Adiponectin shows potential in blocking obesity-related carcinogenesis

Protein hormone inhibits leptin-induced migration of liver cancer cells

2010-10-20

(Press-News.org) A research team from Emory University School of Medicine investigated the role between adiponectin and leptin in obesity-related carcinogenesis. Their findings, published in the November issue of Hepatology, suggest that the protein hormone adiponectin has potential for inhibiting the oncogenic actions of leptin, namely in hepatocellular carcinoma (HCC), and could offer a promising therapy for the disease.

Obesity is on the rise and is associated with increased risk and progression of a number of cancers including colon, prostate, breast, and liver cancers. The World Health Organization declared obesity one of the greatest public health challenges of the 21st century and projects that by 2015, more than 700 million adults will be obese. In the U.S., the Centers for Disease Control and Prevention (CDC) estimates roughly 72.5 million adults are considered obese—having a body mass index (BMI) greater than 30.

Obese populations have higher circulating levels of leptin, the protein hormone that controls appetite, but lower concentrations of adiponectin which regulates glucose levels and the breakdown of fatty acids. Understanding the these hormones play a role in obesity-related cancers and the vast number of individuals who are at risk, Neeraj K. Saxena, Ph.D. and colleagues investigated the protective effect of adiponectin and its impact on leptin in HCC.

"Our study presents important clinical implications since HCC has the highest increased risk associated with obesity compared to other cancers such as prostate, kidney, colon, and stomach," commented Dr. Saxena. Using human cell-lines, mice models of HCC, and tissue microarray researchers determined the antagonistic role of adiponectin on the cancer-causing actions of leptin.

The authors found that adiponectin treatment inhibited leptin-induced proliferation, invasion, and migration of HCC cells. Treatment with adiponectin also slowed leptin-induced HCC tumor growth in vivo. Further analysis showed that leptin expression correlated positively with HCC proliferation and nonalcoholic steatohepatitis (NASH). Adiponectin expression had an inverse correlation with tumor size, and a direct correlation to disease-free survival in human HCC tumor samples.

"Taken together our results suggest an attractive molecular strategy employing adiponectin analogues for potential therapy of metastatic HCC," concluded Dr. Saxena. "With the prevalence of obesity in the U.S., our study could significantly improve overall survival for a vast number of obese liver cancer patients by using adiponectin to inhibit growth, invasion, and migration of HCC cells."

INFORMATION: Article: "Adiponectin Antagonizes The Oncogenic Actions Of Leptin In Hepatocellular Carcinogenesis." Dipali Sharma, Jason Wang, Ping P. Fu, Shvetank Sharma, Arumugam Nagalingam, Jamie Mells, Jeffrey Handy, Andrew J. Page, Cynthia Cohen, Frank A. Anania, Neeraj K. Saxena1. Hepatology; Published Online: August 5, 2010 (DOI: 10.1002/hep.23892); Print Issue Date: November 2010. http://onlinelibrary.wiley.com/doi/10.1002/hep.23892/abstract

This study study is published in Hepatology. Media wishing to receive a PDF of the articles may contact healthnews@wiley.com.

Hepatology is the premier publication in the field of liver disease, publishing original, peer-reviewed articles concerning all aspects of liver structure, function and disease. Each month, the distinguished Editorial Board monitors and selects only the best articles on subjects such as immunology, chronic hepatitis, viral hepatitis, cirrhosis, genetic and metabolic liver diseases and their complications, liver cancer, and drug metabolism. Hepatology is published on behalf of the American Association for the Study of Liver Diseases (AASLD). For more information, please visit http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1527-3350.

Wiley-Blackwell is the international scientific, technical, medical, and scholarly publishing business of John Wiley & Sons, Inc., with strengths in every major academic and professional field and partnerships with many of the world's leading societies. Wiley-Blackwell publishes nearly 1,500 peer-reviewed journals and 1,500+ new books annually in print and online, as well as databases, major reference works and laboratory protocols. For more information, please visit www.wileyblackwell.com or our new online platform, Wiley Online Library (wileyonlinelibrary.com), one of the world's most extensive multidisciplinary collections of online resources, covering life, health, social and physical sciences, and humanities.

Media Advisory

What: The 61st Annual Meeting of the American Association for the Study of Liver Diseases (AASLD)

Founded in 1950, AASLD is the leading organization of scientists and healthcare professionals committed to preventing and curing liver disease. AASLD has grown into an international society responsible for all aspects of hepatology, and the annual meeting attracts 8,500 physicians, surgeons, researchers, and allied health professionals from around the world.

The Liver Meeting® is the premier meeting in the science and practice of hepatology, including the latest findings on new drugs, novel treatments, and the results from pilot and multicenter studies.

When: October 30 – November 2, 2010

Where : Hynes Convention Center
900 Boylston Street
Boston, Massachusetts

Contact: Please contact Ann Haran at 703-299-9766 or aharan@aasld.org to obtain a press pass for this event.

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Adiponectin shows potential in blocking obesity-related carcinogenesis

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