Scientists have found that Erbin, a protein that was thought to be an anti-tumor factor, is highly expressed in breast cancer and is needed by ErbB2 to support breast cancer.

ErbB2, commonly called HER2, is a gene that is prominent in approximately 25 percent of breast cancers.

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When researchers interfered with the interaction of HER2 and Erbin in mice, the tumor development is inhibited, along with its metastasization to the lungs, according to an international team reporting in the "PNAS" scientific journal. The scientists noted the over expression of both in 171 mostly aggressive cases of human breast cancer as well.

The results suggest a new possible therapeutic target to treat breast cancer and potentially a supplement for women who have become resistant to trastuzumab, or Herceptin, the medication generally given to patients that test positive for ErbB2, said the Chairman of the Department of Neuroscience and Regenerative Medicine at the Medical College of Georgia at Georgia Regents University and corresponding author Dr. Lin Mei.

Additionally, Erbin could become a possible diagnostic biomarker that doctors can look for in biopsies of breast tissues, Mei said. The gene, which is also present in healthy breast tissues, is crucial to the action and strength of ErbB2-positive, aggressive breast cancer, according to research.

When the researchers lowered the levels of Erbin, either by the use of a peptide that blocked its interaction with ErbB2 or by a gene therapy method that reduced its production, the growth of breast cancer and its spread was either significantly reduced or completely eliminated.

"Erbin is an intracellular molecule that binds to ErbB2 and stabilizes it," Mei said. "If you take it out, ErbB2 becomes unstable."

On the other hand, ErbB2 generally reaches both inside and outside cancer cells in the breast. Medications such as Herceptin decay excessive amounts of the oncogene by going after the region that juts out of the cell, which can be very effective, leading to a potential cure, Mei said.

"But the tumors are very smart," she added. If only the portions of the ErbB2 that stick out are destroyed, the remaining breast cancer cells can transform so it would no longer have the external points of HER2. The evolution leaves Herceptin without a place to bind.

Infiltrating the cells can prove to be more difficult but the capability of targeting the Erbin found inside the cells could one day make a difference for the breast cancer patients.

"Erbin itself could be a novel target: you disrupt the interaction, and it will be therapeutic," Mei said. "Secondly, when a patient becomes Herceptin-resistant because the extracellular domain of ErbB2 is lost, this approach should still be effective because of the critical interaction of the two."

Tagsbreast cancer, Cancer, Erbin, HER2, ErbB2, herceptin, Trastuzumab, Oncogene