenic activity which is markedly enhanced by CD9, a surface marker of lymphohaemopoietic cells. Therefore, when both proHB-EGF and CD9 are expressed on macrophages, they may strongly promote the development of atherosclerosis. In the present study we have investigated the changes in proHB-EGF and CD9 in THP-1 cells during differentiation into macrophages and by the addition of oxidized low-density lipoproteins (OxLDL) and assessed juxtacrine growth activity of THP-1 macrophages for human aortic SMCs. HB-EGF and CD9 at both the mRNA and the protein level were up-regulated after differentiation into macrophages, and further expression of HB-EGF was induced by the addition of OxLDL or lysophosphatidylcholine. Juxtacrine induction by formalin-fixed growth was suppressed to control levels by an inhibitor of HB-EGF and was partially decreased by anti-CD9 antibodies. These results suggest that co-expression of proHB-EGF and CD9 on macrophages plays an important role in the development of atherosclerosis by a juxtacrine mechanism.

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