Open AccessRatio of Expression of p16 INK4a to p14 ARF Correlates with the Progression of Non‐small Cell Lung Cancer
Author(s) -
Moriyama Satoru,
Nakashima Yoshiaki,
Yano Motoki,
Kaji Masahiro,
Yamakawa Yosuke,
Toyama Tatsuya,
Yamashita Hiroko,
Iwase Hirotaka,
Sasaki Hidefumi,
Saito Yushi,
Kiriyama Masanobu,
Kato Jyoji,
Fujii Yoshitaka
Publication year - 2002
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.2002.tb01320.x
Subject(s) - cancer research , lung cancer , biology , cell cycle , retinoblastoma protein , cell , microbiology and biotechnology , pathology , medicine , genetics
The CDKN2 gene is located on the short arm of chromosome 9p and encodes two unrelated proteins, p16 INK4a and p14 ARF , through the use of independent first exons and shared exons 2 and 3. p16 INK4a is a cyclin‐dependent kinase inhibitor, whereas p14 ARF regulates the cell cycle through a p53 and MDM2–dependent pathway. We have examined the expression of p16 INK4a and p14 ARF using competitive RT‐PCR in 60 non‐small cell lung cancers (NSCLCs) and matching normal lung tissues. The intensities of bands for p16 INK4a and p14 ARF were nearly equal or the intensity of the p16 INK4a band slightly exceeded that of p14 ARF in the normal lung tissues ( n =60). In 38 tumors the intensity of the p16 INK4a band was similar to or slightly weaker than that of p14 ARF . In 6 tumors the intensity of the p16 INK4a band was weaker than that of p14 ARF . In 15 tumors the intensity of the p14 ARF band was very strong and the p16 INK4a band was barely visible. In only one tumor was the intensity of the p16 INK4a band very strong, while the band of p14 ARF was barely visible. The ratio of the intensity of p16 INK4a to p14 ARF had an interesting correlation with the tumor's clinicopathological characteristics. The p stage II‐IV tumors had significantly lower p16 INK4a to p14 ARF ratios than the p stage I tumors ( P =0.036). The T2–4 tumors had significantly lower p16 INK4a to p14 ARF ratios than the T1 tumors ( P =0.005). The N1–3 tumors had significantly lower p16 INK4a to p14 ARF ratios than the NO tumors ( P =0.014). Our results suggest that the ratio of expression of p16 INK4a to p14 ARF tends to decrease during the progression of NSCLC.