Coronin-1B and Its Role in Cell Migration Within Glioblastoma Multiforme Metastasis

By Daniella Gimbosh

Cancer is a destructive disease that has been devastating humankind since time immemorial. Cancer exists in a myriad of different forms within almost any tissue type, thus proving to be even more difficult to research. Importantly, cancer cells have specific properties that allow them to spread, or metastasize, to secondary locations. The ability of these cells to migrate abnormally results in metastases that are extremely difficult to destroy, often leading to death. Hence, tumours in the brain tissue are often difficult to treat and have a low survival rate; more research into brain cancer is vital in order to medically progress in this field.

Glioblastoma multiforme is the most aggressive type of glioma, a brain tumour of the glial cells, able to invade and metastasize locally (Khan et al., 2021). Its extreme invasive and metastatic capacity means that glioblastoma multiforme usually results in the recurrence of tumours and resistance of treatment, with the patient median survival rate being merely 14.6 months (Koshy et al., 2011). Despite recent medical advances in both surgical intervention and molecular therapies (Bhaskaran et al., 2020), glioblastoma multiforme persists as a prognostic and therapeutic challenge with an unfavourable prognosis.

The protein actin is vital for eukaryotic cells and is abundant within them. Actin makes up the cytoskeletal framework of the cell in filament form and is vital for cell motility. Rapid assembly and disassembly of filaments, in combination with help from a variety of different proteins, results in cell ‘crawling’, otherwise known as cell movement (Schaks, Giannone and Rottner, 2019). Hence, it is no surprise that actin is a major research focus when investigating cancer cell migration. Various proteins that interact with actin filaments have been studied, however, many remain undiscovered.

In various glioblastoma multiforme cells, it has been shown that the protein Coronin-1C promotes migration and metastasis through its action on actin-related protein (Arp) 2/3 complexes, thus resulting in elongated actin fibres (Thal et al., 2007). Another coronin protein, Coronin-1B, shares similar properties with Coronin-1C regarding cell motility. However, although a vast amount of research has been conducted to investigate Coronin-1C, little is known about the role of Coronin-1B in glioblastoma multiforme motility. Therefore, more research is required to fill this gap in the literature.

The role of Coronin-1B is different depending on the region – being either at the front, or leading edge, of the cell, or to the rear end of the cell. The Coronin-1B gene is transcribed into a functional Coronin-1B protein which, in filament-dense areas, normally interacts with inactive Arp2/3 complexes, recruiting them to actin filaments (Gandhi et al., 2013). When Arp2/3 complexes bind to actin filaments, this activates the complex to promote filament elongation and branching (Wang et al., 2020). Cofilin is a protein whose severing of actin filaments results in their disassembly. However, Coronin-1B protects the actin filament from cofilin severing at the lamellipodia leading edge. Thus, cell migration and motility are increased, as actin filaments have a vital role in these processes (Cai et al., 2007). Moreover, Coronin-1B has been shown to disassemble Arp2/3 complexes and actin filaments at the rear of lamellipodia networks, essentially performing in the opposite way. It does this by collaborating with cofilin.

With this information in mind, it would be extremely useful to design a study to investigate the role of Coronin-1B in motility and migration within glioblastoma multiforme metastasis. For example, gene-editing technology such as CRISPR-Cas9 can be used to “knock out” the Coronin-1B gene in glioblastoma multiforme cells. Then, cell motility can be observed. The expected result would be that cell motility would decrease if the Coronin-1B gene is knocked out, as Arp2/3 complex interaction with actin filaments would significantly decrease, and increased cofilin severing would result in actin filament disassembly.

Furthermore, the role of Coronin-1B within metastasis to secondary locations specifically could be observed, as well as its role within cell invasion, which is another important aspect to investigate in cancer cell research. Although Coronin-1C has been thoroughly researched and is proposed to play a role in brain tumour progression, its close family member Coronin-1B remains largely undiscovered. Perhaps research on this protein will reveal key findings on cancer cell metastasis and may provide answers to many questions regarding glioblastoma multiforme.


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