Targeting CD82/KAI1 for Precision Therapeutics in Surmounting Metastatic Potential in Breast Cancer

SIMPLE SUMMARY: Breast cancer-related deaths are mainly due to the spread of cancer cells to distant organs (a process termed metastasis). CD82, also known as KAI1, is an established metastasis suppressor that has been documented to be lowly expressed in metastatic breast cancer. Hence, CD82 could possibly be a feasible molecular target for impeding metastases in breast cancer patients. Here, we propose a precision oncology-based model of preventing metastases by an appropriate selection of non-metastatic breast cancer patients with low CD82 expression. Potential therapeutic options for restoring CD82 levels that could be administered include the repurposing of existing chemotherapeutic drugs such as tyrosine kinase inhibitors and etoposide, as well as the use of CD82 peptide mimics and non-coding RNA-based therapeutics. ABSTRACT: Metastasis is the main cause of mortality in breast cancer patients. There is an unmet need to develop therapies that can impede metastatic spread. Precision oncology has shown great promise for the treatment of cancers, as the therapeutic approach is tailored to a specific group of patients who are likely to benefit from the treatment, rather than the traditional approach of “one size fits all”. CD82, also known as KAI1, a glycoprotein belonging to the tetraspanin family and an established metastasis suppressor, could potentially be exploited to hinder metastases in breast cancer. This review explores the prospect of targeting CD82 as an innovative therapeutic approach in precision medicine for breast cancer patients, with the goal of preventing cancer progression and metastasis. Such an approach would entail the selection of a subset of breast cancer patients with low levels of CD82, and instituting an appropriate treatment scheme tailored towards restoring the levels of CD82 in this group of patients. Proposed precision treatment regimens include current modalities of treating breast cancer, in combination with either clinically approved drugs that could restore the levels of CD82, CD82 peptide mimics or non-coding RNA-based therapeutics.