@article{cbc052e5846c4c7abfa72c4cf1d3897c,
title = "Extracellular vesicle RNA signaling in the liver tumor microenvironment",
abstract = "The tumor microenvironment (TME) in liver cancers such as hepatocellular cancer (HCC) consists of a complex milieu of liver tissue-resident cells, infiltrated immune cells, and secreted factors that collectively serve to promote tumor growth and progression. Intercellular crosstalk contributes to tissue homeostasis, and perturbations during injury, inflammation and tumorigenesis that are important for tumor progression. Extracellular vesicle (EV)-mediated transfer of a payload of RNA molecules that serve as an intercellular signaling is an important contributor to tissue homeostasis within the TME. Several types of RNA have been implicated in EV-mediated signaling. Biological processes that can be modulated by EV RNA signaling within the liver include tumor growth, invasion, metastasis, angiogenesis, and modulation of the immune cell activities. This mini-review describes the liver TME, and the biological effects of EV RNA-mediated signaling within the liver to highlight the role of EV RNA in intercellular communication.",
keywords = "Extracellular RNA, Extracellular vesicles, Liver cancer, RNA therapeutics, microRNA",
author = "Piyush Gondaliya and Sayyed, {Adil Ali} and Julia Driscoll and Krishna Patel and Tushar Patel",
note = "Funding Information: This work was supported by the National Cancer Institute [ NIH grant CA217833 ], by the James C and Sarah K Kennedy Deanship and Alfred D and Audrey M Petersen Professorship at Mayo Clinic to Dr Tushar Patel. Funding Information: In the liver, activated HSCs work in concert with HCC CAFs to remodel the liver ECM architecture and modulate the TME in support of HCC progression. The activated HSCs also engage in bidirectional crosstalk with HCC cells to further promote tumor progression. Li et al., reported that HSC-HCC intercellular crosstalk was mediated in part through the exchange of EVs [17,82]. Treatment with hypoxia-conditioned Huh7-EV increased the expression of α-smooth muscle actin and vimentin in LX2 recipients, indicating that EV-treatment induced the activation of and promoted EMT in HSCs. The EV treatment-induced effects were attributed to the horizontal transfer of miR-151, miR-21, and miR-221. Interestingly, these oncomiRs were also enriched in the activated hypoxic-conditioned LX2-EV and were responsible for mediating the LX2-EV pro-tumorigenic effects in recipient Huh7 cells [17].This work was supported by the National Cancer Institute [NIH grant CA217833], by the James C and Sarah K Kennedy Deanship and Alfred D and Audrey M Petersen Professorship at Mayo Clinic to Dr Tushar Patel. Publisher Copyright: {\textcopyright} 2023 Elsevier B.V.",
year = "2023",
month = apr,
day = "1",
doi = "10.1016/j.canlet.2023.216089",
language = "English (US)",
volume = "558",
journal = "Cancer Letters",
issn = "0304-3835",
publisher = "Elsevier Ireland Ltd",
}