Additionally, return it to be activated form. The

Additionally,NF-kB signalling pathway also involved in the prostate cancer development.

NF-kB is an essential protein molecule to enhance the regulation of the geneexpression associated with innate and adaptive immunity and cellproliferation.  When there is no externalstimulus, NF-kB is a dimer remain inactive as they bound with IkB (inhibitor ofkappa B). Through the series of activation, IkB will be degraded which releaseNF-kB  as  free molecule and return it to be activatedform. The degradation is done through the phosphorylation on the specific serineresidues (Ser 177/181 or Ser 176/180) by IkB kinase complex (IKKa or IKKb).Now, free NF-kB dimer can integrate into the nucleus and then bind to theenhancer site in DNA, activate the gene in charge on the inflammatory response,cell growth, metastasis and apoptosis. NF-kB is always at active state causedby the elevated level of tumour necrosis factor (TNF) and this escalates theIkB degradation rate. The expression of NF-kB increases at mRNA and proteinlevel that induced by IL-6 expression. NF-kB also targets on the transcriptionregulatory element of the prostate specific antigen (PSA), a foremost markerfor prostate cancer development and progression.

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This signalling pathway isclosely related with cancer progression, chemoresistance and PSA recurrence.Soft tissue and bone metastasis is also an indication which showed frequentlyin prostate cancer that promoted by NF-kB activation. TNF-? is apro-inflammatory cytokine and acts as inducer of NF-kB with the receptors arefigured out that they are highly expressed in prostate cancer. As a consequence,TNF-? expression was intensified which then cause escalation in terms ofproliferation, angiogenesis, metastasis and resistance to chemotherapeuticdrugs.

Quite a number of studies proved that cross-talk mechanism is presentbetween NF-kB and AR signalling. For instance, p65 of NF-kB can strengthen theendogenous AR expression and its respective downstream target gene causes thegrowth of prostate cancerous cells. 



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