scholarly journals Sgk3 links growth factor signaling to maintenance of progenitor cells in the hair follicle

2005 ◽  
Vol 170 (4) ◽  
pp. 559-570 ◽  
Author(s):  
Laura Alonso ◽  
Hitoshi Okada ◽  
Hilda Amalia Pasolli ◽  
Andrew Wakeham ◽  
Annick Itie You-Ten ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hair Follicle ◽  
Critical Role ◽  
Growth Factor Receptor ◽  
Hair Follicles ◽  
Growth Factor Signaling ◽  
Phosphatidylinositol 3 Kinase ◽  
Life And Death ◽  
Epidermal Growth Factor Signaling ◽  
Epidermal Growth

Tyrosine kinase growth factor receptor signaling influences proliferation, survival, and apoptosis. Hair follicles undergo cycles of proliferation and apoptotic regression, offering an excellent paradigm to study how this transition is governed. Several factors are known to affect the hair cycle, but it remains a mystery whether Akt kinases that are downstream of growth factor signaling impact this equilibrium. We now show that an Akt relative, Sgk (serum and glucocorticoid responsive kinase) 3, plays a critical role in this process. Hair follicles of mice lacking Sgk3 fail to mature normally. Proliferation is reduced, apoptosis is increased, and follicles prematurely regress. Maintenance of the pool of transiently amplifying matrix cells is impaired. Intriguingly, loss of Sgk3 resembles the gain of function of epidermal growth factor signaling. Using cultured primary keratinocytes, we find that Sgk3 functions by negatively regulating phosphatidylinositol 3 kinase signaling. Our results reveal a novel and important function for Sgk3 in controlling life and death in the hair follicle.

Melatonin attenuates growth factor receptor signaling required for SARS-CoV-2 replication

2020 ◽  
Vol 3 (4) ◽  
pp. 534-537
Author(s):  
Jan Tesarik
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Published Data ◽  
Growth Factor Signaling ◽  
Melatonin Treatment ◽  
Epidermal Growth Factor Signaling ◽  
Infected Cells ◽  
Epidermal Growth ◽  
Growth Factor Receptor Signaling ◽  
Specific Agent

Melatonin has recently been suggested as a non-specific agent to prevent early (asymptomatic or moderate) infections with SARS-CoV-2 virus, the agent responsible for COVID-19, from developing to severe conditions requiring hospitalization. This recommendation was based on the ability of melatonin to suppress excessive inflammatory reactions and to modulate the immune system by attenuating the innate (blind and potentially harmful) response and potentiating the adaptive (selective and helpful) one. Recent data on the molecular mechanism of COVID-19 infection show that growth factor signaling is required for SARS-CoV-2 replication in the infected cells. When confronted with previously published data on the effects of melatonin on epidermal growth factor signaling, these data strongly suggest that melatonin can also act against the virus itself. Taken together, these data represent an additional argument in favor of using melatonin treatment as both a preventive and curative measure against COVID-19.

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.

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