Scientists reveal the mechanism of cell metastasis in breast cancer

U.S. scientists have discovered a protein that allows breast cancer cells to survive as they move around the body and form new tumors, a process known as metastasis. Their conclusions are based on laboratory experiments and mouse models that explain the metastasis mechanism in the most common type of breast cancer, insumptive catheter cancer. The protein, known as E-calcium mucous protein, appears to limit the molecular stress in cancer cells, allowing them to survive enough to form new tumors.
, published September 4 in the journal Nature, could lead to new ways to prevent the recurrence of breast cancer.
previously believed that cancer cells had to lose E-calcium muctin to metaspose. "It's hard to explain why breast tumors in patients usually continue to express E-calcium mucous proteins," said Andrew Ewald, a professor of cell biology and co-director of the Cancer Invasion and Metastasis Program at Johns Hopkins Kimmel Cancer Center. Our study aims to test the role of this protein in the metastasis of the most common breast cancer subtype, immersive catheterized cancer. Ewald
that the vast majority of deaths from breast cancer and other cancers are caused by metastasis, so preventing metastasis is a key goal of cancer research.
From a scientific point of view, metastasis is divided into many different stages, including cancer cells invading healthy breast tissue, escaping primary tumors, entering and surviving blood vessels, entering new organs, and surviving and sowing new tumors in distant organs such as the lungs.
cancer cells break away from primary tumors early in metastasis, and a number of studies have focused on how cancer cells adhere to each other at the molecular level through E-calcium mucosa. In some cancers, such as the type of breast cancer known as leaching small leaf cancer (ILC), the genetic mutation that removes E-calcium mucous proteins appears to be a key factor in metastasis.
However, in some other types of cancer, such as immersive catheter cancer (IDC, the most common type of breast cancer, accounting for more than 80 percent of all breast cancer diagnoses), this protein is preserved or even overexposed, which scientists have so far been unable to explain the contradiction.
To study the problem, Ewald and his colleagues tested the role of E-calcium mucoprotein in three experimental models of insulative catheter cancer that represent the common subtypes of human breast cancer: tube-cavity breast cancer, substrate-like breast cancer, and triple-negative breast cancer. These different subsypes have different gene expression patterns and different average patient prognostics.
first tested the role of E-calcium mucous protein during cancer invasion. In all three models, the absence of the E-calcium mucous protein gene significantly improved the ability of cancer cells to invade healthy tissue. For example, in mouse models, tumors that produced E-calcium mucous protein invaded 6% of their tumor edges, while tumors that did not produce E-calcium mucous protein invaded 82% of their edges.
in laboratory experiments and animal models, the absence of E-calcin interferes with all other biological metastasis stages in the three breast cancer models. Cells without E-calcium mucous proteins are lost during migration and die in large numbers at every step of the way after leaving the primary tumor. Ewald says very few cells that have successfully migrated and survived have not multiplyed in new organs and rarely form new tumors.
news is that our research shows that the transfer process seems to be very inefficient, even in an ideal laboratory environment," Ewald said. "Studies have shown that about 99% of cells that are separated from the primary tumor die and never form a new tumor.
that breast cancer cells need to adhere to the connection to survive and eventually spread and cause death. "Our future research looks at how to target survival signals associated with E-calcium mucous proteins to prevent metastasis and thus save patients' lives." Ewald said. (Source: China Science Journal Zhao Xixi)
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