Journal
CANCER RESEARCH
Volume 75, Issue 2, Pages 415-425Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-14-2740
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Funding
- Children's Cancer Institute Australia
- Sydney Children's Hospital
- National Health and Medical Research Council [NHMRC APP1008719]
- Cancer Council New South Wales
- Cancer Institute New South Wales Career Development Fellowship
- NHMRC Senior Research Fellowships [658611, APP1058299]
- Australian Research Council Centre of Excellence in Convergent Bio-Nano Science and Technology [CE140100036]
- Cancer Institute of New South Wales infrastructure award
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beta III-tubulin (encoded by TUBB3) expression is associated with therapeutic resistance and aggressive disease in non-small cell lung cancer (NSCLC), but the basis for its pathogenic influence is not understood. Functional and differential proteomics revealed that beta III-tubulin regulates expression of proteins associated with malignant growth and metastases. In particular, the adhesion-associated tumor suppressor maspin was differentially regulated by beta III-tubulin. Functionally, beta III-tubulin suppression altered cell morphology, reduced tumor spheroid outgrowth, and increased sensitivity to anoikis. Mechanistically, the PTEN/AKT signaling axis was defined as a critical pathway regulated by beta III-tubulin in NSCLC cells. beta III-Tubulin blockage in vivo reduced tumor incidence and growth. Overall, our findings revealed how beta III-tubulin influences tumor growth in NSCLC, defining new biologic functions and mechanism of action of beta III-tubulin in tumorigenesis.
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