Is there a CDKN2A-centric network in pancreatic ductal adenocarcinoma?

Abstract

Pancreatic cancer has a high mortality rate and its incidence has risen rapidly in recent years. Meanwhile, the diagnosis and treatment of this cancer remain challenging. Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic cancer, but, currently, no sufficiently effective modalities for its treatment exist. The early diagnosis rate of pancreatic cancer is low and most patients have reached an advanced stage at the time of diagnosis. PDAC evolves from precancerous lesions and is highly aggressive and metastatic. It is essential to understand how the disease progresses and metastasizes. CDKN2A mutations are very common in PDAC. Therefore, here, we have performed a literature review and discuss the role of CDKN2A and some related genes in the development of PDAC, as well as the basis of gene targeting with a correlation coefficient of CDKN2A above 0.9 on the STRING website. It is noteworthy that the interaction of CDKN2A with each gene has been reported in the literature. The role of these genes and CDKN2A in PDAC may provide new directions that will advance the current knowledge base and treatment options since cancer progression is realized through interactions among cells. Our findings provide new insights into the treatment of PADC that can, to some extent, improve the diagnosis rate and quality of life of patients.

Keywords: CDKN2A; PDAC; biomarkers; cell cycle; genes.

Figure 1

CDKN2A-centric network regulation. Interaction network diagram of CDKN2A on the STRING webpage (correlation coefficient more than 0.9 and no more than 5 interactors) including CDK4, CDK6, MYC, TP53, MDM2 and KRAS, SMAD4. In this picture, CDKN2A, TP53, SMAD4 are tumor suppressor genes, while CDK4, CDK6, MYC, MDM2 and KRAS are oncogenes in almost cancer cells. Lines represent interactions between two genes and we can find out CDKN2A has relationships with these genes in PADC.