Novel role of forkhead box O 4 transcription factor in cancer: Bringing out the good or the bad

2018 ◽  
Vol 50 ◽  
pp. 1-12 ◽  
Author(s):  
Shuai Jiang ◽  
Zhi Yang ◽  
Shouyin Di ◽  
Wei Hu ◽  
Zhiqiang Ma ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Forkhead Box

473 Role of the transcription factor forkhead box p3 in breast cancer and metastasis

2010 ◽  
Vol 8 (5) ◽  
pp. 121
Author(s):  
V. Uva ◽  
L. Sfondrini ◽  
T. Triulzi ◽  
P. Casalini ◽  
R. Orlandi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Forkhead Box P3 ◽  
Forkhead Box

scholarly journals The Role of Forkhead Box Protein M1 in Breast Cancer Progression and Resistance to Therapy

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Raya Saba ◽  
Alhareth Alsayed ◽  
James P. Zacny ◽  
Arkadiusz Z. Dudek
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Regulatory Pathways ◽  
Forkhead Box ◽  
Epidermal Growth

The Forkhead box M1 (FOXM1) is a transcription factor that has been implicated in normal cell growth and proliferation through control of cell cycle transition and mitotic spindle. It is implicated in carcinogenesis of various malignancies where it is activated by either amplification, increased stability, enhanced transcription, dysfunction of regulatory pathways, or activation of PI3K/AKT, epidermal growth factor receptor, Raf/MEK/MAPK, and Hedgehog pathways. This review describes the role of FOXM1 in breast cancer. This includes how FOXM1 impacts on different subtypes of breast cancer, that is, luminal/estrogen receptor positive (ER+), expressing human epidermal growth factor receptor 2 (HER2), basal-like breast cancer (BBC), and triple negative breast cancer (TNBC). The review also describes different tested preclinical therapeutic strategies targeting FOXM1. Developing clinically applicable therapies that specifically inhibit FOXM1 activity is a logical next step in biomarker-driven approaches against breast cancer but will not be without its challenges due to the unique properties of this transcription factor.

scholarly journals FOXL2: a central transcription factor of the ovary

2013 ◽  
Vol 52 (1) ◽  
pp. R17-R33 ◽  
Author(s):  
Adrien Georges ◽  
Aurelie Auguste ◽  
Laurianne Bessière ◽  
Anne Vanet ◽  
Anne-Laure Todeschini ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Forkhead Transcription Factor ◽  
Gene Encoding ◽  
Post Translational Modifications ◽  
Forkhead Box ◽  
Molecular Aspects ◽  
And Function ◽  
Craniofacial Defects ◽  
The Impact

Forkhead box L2 (FOXL2) is a gene encoding a forkhead transcription factor preferentially expressed in the ovary, the eyelids and the pituitary gland. Its germline mutations are responsible for the blepharophimosis ptosis epicanthus inversus syndrome, which includes eyelid and mild craniofacial defects associated with primary ovarian insufficiency. Recent studies have shown the involvement of FOXL2 in virtually all stages of ovarian development and function, as well as in granulosa cell (GC)-related pathologies. A central role of FOXL2 is the lifetime maintenance of GC identity through the repression of testis-specific genes. Recently, a highly recurrent somatic FOXL2 mutation leading to the p.C134W subtitution has been linked to the development of GC tumours in the adult, which account for up to 5% of ovarian malignancies. In this review, we summarise data on FOXL2 modulators, targets, partners and post-translational modifications. Despite the progresses made thus far, a better understanding of the impact of FOXL2 mutations and of the molecular aspects of its function is required to rationalise its implication in various pathophysiological processes.

scholarly journals An Essential Role of the Forkhead-Box Transcription Factor Foxo1 in Control of T Cell Homeostasis and Tolerance

Immunity ◽  
2009 ◽  
Vol 30 (3) ◽  
pp. 358-371 ◽  
Author(s):  
Weiming Ouyang ◽  
Omar Beckett ◽  
Richard A. Flavell ◽  
Ming O. Li
Keyword(s):  
Transcription Factor ◽  
T Cell ◽  
Essential Role ◽  
T Cell Homeostasis ◽  
Cell Homeostasis ◽  
Forkhead Box

scholarly journals Role of the transcription factor forkhead box P3 in breast cancer and metastasis

