Open AccessExpression and role of p16 and GLUT1 in malignant diseases and lung cancer: A review
Author(s) -
Pezzuto Aldo,
D'Ascanio Michela,
Ricci Alberto,
Pagliuca Alessandra,
Carico Elisabetta
Publication year - 2020
Publication title -
thoracic cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 28
eISSN - 1759-7714
pISSN - 1759-7706
DOI - 10.1111/1759-7714.13651
Subject(s) - carcinogenesis , cancer research , glut1 , cell cycle , medicine , lung cancer , glucose transporter , cancer , cell growth , cell cycle checkpoint , cell , retinoblastoma , biology , oncology , genetics , gene , insulin
Non‐small cell lung cancer (NSCLC) is the leading cause of cancer death and in most cases it is often diagnosed at an advanced stage. Many genetic and microenvironmental factors are able to modify the cell cycle inducing carcinogenesis and tumor growth. Among the metabolic and genetic factors that come into play in carcinogenesis and tumor cell differentiation and growth there are two different proteins that should be considered which are glucose transporters (GLUTs) and p16 INK4 The first are glucose transporters which are strongly involved in tumor metabolism, notably accelerating cancer cell metabolism both in aerobic and anaerobic conditions. There are different subtypes of GLUT family factors of which GLUT 1 is the most important and widely expressed. By contrast, p16 is mainly a tumor‐suppressor protein that acts on cyclin‐dependent kinase favoring cell cycle arrest in the G1 phase. Our search focused on the action of the aforementioned factors.