By Jin-Ming Yang
This quantity will aspect the present kingdom and views of autophagy-based melanoma treatment. overlaying quite a lot of themes, it is going to contain an outline of autophagy as a healing aim in melanoma, autophagy modulators as melanoma healing brokers, implications of micro-RNA-regulated autophagy in melanoma remedy, modulation of autophagy via focusing on PI3 kinase in melanoma treatment, concentrating on autophagy in melanoma stem cells, and roles of autophagy in melanoma immunotherapy. additionally, the quantity will assessment purposes of method biology and bioinformatics techniques to studying melanoma healing pursuits within the autophagy regulatory community.
The quantity could be useful for various simple and medical scientists, together with melanoma biologists, autophagy researchers, pharmacologists, and scientific oncologists who desire to delve extra deeply into this box of melanoma research.
This quantity would be the first ebook to concentration completely on autophagy as a objective in melanoma treatment. in addition, it's going to comprehensively speak about the jobs of autophagy in so much presently to be had melanoma treatments.
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Additional info for Targeting Autophagy in Cancer Therapy
1 mTOR Inhibitors mTOR (mammalian Target Of Rapamycin) senses cellular nutrient and energy levels, and negatively regulates autophagy. mTOR forms two distinct signaling complexes, mTORC1 and mTORC2. The molecular mechanism of how mTORC2 is regulated by its upstream effectors is largely unknown. mTORC1 (hereafter mTOR) is a master regulator of cellular metabolism and autophagy, regulated by the growth factor/ PI3K/AKT signaling pathway. It integrates nutrient and growth factors which signal to promote anabolic metabolism, such as protein synthesis and lipid synthesis, and to inhibit catabolic pathways, such as lysosomal biogenesis and autophagy (Laplante and Sabatini 2012).
Thymoquinone, derived from Nigella sativa seed, was reported to inhibit proliferation in glioblastoma cells. It induced lysosomal membrane permeabilization, resulting in a leakage of cathepsin B into the cytosol, which mediates caspaseindependent cell death (Racoma et al. 2013). Cathepsins are proteases distributed in almost all mammalian cells, with functions in tumor progression (Nomura and Katunuma 2005). Most of the members of cathepsins become activated at the low pH level in lysosomes. Their activities are closely linked with the lysosomal function.
It conﬁrms the role for autophagy in protecting the genome in a cellular spontaneous mechanism of tumor suppression (Mathew et al. 2007). A direct link between autophagy and tumor suppression is the discovery that Beclin 1 could function as a tumor suppressor (Liang et al. 1999). The autophagy gene Beclin 1 is mono-allelic deleted in 40–75 % of cases of human sporadic breast, ovarian, and prostate cancer. Disruption of Beclin 1 increases the frequency of spontaneous malignancies and accelerates the development of hepatitis B virusinduced premalignant lesions in a targeted mutant mouse model (Qu et al.