Expression of the SEPT9_i4 isoform confers resistance to microtubule-interacting drugs

Background The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis, apoptosis, membrane dynamics and vesicle trafficking. Septin proteins can form hetero-oligomeric complexes and interact with other proteins in...

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Published inCellular oncology (Dordrecht) Vol. 35; no. 2; pp. 85 - 93
Main Authors Chacko, Alex D., McDade, Simon S., Chanduloy, Severine, Church, Stewart W., Kennedy, Richard, Price, John, Hall, Peter A., Russell, S. E. Hilary
Format Journal Article
LanguageEnglish
Published Dordrecht Springer Netherlands 01.04.2012
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Abstract Background The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis, apoptosis, membrane dynamics and vesicle trafficking. Septin proteins can form hetero-oligomeric complexes and interact with other proteins including actin and tubulin. The human SEPT9 gene on chromosome 17q25.3 has a complex genomic architecture with 18 different transcripts that can encode 15 distinct polypeptides. Two distinct transcripts with unique 5′ ends (SEPT9_v4 and SEPT9_v4*) encode the same protein. In tumours the ratio of these transcripts changes with elevated levels of SEPT9_v4* mRNA, a transcript that is translated with enhanced efficiency leading to increased SEPT9_i4 protein. Methods We have examined the effect of over-expression of SEPT9_i4 on the dynamics of microtubule polymer mass in cultured cells. Results We show that the microtubule network in SEPT9_i4 over-expressing cells resists disruption by paclitaxel or cold incubation but also repolymerises tubulin more slowly after microtubule depolymerisation. Finally we show that SEPT9_i4 over-expressing cells have enhanced survival in the presence of clinically relevant microtubule acting drugs but not after treatment with DNAinteracting agents. Conclusions Given that SEPT9 over-expression is seen in diverse tumours and in particular ovarian and breast cancer, such data indicate that SEPT9_v4 expression may be clinically relevant and contribute to some forms of drug resistance.
AbstractList BACKGROUNDThe evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis, apoptosis, membrane dynamics and vesicle trafficking. Septin proteins can form hetero-oligomeric complexes and interact with other proteins including actin and tubulin. The human SEPT9 gene on chromosome 17q25.3 has a complex genomic architecture with 18 different transcripts that can encode 15 distinct polypeptides. Two distinct transcripts with unique 5' ends (SEPT9_v4 and SEPT9_v4*) encode the same protein. In tumours the ratio of these transcripts changes with elevated levels of SEPT9_v4* mRNA, a transcript that is translated with enhanced efficiency leading to increased SEPT9_i4 protein. METHODSWe have examined the effect of over-expression of SEPT9_i4 on the dynamics of microtubule polymer mass in cultured cells. RESULTSWe show that the microtubule network in SEPT9_i4 over-expressing cells resists disruption by paclitaxel or cold incubation but also repolymerises tubulin more slowly after microtubule depolymerisation. Finally we show that SEPT9_i4 over-expressing cells have enhanced survival in the presence of clinically relevant microtubule acting drugs but not after treatment with DNAinteracting agents. CONCLUSIONSGiven that SEPT9 over-expression is seen in diverse tumours and in particular ovarian and breast cancer, such data indicate that SEPT9_v4 expression may be clinically relevant and contribute to some forms of drug resistance.
The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis, apoptosis, membrane dynamics and vesicle trafficking. Septin proteins can form hetero-oligomeric complexes and interact with other proteins including actin and tubulin. The human SEPT9 gene on chromosome 17q25.3 has a complex genomic architecture with 18 different transcripts that can encode 15 distinct polypeptides. Two distinct transcripts with unique 5' ends (SEPT9_v4 and SEPT9_v4*) encode the same protein. In tumours the ratio of these transcripts changes with elevated levels of SEPT9_v4* mRNA, a transcript that is translated with enhanced efficiency leading to increased SEPT9_i4 protein. We have examined the effect of over-expression of SEPT9_i4 on the dynamics of microtubule polymer mass in cultured cells. We show that the microtubule network in SEPT9_i4 over-expressing cells resists disruption by paclitaxel or cold incubation but also repolymerises tubulin more slowly after microtubule depolymerisation. Finally we show that SEPT9_i4 over-expressing cells have enhanced survival in the presence of clinically relevant microtubule acting drugs but not after treatment with DNAinteracting agents. Given that SEPT9 over-expression is seen in diverse tumours and in particular ovarian and breast cancer, such data indicate that SEPT9_v4 expression may be clinically relevant and contribute to some forms of drug resistance.
