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The Ras Gene

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...

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Concurrent PEDF deficiency and Kras mutation induce invasive pancreatic cancer and adipose-rich stroma in mice.

Paul J Grippo¹, Philip S Fitchev, David J Bentrem

¹Department of Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. p-grippo@northwestern.edu

|January 12, 2012

Summary

Pigment epithelium-derived factor (PEDF) deficiency promotes pancreatic cancer by increasing adiposity and invasion. Loss of PEDF in mice led to invasive pancreatic ductal adenocarcinoma (PDAC) with enhanced fat accumulation and tumor spread, highlighting PEDF as a key regulator.

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Area of Science:

Oncology
Metabolic Research
Molecular Biology

Background:

Pigment epithelium-derived factor (PEDF) is a SERPIN with antiangiogenic properties implicated in metabolism and adipogenesis.
Pancreatic cancer progression is influenced by adipogenesis, with increased pancreatic fat correlating to tumor dissemination.
PEDF deficiency in mice and oncogenic Ras mutations in pancreatic ductal adenocarcinoma (PDAC) both promote adipogenesis and premalignant lesions.

Purpose of the Study:

To determine if concurrent loss of PEDF is sufficient to promote adipogenesis and tumorigenesis in the pancreas.
To investigate the role of PEDF in the context of oncogenic Ras-driven pancreatic neoplasms.

Main Methods:

Ablation of PEDF in an EL-Kras(G12D) mouse model.
Analysis of invasive PDAC development, matrix metalloproteinase (MMP) expression, and peripancreatic fat accumulation.
Assessment of lipid droplet-associated proteins (TIP47, ADRP) and lipolysis factors in pancreatic stroma.
Measurement of PEDF, TIP47, and VEGF levels in human PDAC tissues and serum.

Main Results:

EL-Kras(G12D)/PEDF deficient mice developed invasive PDAC with increased MMP-2 and MMP-9 expression.
These mice exhibited increased peripancreatic fat, adipocyte hypertrophy, and pancreatic steatosis.
Increased adipogenesis markers (TIP47, ADRP) and decreased lipolysis (adipose triglyceride lipase) were observed.
Human PDAC patients showed decreased PEDF, increased stromal TIP47, and an elevated VEGF to PEDF ratio.

Conclusions:

Loss of PEDF significantly contributes to pancreatic adiposity and tumor invasion.
PEDF is identified as a critical negative regulator of pancreatic adiposity and tumor spread.
These findings underscore the importance of lipid metabolism within the tumor microenvironment.