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How We Can Stop Fat Cells From Fueling Cancer.

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Cancer cells constantly grow and divide, which means that they need a consistent energy supply. A new study looks at how cancer derives fuel from fat cells and finds a potential mechanism to starve the tumor of its nutrition.

Cancer is an increasingly complex area of study, with every perceivable angle of attack being plumbed by researchers.

Despite millions of hours of experimentation, however, there are still many questions left unanswered.


As we learn more about cancer, it becomes more and more clear that it needs to be approached as a whole-body disease.

For cancer to survive and thrive, it needs to draw energy from the body’s cells and tissues, utilize the circulatory system, and avoid the immune system. Tumors need to work intelligently to sustain their growth and become integrated in the body.

Researchers are now focusing on attacking not just the cancerous cells, but also the systems that tumors rely on to sustain them.

Tumor, metabolism, and fat

Researchers from Sanford Prebys Medical Discovery Institute in San Diego, CA, are now particularly interested in the way that tumors communicate with fat cells. Co-senior study author Maria Diaz-Meco, Ph.D., explains further.

“We need to consider,” she states, “other aspects of cancer therapeutics beyond the better-known genetics. That is, we need to invest more in the research of cancer metabolism, which deals with the identification of metabolic vulnerabilities that should be common to all types of cancers.”

In the United States, prostate cancer is the second leading cause of cancer-related death among men. Obesity is known to be a major risk factor and predicts how aggressively the cancer will behave. But exactly how obesity worsens prostate cancer outcomes is not yet known.

To date, many studies exploring obesity and prostate cancer have focused on mice that have been fed a high-fat diet. Co-senior study author Jorge Moscat, Ph.D., explains why this is not ideal.

Although this mimics some of the situations in patients,” he says, “it prevents a real understanding of the signaling pathways that control the bidirectional communication between tumors and adipocytes, or fat cells.”

“This is essential,” adds Moscat, “if we want to identify therapeutic targets that can be harnessed to prevent the pro-tumorigenic signals emanating from the adipose tissue.”

Moscat and Diaz-Meco approached this problem from a new direction: they used a mouse model that lacks a particular protein known as p62 in its fat cells. Mice deficient in this protein become obese even when fed a standard diet.

Tumors use fat cells for fuel.

They found that p62 plays an important role in the communication between fat tissue and tumors. The protein appears to support the “metabolic fitness” of cancer, promoting progression and metastasis. It achieves this by inhibiting a second protein called mTORC1.

When mTORC1 is suppressed, so are the energy-consuming activities of fat cells, such as oxidative phosphorylation and “fatty acid metabolism in white fat tissue.” With these processes halted, there are more fatty acids and other nutrients available for the tumor to use to grow and develop.



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