Background The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis, apoptosis, membrane dynamics and vesicle trafficking. Septin proteins can form hetero-oligomeric complexes and interact with other proteins including actin and tubulin. The human SEPT9 gene on chromosome 17q25.3 has a complex genomic architecture with 18 different transcripts that can encode 15 distinct polypeptides. Two distinct transcripts with unique 5' ends (SEPT9_v4 and SEPT9_v4*) encode the same protein. In tumours the ratio of these transcripts changes with elevated levels of SEPT9_v4* mRNA, a transcript that is translated with enhanced efficiency leading to increased SEPT9_i4 protein.
Background The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis, apoptosis, membrane dynamics and vesicle trafficking. Septin proteins can form hetero-oligomeric complexes and interact with other proteins including actin and tubulin. The human SEPT9 gene on chromosome 17q25.3 has a complex genomic architecture with 18 different transcripts that can encode 15 distinct polypeptides. Two distinct transcripts with unique 5′ ends (SEPT9_v4 and SEPT9_v4*) encode the same protein. In tumours the ratio of these transcripts changes with elevated levels of SEPT9_v4* mRNA, a transcript that is translated with enhanced efficiency leading to increased SEPT9_i4 protein. Methods We have examined the effect of over-expression of SEPT9_i4 on the dynamics of microtubule polymer mass in cultured cells. Results We show that the microtubule network in SEPT9_i4 over-expressing cells resists disruption by paclitaxel or cold incubation but also repolymerises tubulin more slowly after microtubule depolymerisation. Finally we show that SEPT9_i4 over-expressing cells have enhanced survival in the presence of clinically relevant microtubule acting drugs but not after treatment with DNAinteracting agents. Conclusions Given that SEPT9 over-expression is seen in diverse tumours and in particular ovarian and breast cancer, such data indicate that SEPT9_v4 expression may be clinically relevant and contribute to some forms of drug resistance.
Author Chacko, Alex D.
Kennedy, Richard
Chanduloy, Severine
Hall, Peter A.
McDade, Simon S.
Price, John
Church, Stewart W.
Russell, S. E. Hilary
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  surname: Chacko
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  surname: McDade
  fullname: McDade, Simon S.
  organization: Centre for Cancer Research and Cell Biology, Queen’s University Belfast
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  surname: Chanduloy
  fullname: Chanduloy, Severine
  organization: Centre for Cancer Research and Cell Biology, Queen’s University Belfast
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  givenname: Stewart W.
  surname: Church
  fullname: Church, Stewart W.
  organization: Centre for Cancer Research and Cell Biology, Queen’s University Belfast
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  givenname: Richard
  surname: Kennedy
  fullname: Kennedy, Richard
  organization: Centre for Cancer Research and Cell Biology, Queen’s University Belfast
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  surname: Price
  fullname: Price, John
  organization: Department of Gynaecology, Tower Block, Belfast City Hospital
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  givenname: S. E. Hilary
  surname: Russell
  fullname: Russell, S. E. Hilary
  email: seh.russell@gmail.com
  organization: Centre for Cancer Research and Cell Biology, Queen’s University Belfast
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Keywords SEPT9
Drug resistance
Septin
Microtubules
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Snippet Background The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis,...
The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis, apoptosis,...
Background The evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis,...
BACKGROUNDThe evolutionarily conserved septin family of genes encode GTP binding proteins involved in a variety of cellular functions including cytokinesis,...
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StartPage 85
SubjectTerms Biomedical and Life Sciences
Biomedicine
Cancer Research
Cell Line, Tumor
DNA Damage
Drug Resistance, Neoplasm - drug effects
Flow Cytometry
Humans
Ice
Microtubules - drug effects
Microtubules - metabolism
Oncology
Original Paper
Paclitaxel - pharmacology
Pathology
Polymerization - drug effects
Protein Isoforms - metabolism
Septins - metabolism
Vinblastine - analogs & derivatives
Vinblastine - pharmacology
Vinorelbine
Title Expression of the SEPT9_i4 isoform confers resistance to microtubule-interacting drugs
URI https://link.springer.com/article/10.1007/s13402-011-0066-0
https://www.ncbi.nlm.nih.gov/pubmed/22278362
https://search.proquest.com/docview/1430851981
https://search.proquest.com/docview/929119782
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