predictions of how different actions may affect cellular processes in cancer cells; for example, upregulation of one isoform may advantageously alter β-tubulin but also alter the expression and behaviour of neighbouring β-tubulin isoforms []. 1.5.4. The roles of isotypes in cancer β-tubulin The different expression patterns of isoforms between cancer cells and β-tubulin normal cells may reflect how they oppose normal MT function [, ]. Changes in expression patterns have been observed in early and advanced stage tumours [, ]. MT metabolic adaptions have been implicated in enhanced proliferation, drug resistance and the grade and advancement of cancer []. The β3-tubulin, β1-tubulin and isotypes have all been associated with cancer progression [, ]. β2c-tubulin is almost exclusively found in neuronal cells where it is associated with glioma in brain tumours []. It is only present at very low levels in other tissues and almost absent in neoplastic tumours and well-differentiated tumours [, ]. However its overexpression in almost all other cancer tissue types is associated with the most advanced, invasive and poorly differentiated tumours [, ]. and are linked to drug resistance [, ] and over-expression Both β3-tubulin β1-tubulin of and has been found to destabilise MT-dynamics in ovarian β3-tubulin β5-tubulin and lung cancer cells [, ] and may be implicated in opposing the effect of anti-microtubule drugs, such as paclitaxels. Both and β3-tubulin β6-tubulin overexpression are being explored as biomarkers [, ]. The expression patterns of isoforms are often different between tumour β-tubulin tissues (in vivo) and cell lines (in vitro) []. For example, ovarian, kidney, prostate,
predictions of how different actions may affect cellular processes in cancer cells; for example, upregulation of one β-tubulin isoform may advantageously alter but also alter the expression and behaviour of neighbouring β-tubulin isoforms []. 1.5.4. The roles of β-tubulin isotypes in cancer The different expression patterns of β-tubulin isoforms between cancer cells and normal cells may reflect how they oppose normal MT function [, ]. Changes in expression patterns have been observed in early and advanced stage tumours [, ]. MT metabolic adaptions have been implicated in enhanced proliferation, drug resistance and the grade and advancement of cancer []. The β3-tubulin, β1-tubulin and β2c-tubulin isotypes have all been associated with cancer progression [, ]. is almost exclusively found in neuronal cells where it is associated with glioma in brain tumours []. It is only present at very low levels in other tissues and almost absent in neoplastic tumours and well-differentiated tumours [, ]. However its overexpression in almost all other cancer tissue types is associated with the most advanced, invasive and poorly differentiated tumours [, ]. Both β3-tubulin and β1-tubulin are linked to drug resistance [, ] and over-expression of β3-tubulin and β5-tubulin has been found to destabilise MT-dynamics in ovarian and lung cancer cells [, ] and may be implicated in opposing the effect of anti-microtubule drugs, such as paclitaxels. Both β3-tubulin and β6-tubulin overexpression are being explored as biomarkers [, ]. The expression patterns of β-tubulin isoforms are often different between tumour tissues (in vivo) and cell lines (in vitro) []. For example, ovarian, kidney, prostate,