Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer

C Gamell; T Gulati; B Solomon; S Haupt; Y Haupt

doi:10.1080/23723556.2017.1299273

Uncovering a novel pathway for p16 silencing: Therapeutic implications for lung cancer

Mol Cell Oncol. 2017 Mar 7;4(5):e1299273. doi: 10.1080/23723556.2017.1299273. eCollection 2017.

Authors

C Gamell^{1

2}, T Gulati^{1

2}, B Solomon^{1

3}, S Haupt^{1

2}, Y Haupt^{1

2

4

5}

Affiliations

¹ The Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, VIC, Australia.
² Tumor Suppression Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
³ Molecular Therapeutics and Biomarkers Laboratory, Peter MacCallum Cancer Centre, Melbourne, VIC, Australia.
⁴ Department of Biochemistry and Molecular Biology, Monash University, Melbourne, VIC, Australia.
⁵ Department of Pathology, The University of Melbourne, Melbourne, VIC, Australia.

Abstract

A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16^INK4a (best known as p16), commonly due to promoter hypermethylation. We recently reported a novel regulatory pathway involving E6-associated protein and cell division control protein 6, which provides a methylation-independent mechanism for p16 silencing in patients with a particularly aggressive form of NSCLC.

Keywords: CDC6; E6AP; INK4/ARF; NSCLC; p16; tumor suppression.