Breast cancer remains one of the most prevalent and deadly cancers affecting women in the United States, accounting for 15.3 percent of all new cancer cases and 6.7 percent of all cancer deaths in 2018, with an estimated 266,120 new diagnoses and 40,920 deaths in that year alone. While treatments have advanced significantly, metastasis, the spread of cancer from the primary tumor to distant sites such as the lungs, remains a leading cause of mortality. New research from LSU Health New Orleans has uncovered a previously unknown mechanism by which a tumor suppressor protein controls the spread of breast cancer, with direct implications for the development of targeted therapies.
At FOMAT, breast cancer research represents a deep commitment given how significantly the disease affects women across all of our patient communities. The discovery of new tumor suppressor mechanisms like this one opens promising avenues for targeted therapies that could work alongside existing treatments to stop cancer from spreading. Research that identifies how tumors communicate and seed metastasis is exactly the kind of foundational science that shapes the next generation of oncology trials.
What Nischarin Does in Breast Cancer Cells
The protein Nischarin was originally discovered by the laboratory of Suresh Alahari, PhD, the Fred Brazda Professor of Biochemistry and Molecular Biology at LSU Health New Orleans School of Medicine. Previous research from his lab established that Nischarin functions as a tumor suppressor involved in regulating breast cancer cell migration and movement. The current study, published in Cancer Research, extends that understanding by revealing a new role for Nischarin in controlling exosome release, a process directly tied to how tumors spread.
Exosomes are nano sized vesicles, essentially tiny fluid filled sacs, that carry proteins, genetic material, and other signaling molecules between cells. Tumor derived exosomes act as intercellular messengers that promote tumor progression and metastasis by influencing the behavior of cells within the tumor microenvironment. Primary tumors actively release these exosomes to prepare distant sites for the arrival and growth of metastatic cancer cells.
How Nischarin Controls Breast Cancer Metastasis Through Exosomes
The research team found that Nischarin regulates cell attachment and alters the properties of the exosomes that breast cancer cells release. Cells that express Nischarin release fewer exosomes overall, and the exosomes they do release have measurably different effects on surrounding tissue. When breast cancer cells were co cultured with exosomes from Nischarin positive cells, tumor growth and lung metastasis both decreased. Nischarin positive exosomes also reduced breast cancer cell motility and adhesion, as well as overall tumor volume. Cell survival in the presence of Nischarin expression was also decreased.
These findings collectively demonstrate that Nischarin does not merely suppress tumor growth at the primary site but actively reshapes the exosome mediated communication network that tumors rely on to spread.
Why This Matters for Breast Cancer Treatment Development
According to Dr. Alahari, the discovery of this novel role for Nischarin increases understanding of exosome biology and identifies new targets for modulating breast cancer metastasis. Inhibiting exosome secretion, he notes, may serve as an effective therapeutic strategy for breast cancer patients.
Beyond targeting exosome release directly, the research points to another promising application. Exosomes have already been explored as drug delivery vehicles in oncology research. Dr. Alahari suggests that Nischarin expressing exosomes used in combination with existing drug therapies could produce a meaningful therapeutic effect, potentially enhancing the precision and efficacy of breast cancer treatment in ways that conventional approaches cannot achieve alone.
The Path Forward in Breast Cancer Research
This study adds to a growing body of evidence that the tumor microenvironment and its intercellular communication systems are viable therapeutic targets. As researchers continue to map how proteins like Nischarin regulate exosome biology, the findings are expected to inform both biomarker development and the design of next generation clinical trials targeting metastatic breast cancer.
FOMAT conducts oncology clinical trials at sites across the United States, including studies focused on breast cancer. To learn more about active studies, visit FOMAT’s patient studies page.
For the full source, see the original publication in Cancer Research.