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Review
. 2022 May 2;20(1):208.
doi: 10.1186/s12951-022-01382-0.

Extracellular vesicle-mediated crosstalk between pancreatic cancer and stromal cells in the tumor microenvironment

Affiliations
Review

Extracellular vesicle-mediated crosstalk between pancreatic cancer and stromal cells in the tumor microenvironment

Ying Li et al. J Nanobiotechnology. .

Abstract

Pancreatic ductal adenocarcinoma (PDAC) interacts closely with the tumor microenvironment (TME). The TME is remodeled by crosstalk between pancreatic cancer cells and stromal cells, and is critical for cancer progression. Extracellular vesicles (EVs), including exosomes and microvesicles, help facilitate an exchange of information both within the TME and to distant organs. EVs have also been identified as potential diagnostic biomarkers, therapeutic targets, and drug carriers for pancreatic cancer treatment. Thus, understanding the selective packaging of EVs cargo and its mechanistic impact will increase our understanding of cancer biology. In this review, we collect and analyze recent findings of the pancreatic cancer-stromal cell interactions mediated by EVs and the mechanisms involved in cancer-related immunity and chemoresistance. These studies demonstrate the vital role of EVs in pancreatic cancer reprogramming and TME remodeling. We also summarize the EVs identified as potential PDAC diagnostic biomarkers and possible therapeutic targets. This greater understanding is a promising avenue for transitioning EVs from bench to bedside.

Keywords: Clinical applications; Communication; Extracellular vesicles; Pancreatic cancer; Tumor microenvironment.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Multiple roles of pancreatic ductal adenocarcinoma (PDAC)-derived extracellular vesicles (EVs) in altering the phenotypes of recipient stromal cells in the tumor microenvironment (TME) and shaping a pathologically active environment favoring tumor progression. Cancer cells and stromal cells both utilize EVs to influence surrounding cells within the TME niche by transferring bioactive molecules, including microRNAs
Fig. 2
Fig. 2
Extracellular vesicles (EVs) released from stromal cells in the tumor microenvironment (TME) can affect pancreatic ductal adenocarcinoma (PDAC) biology via delivering molecular cargo molecules. The malignant properties of PDAC, such as carcinogenesis, metastasis, drug resistance, and immune suppression, can be significantly affected by EVs released from stromal cells in the TME

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References

    1. Stathis A, Moore MJ. Advanced pancreatic carcinoma: current treatment and future challenges. Nat Rev. 2010;7:163–172. - PubMed
    1. Miller AL, Garcia PL, Yoon KJ. Developing effective combination therapy for pancreatic cancer: an overview. Pharmacol Res. 2020;155:104740. doi: 10.1016/j.phrs.2020.104740. - DOI - PMC - PubMed
    1. Zhou W, Zhou Y, Chen X, Ning T, Chen H, Guo Q, Zhang Y, Liu P, Zhang Y, Li C, et al. Pancreatic cancer-targeting exosomes for enhancing immunotherapy and reprogramming tumor microenvironment. Biomaterials. 2021;268:120546. doi: 10.1016/j.biomaterials.2020.120546. - DOI - PubMed
    1. Daßler-Plenker J, Küttner V, Egeblad M. Communication in tiny packages: Exosomes as means of tumor-stroma communication. Biochim Biophys Acta Rev Cancer. 2020;1873:188340. doi: 10.1016/j.bbcan.2020.188340. - DOI - PubMed
    1. Becker A, Thakur BK, Weiss JM, Kim HS, Peinado H, Lyden D. Extracellular vesicles in cancer: cell-to-cell mediators of metastasis. Cancer Cell. 2016;30:836–848. doi: 10.1016/j.ccell.2016.10.009. - DOI - PMC - PubMed