What are some cancer therapeutic drugs/treatments/strategies that target HER2 and HER3? How do they disrupt signaling pathway?
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I’d like to begin this topic by introducing HER2 and HER3 and their involvement in signaling that leads to cancer. There are four members in the HER family, HER1, HER2, HER3, and HER4. They are cytoplasmic membrane-anchored proteins with an extracellular ligand-binding domain, a transmembrane domain, and the intracellular tyrosine kinase domain. HER3 lacks RTK activity and relies on dimerization with HER2for phosphorylation. Once phosphorylated, HER3 serves as a binding site for proteins that lead to downstream signaling pathways such as PI3K/AKT and more that regulate cell survival, proliferation, and apoptosis. The HER2/HER3 heterodimer is one of the main activators of the PI3K/AKT and Ras/MEK/ERK signaling pathways. Downstream of these pathways are key regulations that would upregulate mesenchymal transition and lead to metastasis of breast cancer. HER2 does not directly to bind to any ligand but dimerizes with HER3 as previously mentioned as HER3 lacks RTK activity on its own. In cancer, HER2 homodimerize with itself when there is a high concentration. HER2 can localize to the nucleus and initiate transcriptional activity. Nuclear HER2 also acts as a STAT3 transcriptional co-activator. This stimulates breast cancer cell growth.
What are some cancer therapeutic drugs/treatments/strategies that target HER2 and HER3? How do they disrupt signaling pathway?
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What are some cancer therapeutic drugs/treatments/strategies that target HER2 and HER3? How do they disrupt signaling pathway?
Some cancer therapeutic drugs that target HER2 and HER3 are trastuzumab (Herceptin), pertuzumab (Perjeta), lapatinib (Tykerb), and neratinib (Nerlynx). These drugs disrupt the signaling pathway by inhibiting the activity of the HER2/HER3 heterodimer. This, in turn, will inhibit cell growth and metastasis. As mentioned earlier, one of the downstream effects of the HER2/HER3 heterodimer is the upregulation of mesenchymal transition (Dey, Williams, Leyland-Jones, & De, 2015). If this signaling pathway can be disrupted, it may help prevent or stop metastasis from occurring. There are many other drugs in development that also target HER2 and HER3, so, hopefully, more therapies will be available in the future to help patients with cancer.
HER3 inhibitors are a relatively new class of anti-cancer drugs and are being investigated in multiple clinical trials for various tumor types. Some of these inhibitors include gefitinib (Iressa), erlotinib (Tarceva), afatinib (Gilotrif), and dacomitinib (Vizimpro). These drugs work by blocking the HER3 receptor, which inhibits the activity of the HER2/HER3 heterodimer. As a result, cell growth and metastasis are disrupted.
It is still early in developing these drugs, but they have shown promise in preclinical studies. More research is needed to determine the efficacy and safety of these inhibitors, but they offer a potential new treatment option for patients with cancer (Kim & Bae, 2011).
So far, trastuzumab (Herceptin) and lapatinib (Tykerb) are the only drugs that the FDA has approved to treat patients with HER2-positive breast cancer. These drugs work by inhibiting the HER2/HER3 heterodimer activity, which disrupts the signaling pathway and helps to stop or slow tumor growth (Aceto et al., 2012). Many other drugs are currently in development that targets HER2 and HER3, so hopefully, more therapies will be available in the future to help patients with cancer.
Question: What are the downstream effects of the HER2/HER3 heterodimer?
Image:
Image: General features of the HER family (Saba, Yom, Haigentz, & El-Rayes, 2012)
References
Aceto, N., Duss, S., MacDonald, G., Meyer, D. S., Roloff, T. C., Hynes, N. E., & Bentires-Alj, M. (2012). Co-expression of HER2 and HER3 receptor tyrosine kinases enhances invasion of breast cells via stimulation of interleukin-8 autocrine secretion. Breast Cancer Research, 14(5), 1-11.
Dey, N., Williams, C., Leyland-Jones, B., & De, P. (2015). A critical role for HER3 in HER2-amplified and non-amplified breast cancers: function of a kinase-dead RTK. American journal of translational research, 7(4), 733.
Kim, H. J., & Bae, S. C. (2011). Histone deacetylase inhibitors: molecular mechanisms of action and clinical trials as anti-cancer drugs. American journal of translational research, 3(2), 166.
Saba, N. F., Yom, S. S., Haigentz, M., & El-Rayes, B. (2012). Monoclonal Antibodies against Epidermal Growth Factor Receptor in Solid Tumors. Chemotherapy research and practice, 2012. https://www.hindawi.com/journals/cherp/2012/817304/
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