The discovery of proteins that initiate the muscle wasting caused by tumors could lead to new treatments for this hard-to-treat and often fatal condition called cancer-induced cachexia or cancer cachexia, reported scientists with The University of Texas Health Science Center at Houston (UTHealth) in a proof-of-concept study in the journal Nature Communications.

The UTHealth researchers found that in mouse cancer models, when they blocked the activity of the proteins named Hsp70 and Hsp90 in the bloodstream, the development of cancer cachexia stalled. The researchers used antibodies to neutralize the proteins in one model and silenced the genes that create them in cancer cells in another.

“We are the first to link elevated serum levels of Hsp70 and Hsp90 to cachexia in mice, and show that these proteins drive both muscle wasting and inflammation,” said Yi-Ping Li, PhD, the senior author and a professor of integrative biology and pharmacology at McGovern Medical School at UTHealth. “These proteins are promising therapeutic targets for defeating cachexia.”

Cancer cachexia primarily occurs in solid tumors including lung, pancreatic, colorectal and gastric cancer. “We show that all of these tumor cells from humans release high levels of Hsp70 and Hsp90, which explains the previous clinical findings that patients with these tumors tend to have elevated serum levels of these proteins,” Li added.

The next step in the research will involve investigations on cancer patients to determine if these proteins are biomarkers of cancer cachexia in humans, Li said.

Li said their findings could help in the understanding of other conditions that cause muscle loss such as chronic obstructive pulmonary disease and congestive heart failure, where circulating Hsp70 is also elevated.

The paper is titled, “Tumor induces muscle wasting in mice through releasing extracellular Hsp70 and Hsp90.”