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Review
. 2021 Dec 10:9:806482.
doi: 10.3389/fcell.2021.806482. eCollection 2021.

Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis

Sarah Bui  1 , Isabel Mejia  2 , Begoña Díaz  2   3 , Yanzhuang Wang  1   4
Affiliations
Review

Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis

Sarah Bui et al. Front Cell Dev Biol. .

Abstract

The Golgi apparatus plays a central role in normal cell physiology by promoting cell survival, facilitating proliferation, and enabling cell-cell communication and migration. These roles are partially mediated by well-known Golgi functions, including post-translational modifications, lipid biosynthesis, intracellular trafficking, and protein secretion. In addition, accumulating evidence indicates that the Golgi plays a critical role in sensing and integrating external and internal cues to promote cellular homeostasis. Indeed, the unique structure of the mammalian Golgi can be fine-tuned to adapt different Golgi functions to specific cellular needs. This is particularly relevant in the context of cancer, where unrestrained proliferation and aberrant survival and migration increase the demands in Golgi functions, as well as the need for Golgi-dependent sensing and adaptation to intrinsic and extrinsic stressors. Here, we review and discuss current understanding of how the structure and function of the Golgi apparatus is influenced by oncogenic transformation, and how this adaptation may facilitate cancer cell invasion and metastasis.

Keywords: Golgi; cancer; dissemination; metastasis; oncogenic transformation; proliferation; signaling; tumorigenesis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Golgi morphology in cancer cell lines. Carcinoma cell lines, HeLa (cervical), H1650 (lung), and SU.86.86 (pancreatic), were stained for GM130 (cis-Golgi marker) and DAPI (blue). Images represent distinct Golgi morphologies in different carcinoma cell lines. Arrowheads indicate outlined cells that are magnified in the right column (zoom-in).
FIGURE 2
FIGURE 2
Diagram illustrating the main steps of metastatic cascade. 1) Local invasion: cells at the primary tumor site invade the surrounding stroma; 2) intravasation of cancer cell into blood vessels; 3) dissemination of cancer cells in blood vessels to distant sites; 4) extravasation of cancer cell from blood vessel to a secondary tissue; 5) colonization of a secondary tissue to form metastasis.
FIGURE 3
FIGURE 3
Golgi associated factors in Epithelial-to-Mesenchymal Transition (EMT). A number of Golgi-localized proteins, including Golgi matrix proteins and enzymes, are linked to changes in Golgi structure and function as cancer cells acquire a mesenchymal-like migratory phenotype.
FIGURE 4
FIGURE 4
Golgi response to the tumor microenvironment. (A) Variety of stresses are found in the tumor microenvironment, (B) capable of activating Golgi-associated degradation (GARD), autophagy, unconventional protein secretion (ups), cleavage of Golgi proteins and (C) Golgi Stress Response pathways.
See this image and copyright information in PMC

References

    1. Ahat E., Xiang Y., Zhang X., Bekier M. E., Wang Y. (2019). GRASP Depletion-Mediated Golgi Destruction Decreases Cell Adhesion and Migration via the Reduction of α5β1 Integrin. MBoC 30, 766–777. 10.1091/mbc.E18-07-0462 - DOI - PMC - PubMed
    1. Anglesio M. S., Evdokimova V., Melnyk N., Zhang L., Fernandez C. V., Grundy P. E., et al. (2004). Differential Expression of a Novel Ankyrin Containing E3 Ubiquitin-Protein Ligase, Hace1, in Sporadic Wilms' Tumor versus normal Kidney. Hum. Mol. Genet. 13, 2061–2074. 10.1093/hmg/ddh215 - DOI - PubMed
    1. Asada M., Furukawa K., Segawa K., Endo T., Kobata A. (1997). Increased Expression of Highly Branched N-Glycans at Cell Surface Is Correlated with the Malignant Phenotypes of Mouse Tumor Cells. Cancer Res. 57, 1073–1080. - PubMed
    1. Avraamides C. J., Garmy-Susini B., Varner J. A. (2008). Integrins in Angiogenesis and Lymphangiogenesis. Nat. Rev. Cancer 8, 604–617. 10.1038/nrc2353 - DOI - PMC - PubMed
    1. Awwad R. A., Sergina N., Yang H., Ziober B., Willson J. K., Zborowska E., et al. (2003). The Role of Transforming Growth Factor Alpha in Determining Growth Factor independence. Cancer Res. 63, 4731–4738. - PubMed

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