Towards Targeting PI3K-Dependent Regulation of Gene Expression in Brain Cancer

Mantamadiotis, Theo

doi:10.3390/cancers9060060

Cited by 24 publications

(16 citation statements)

References 89 publications

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“…As FGF10 activates both ERK1/2 and PI3K all the known transcription factors that depend on these kinases (e.g., ATF2, ELK1, FOS and FOXO, NFkB, CREB, respectively) ( Yang et al, 2013 ; Mantamadiotis, 2017 ) should play a role in FGF10-dependent responses. However, it is not the case for ERK1/2-regulated activation of c-FOS ( Taniguchi et al, 2003 ), suggesting that transcriptional regulation in response to FGF10/ERK1/2 signaling is complex and requires further investigation.…”

Section: Fgf10-dependent Regulators Of Intracellular Signalingmentioning

confidence: 99%

Regulation of FGF10 Signaling in Development and Disease

Watson

Francavilla

2018

Front. Genet.

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Fibroblast Growth Factor 10 (FGF10) is a multifunctional mesenchymal-epithelial signaling growth factor, which is essential for multi-organ development and tissue homeostasis in adults. Furthermore, FGF10 deregulation has been associated with human genetic disorders and certain forms of cancer. Upon binding to FGF receptors with heparan sulfate as co-factor, FGF10 activates several intracellular signaling cascades, resulting in cell proliferation, differentiation, and invasion. FGF10 activity is modulated not only by heparan sulfate proteoglycans in the extracellular matrix, but also by hormones and other soluble factors. Despite more than 20 years of research on FGF10 functions, context-dependent regulation of FGF10 signaling specificity remains poorly understood. Emerging modes of FGF10 signaling regulation will be described, focusing on the role of FGF10 trafficking and sub-cellular localization, heparan sulfate proteoglycans, and miRNAs. Systems biology approaches based on quantitative proteomics will be considered for globally investigating FGF10 signaling specificity. Finally, current gaps in our understanding of FGF10 functions, such as the relative contribution of receptor isoforms to signaling activation, will be discussed in the context of genetic disorders and tumorigenesis.

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Section: Fgf10-dependent Regulators Of Intracellular Signalingmentioning

confidence: 99%

Regulation of FGF10 Signaling in Development and Disease

Watson

Francavilla

2018

Front. Genet.

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“…Phosphatase and tensin homolog (PTEN) a tumor suppressor gene, has been reported to be involved in various types of cancer ( 15 , 16 ). Mutations in PTEN have been reported to be involved in the development of cancer ( 17 , 18 ). In various types of cancer the mutation frequency of PTEN is very high ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

Doxorubicin resistance induces IL6 activation in the colon cancer cell line LS180

Liao

Wang

et al. 2018

Oncol Lett

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Despite improvements in the development of drugs for the treatment of cancer, drug resistance remains a major obstacle. In colon cancer, following an initially promising response, patients develop drug resistance, which impacts the efficacy and halts the response of cancerous cells towards drugs. In the present study, a phosphatase and tensin homolog (PTEN) knockdown model of LS180 cells, doxorubicin-resistant models of LS180 cells as well as doxorubicin-resistant LS180 (PTEN) knockdown model were established. The present study demonstrated that doxorubicin resistance led to the activation of interleukin (IL)6 signalling pathway which was enhanced by knockdown of PTEN. There was also an increase in the levels of IL8 and IL2 which were further enchanced by knockdown of PTEN. Doxorubicin resistance also led to an increase in the population of cancer stem cells in LS180 and shPTEN-treated LS180 cells. Notably, doxorubicin resistance also induced epithelial to mesenchymal transition and increased the formation of mammospheres. Furthermore, the present study also reported that IL6 receptor antibody not only decreased IL6 levels but also led to a significant decreased number of cancer stem cell like population and mammosphere formation. In conclusion, in the present study it was demonstrated that doxorubicin resistance led to activation of IL6 signalling pathway which was further elevated by the knockdown of PTEN in the colon cancer cell line LS180. Thus, inhibiting the IL6 loop may provide an alternative pathway to tackle doxorubicin resistance.

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“…Conversely, mTORC2 is insensitive to rapamycin, which drives the glial cell proliferation, motility, and survival through the activation of AGC protein kinases [64][65][66]. However, it is found that overactivation of the PI3K/AKT/mTOR pathway reduces in the survival of glioblastoma patients and increases in the aggression of the tumor as it overstimulates processes responsible for cell proliferation, survival and migration in glioblastoma [67,68]. Therefore, researchers have identified PI3K, AKT, and mTOR as molecular targets for glioblastomas.…”

Section: Pi3k/akt/mtor Pathwaymentioning

confidence: 99%

Glioblastoma: Pathogenesis and Current Status of Chemotherapy and Other Novel Treatments

Rajaratnam

Islam

Yang

et al. 2020

Cancers

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Glioblastoma is one of the most common and detrimental forms of solid brain tumor, with over 10,000 new cases reported every year in the United States. Despite aggressive multimodal treatment approaches, the overall survival period is reported to be less than 15 months after diagnosis. A widely used approach for the treatment of glioblastoma is surgical removal of the tumor, followed by radiotherapy and chemotherapy. While there are several drugs available that are approved by the Food and Drug Administration (FDA), significant efforts have been made in recent years to develop new chemotherapeutic agents for the treatment of glioblastoma. This review describes the molecular targets and pathogenesis as well as the current progress in chemotherapeutic development and other novel therapies in the clinical setting for the treatment of glioblastoma.

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Towards Targeting PI3K-Dependent Regulation of Gene Expression in Brain Cancer

Cited by 24 publications

References 89 publications

Regulation of FGF10 Signaling in Development and Disease

Regulation of FGF10 Signaling in Development and Disease

Doxorubicin resistance induces IL6 activation in the colon cancer cell line LS180

Glioblastoma: Pathogenesis and Current Status of Chemotherapy and Other Novel Treatments

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