2013 ◽  
Vol 4 ◽  
Author(s):  
Sfondrini Lucia ◽  
Cataldo Alessandra ◽  
Uva Valentina ◽  
Triulzi Tiziana ◽  
Casalini Patrizia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Forkhead Box P3 ◽  
Forkhead Box

scholarly journals Role of IGF-I and the TNFα/NF-κB pathway in the induction of muscle atrogenes by acute inflammation

2012 ◽  
Vol 303 (6) ◽  
pp. E729-E739 ◽  
Author(s):  
O. Schakman ◽  
M. Dehoux ◽  
S. Bouchuari ◽  
S. Delaere ◽  
P. Lause ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factor ◽  
Acute Inflammation ◽  
Ru 486 ◽  
Forkhead Box ◽  
Igf I ◽  
Ubiquitin Proteasome ◽  
Circulating Levels ◽  
Muscular Activation

Several catabolic states (sepsis, cancer, etc.) associated with acute inflammation are characterized by a loss of skeletal muscle due to accelerated proteolysis. The main proteolytic systems involved are the autophagy and the ubiquitin-proteasome (UPS) pathways. Among the signaling pathways that could mediate proteolysis induced by acute inflammation, the transcription factor NF-κB, induced by TNFα, and the transcription factor forkhead box O (FOXO), induced by glucocorticoids (GC) and inhibited by IGF-I, are likely to play a key role. The aim of this study was to identify the nature of the molecular mediators responsible for the induction of these muscle proteolytic systems in response to acute inflammation caused by LPS injection. LPS injection robustly stimulated the expression of several components of the autophagy and the UPS pathways in the skeletal muscle. This induction was associated with a rapid increase of circulating levels of TNFα together with a muscular activation of NF-κB followed by a decrease in circulating and muscle levels of IGF-I. Neither restoration of circulating IGF-I nor restoration of muscle IGF-I levels prevented the activation of autophagy and UPS genes by LPS. The inhibition of TNFα production and muscle NF-κB activation, respectively by using pentoxifilline and a repressor of NF-κB, did not prevent the activation of autophagy and UPS genes by LPS. Finally, inhibition of GC action with RU-486 blunted completely the activation of these atrogenes by LPS. In conclusion, we show that increased GC production plays a more crucial role than decreased IGF-I and increased TNFα/NF-κB pathway for the induction of the proteolytic systems caused by acute inflammation.

scholarly journals SP1 governs primordial folliculogenesis by regulating pregranulosa cell development in mice

2019 ◽  
Vol 12 (3) ◽  
pp. 230-244 ◽  
Author(s):  
Han Cai ◽  
Bingying Liu ◽  
Huarong Wang ◽  
Guanghong Sun ◽  
Lizhao Feng ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Molecular Level ◽  
Critical Role ◽  
Somatic Cells ◽  
Primordial Follicle ◽  
Cell Development ◽  
Reporter Mouse ◽  
Forkhead Box

Abstract Establishment of the primordial follicle (PF) pool is pivotal for the female reproductive lifespan; however, the mechanism of primordial folliculogenesis is poorly understood. Here, the transcription factor SP1 was shown to be essential for PF formation in mice. Our results showed that SP1 is present in both oocytes and somatic cells during PF formation in the ovary. Knockdown of Sp1 expression, especially in pregranulosa cells, significantly suppressed nest breakdown, oocyte apoptosis, and PF formation, suggesting that SP1 expressed by somatic cells functions in the process of primordial folliculogenesis. We further demonstrated that SP1 governs the recruitment and maintenance of Forkhead box L2-positive (FOXL2+) pregranulosa cells using an Lgr5-EGFP-IRES-CreERT2 (Lgr5-KI) reporter mouse model and a FOXL2+ cell-specific knockdown model. At the molecular level, SP1 functioned mainly through manipulation of NOTCH2 expression by binding directly to the promoter of the Notch2 gene. Finally, consistent with the critical role of granulosa cells in follicle survival in vitro, massive loss of oocytes in Sp1 knockdown ovaries was evidenced before puberty after the ovaries were transplanted under the renal capsules. Conclusively, our results reveal that SP1 controls the establishment of the ovarian reserve by regulating pregranulosa cell development in the mammalian ovary.

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