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Review
. 2022 Oct 8;14(19):4925.
doi: 10.3390/cancers14194925.

The Role of MARCKS in Metastasis and Treatment Resistance of Solid Tumors

Chun-Lung Chiu  1 , Hongjuan Zhao  1 , Ching-Hsien Chen  2   3 , Reen Wu  2   4 , James D Brooks  1
Affiliations
Review

The Role of MARCKS in Metastasis and Treatment Resistance of Solid Tumors

Chun-Lung Chiu et al. Cancers (Basel). .

Abstract

The myristoylated alanine-rich C-kinase substrate (MARCKS) is a membrane-associated protein kinase C (PKC) substrate ubiquitously expressed in eukaryotic cells. MARCKS plays important roles in multiple cellular processes, including cell adhesion and motility, mucin secretion, exocytosis, and inflammatory response. Aberrant MARCKS signaling has been observed in the development and progression of multiple cancer types. In addition, MARCKS facilitates cancer metastasis through modulating cancer cell migration and invasion. Moreover, MARCKS contributes to treatment resistance, likely by promoting cancer stem cell renewal as well as immunosuppression. In this review, we describe MARCKS protein structure, cellular localization, and biological functions. We then discuss the role of MARCKS in cancer metastasis as well as its mechanisms of action in solid tumors. Finally, we review recent advances in targeting MARCKS as a new therapeutic strategy in cancer management.

Keywords: MARCKS; cancer metastasis; cancer stemness; treatment resistance.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The publication trend of MARCKS research related to solid tumors in PubMed from 1989 to 2021. The black dots represent the publication ratio (%) of each year in which the publications of MARCKS research related to solid tumors were divided by the total publications of MARCKS research. The red line demonstrates the trend of the non-linear regression fit curve analyzed from each year’s publication ratio by GraphPad Prism (v6.07).
Figure 2
Figure 2
MARCKS participates in mediating target signaling pathways to drive malignant phenotypes that lead to cancer metastasis (through actin rearrangement, MMP9, ErbB2, NF-κB, and AKT pathways), cancer stemness (through the NF-κB pathway), and therapeutic resistance (through AKT, ABCB1, and stemness genes—SOX2, OCT4, and CD133).
See this image and copyright information in PMC

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