scholarly journals Epidermal growth factor receptor kinase activity is required for gap junction closure and for part of the decrease in ovarian follicle cGMP in response to LH

Reproduction ◽  
2010 ◽  
Vol 140 (5) ◽  
pp. 655-662 ◽  
Author(s):  
Rachael P Norris ◽  
Marina Freudzon ◽  
Viacheslav O Nikolaev ◽  
Laurinda A Jaffe

The meiotic cell cycle in mouse oocytes is arrested in prophase, and then restarted when LH acts on the surrounding granulosa cells. The granulosa cells keep meiosis arrested by providing a source of cGMP that diffuses into the oocyte through gap junctions, and LH restarts the cell cycle by closing the junctions and by decreasing granulosa cell cGMP, thus lowering oocyte cGMP. Epidermal growth factor receptor (EGFR) activation is an essential step in triggering LH-induced meiotic resumption, but its relationship to the cGMP decrease in the follicle is incompletely understood, and its possible function in causing gap junction closure has not been investigated. Here, we use EGFR agonists (epiregulin and amphiregulin) and an EGFR kinase inhibitor (AG1478) to study the function of the EGFR in the signaling pathways leading to the release of oocytes from prophase arrest. Our results indicate that the EGFR kinase contributes to LH-induced meiotic resumption in two different ways. First, it is required for gap junction closure. Second, it is required for an essential component of the decrease in follicle cGMP. Our data show that the EGFR kinase-dependent component of the cGMP decrease is required for LH-induced meiotic resumption, but they also indicate that an as yet unidentified pathway accounts for a large part of the cGMP decrease.

RSC Advances ◽  
2016 ◽  
Vol 6 (81) ◽  
pp. 77717-77734 ◽  
Author(s):  
Monika Chauhan ◽  
Gaurav Joshi ◽  
Harveen Kler ◽  
Archana Kashyap ◽  
Suyog M. Amrutkar ◽  
...  

Based on the quinazoline bearing EGFR inhibitors, a series of thirty four compounds having a quinoline scaffold were synthesized and evaluated in vitro for EGFR kinase inhibitory and anticancer activities.


2018 ◽  
Vol 54 (54) ◽  
pp. 7479-7482 ◽  
Author(s):  
Mu Yang ◽  
Hanzhi Wu ◽  
Julie Chu ◽  
Lucas A. Gabriel ◽  
Y. Kim ◽  
...  

Platinum-modified tyrosine kinase inhibitors show strong and selective EGFR kinase binding and form adducts with a pharmacologically relevant cysteine residue.


2018 ◽  
Vol 45 (2) ◽  
pp. 523-536 ◽  
Author(s):  
Xiaohui Gong ◽  
Xianjin Du ◽  
Yong Xu ◽  
Wenze Zheng

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.


2009 ◽  
Vol 4 (4) ◽  
pp. 559 ◽  
Author(s):  
Vamsidhar Velcheti ◽  
Yumi Kasai ◽  
Avinash K. Viswanathan ◽  
Jon Ritter ◽  
Ramaswamy Govindan

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