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- W3136175339 startingPage "166129" @default.
- W3136175339 abstract "Hexosamine biosynthetic (HBP) and PI3K/AKT/mTOR pathways are found to predominate the proliferation and survival of prostate cancer cells. Both these pathways have their own specific intermediates to propagate the secondary signals in down-stream cascades and besides having their own structured network, also have shared interconnecting branches. These interconnections are either competitive or co-operative in nature depending on the microenvironmental conditions. Specifically, in prostate cancer HBP and mTOR pathways increases the expression and protein level of androgen receptor in order to support cancer cell proliferation, advancement and metastasis. Pharmacological inhibition of a single pathway is therefore insufficient to stop disease progression as the cancer cells manage to alter the signalling channel. This is one of the primary reasons for the therapeutic failure in prostate cancer and emergence of chemoresistance. Inhibition of these multiple pathways at their common junctures might prove to be of benefit in men suffering from an advanced disease state. Hence, a thorough understanding of these cellular intersecting points and their significance with respect to signal transduction mechanisms might assist in the rational designing of combinations for effective management of prostate cancer. • Hexosamine biosynthetic (HBP) and PI3K/AKT/mTOR pathways modulate the proliferation and survival of prostate cancer cells. • In Prostate Cancer, these pathways influence cell proliferation, advancement and metastasis. • Targeting these pathways may be a viable therapeutic target." @default.
- W3136175339 created "2021-03-29" @default.
- W3136175339 creator A5028708552 @default.
- W3136175339 creator A5030695851 @default.
- W3136175339 creator A5053478067 @default.
- W3136175339 date "2021-07-01" @default.
- W3136175339 modified "2023-09-26" @default.
- W3136175339 title "Signalling transduction of O-GlcNAcylation and PI3K/AKT/mTOR-axis in prostate cancer" @default.
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