Abstract
A key step during onset of most cases of non-small cell lung cancer (NSCLC) is the loss of the tumor suppressor p16INK4a (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.
Original language | English |
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Article number | e1299273 |
Number of pages | 3 |
Journal | Molecular and Cellular Oncology |
Volume | 4 |
Issue number | 5 |
DOIs | |
Publication status | Published - 3 Sep 2017 |
Keywords
- CDC6
- E6AP
- INK4/ARF
- NSCLC
- p16
- tumor suppression