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Review Article Open Access
Volume 4 | Issue 2 | DOI: https://doi.org/10.33696/Signaling.4.091

Potential Mechanism of CDC42 Promoting HCC Metastasis

  • 1Department of Oncology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China
  • 2Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China
  • #These authors contributed equally
+ Affiliations - Affiliations

Corresponding Author

Jun Li, lijun37@mail.sysu.edu.cn;

Miaoling Tang, tangmling3@mail2.sysu.edu.cn 

Received Date: March 14, 2023

Accepted Date: April 21, 2023

Abstract

Hepatocellular carcinoma (HCC) is an aggressive malignancy with increasing morbidity and mortality worldwide. The migration and motility of HCC tumor cells are enhanced by the formation of invadopodia, which comprise membrane protrusions at the leading edge. Previous studies have showed that cell division cycle 42 (CDC42) plays an essential role in remodeling the cytoskeleton, which is associated with invadopodia formation and thus mediates cellular movement. Therefore, aberrant expression of CDC42 is hypothesized to promote tumor cell migration. In this review, we discuss the important role of CDC42 activation induced by guanine nucleotide-exchange factors (GEFs), which function as upstream regulators to activate CDC42, thereby mediating HCC invasion and metastasis by facilitating invadopodia formation. Furthermore, inhibitors targeting the CDC42-GEF interaction might be developed as an intervention against HCC metastasis.

Keywords

CDC42, GEFs, HCC, Cell motility, Invadopodia, Metastasis, Inhibitors

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