Current Cancer Therapies
Question
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In terms of tumor progression, cells undergo stiffening just prior to becoming malignant, capable of uncontrolled growth and migration. Recent studies indicate that cell stiffening plays a role in promoting proliferation or metastatic growth, which is subsequently followed by stress fiber disassembly to allow cell migration. This transition was found to coincide with the change in the levels of activity of downstream elements of the signaling pathway, such as the kinase Src, that regulate changes in the actin cytoskeleton. As shown in the attached figure below, low Src activity promotes stress fiber assembly leading to cell stiffening, whereas high Src activity has the opposite effect allowing for cell migration.
In light of this, are there any current cancer therapies targeting actin regulation?
REF
Tavares, S., Vieira, A., Taubenberger, A. et al. Actin stress fiber organization promotes cell stiffening and proliferation of pre-invasive breast cancer cells. Nat Commun 8, 15237 (2017). https://doi.org/10.1038/ncomms15237
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Solution
Current Cancer Therapies
Cancer therapy has advanced in the last 20 years. Currently, there are over a dozen therapies available that target actin regulation. One example is the Src inhibitor Saracatinib (Jung and Park, 2020). Saracatinib has been approved to treat certain non-small cell lung carcinoma, metastatic breast cancer, and acute lymphoblastic leukemia. Another example is Gleevec which targets Bcr-Abl. Gleevec has been approved to treat Chronic Myelogenous Leukemia (CML) and certain gastrointestinal stromal tumors (GIST).
Others are:
● Those that induce actomyosin contractility.
● Another type of drug can target proteins involved in the assembly and disassembly of the cytoskeleton.
The positively charged monomeric G-actin binds to the negatively charged F-actin polymers, which causes them to break down. This is demonstrated by the natural product CytD, which increases G-actin levels and regulates F-actin polymers (Tavares et al., 2017). CytD is a well-studied drug that is highly effective at inhibiting the polymerization of F-actin in vitro. In addition to CytD, several other drugs target actin polymerization. Actomyosin contractility regulates many important cellular processes such as cell shape changes, cell motility, and cytokinesis. Several drugs have been developed to stop myosin from working. One example is jasplakinolide, a chemical that helps to keep cells stable (Shang et al., 2018). The drug latrunculin A induces depolymerization of filamentous actin and has also been proposed as a potential anticancer agent, with studies suggesting its ability to inhibit metastasis by impeding the tumor cells’ motility.
The actin cytoskeleton plays a key role in shaping individual cells and tissues. In terms of tumor progression, cells undergo stiffening before becoming malignant, capable of uncontrolled growth and migration. Cancer therapies that target actin regulation are still in their early phases of development. However, FDA has approved a few and are available for clinical use, like cytochalasin D and Saracatinib.
References
Jung, Y. S., & Park, J. I. (2020). Wnt signaling in cancer: therapeutic targeting of Wnt signaling beyond β-catenin and the destruction complex. Experimental & Molecular Medicine, 52(2), 183-191.
Shang, W., Jiang, Y., Boettcher, M., Ding, K., Mollenauer, M., Liu, Z., ... & Wang, H. (2018). Genome-wide CRISPR screen identifies FAM49B as a key regulator of actin dynamics and T cell activation. Proceedings of the National Academy of Sciences, 115(17), E4051-E4060.
Tavares, S., Vieira, A., Taubenberger, A. et al. (2017). Actin stress fiber organization promotes cell stiffening and proliferation of pre-invasive breast cancer cells. Nat Commun 8, 15237
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