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Article: Tumor-associated neutrophils attenuate the immunosensitivity of hepatocellular carcinoma

TitleTumor-associated neutrophils attenuate the immunosensitivity of hepatocellular carcinoma
Authors
Issue Date5-Dec-2024
PublisherRockefeller University Press
Citation
Journal of Experimental Medicine, 2025, v. 222, n. 1 How to Cite?
AbstractTumor-associated neutrophils (TANs) are heterogeneous; thus, their roles in tumor development could vary depending on the cancer type. Here, we showed that TANs affect metabolic dysfunction-associated steatohepatitis hepatocellular carcinoma (MASH-related HCC) more than viral-associated HCC. We attributed this difference to the predominance of SiglecFhi TANs in MASH-related HCC tumors. Linoleic acid and GM-CSF, which are commonly elevated in the MASH-related HCC microenvironment, fostered the development of this c-Myc-driven TAN subset. Through TGFβ secretion, SiglecFhi TANs promoted HCC stemness, proliferation, and migration. Importantly, SiglecFhi TANs supported immune evasion by directly suppressing the antigen presentation machinery of tumor cells. SiglecFhi TAN removal increased the immunogenicity of a MASH-related HCC model and sensitized it to immunotherapy. Likewise, a high SiglecFhi TAN signature was associated with poor prognosis and immunotherapy resistance in HCC patients. Overall, our study highlights the importance of understanding TAN heterogeneity in cancer to improve therapeutic development.
Persistent Identifierhttp://hdl.handle.net/10722/358361
ISSN
2023 Impact Factor: 12.6
2023 SCImago Journal Rankings: 6.838

 

DC FieldValueLanguage
dc.contributor.authorTeo, Jia Ming Nickolas-
dc.contributor.authorChen, Zhulin-
dc.contributor.authorChen, Weixin-
dc.contributor.authorTan, Rachael Julia Yuenyinn-
dc.contributor.authorCao, Qi-
dc.contributor.authorChu, Yingming-
dc.contributor.authorMa, Delin-
dc.contributor.authorChen, Liting-
dc.contributor.authorYu, Huajian-
dc.contributor.authorLam, Ka Hei-
dc.contributor.authorLee, Terence Kin Wah-
dc.contributor.authorChakarov, Svetoslav-
dc.contributor.authorBecher, Burkhard-
dc.contributor.authorZhang, Ning-
dc.contributor.authorLi, Zhao-
dc.contributor.authorMa, Stephanie-
dc.contributor.authorXue, Ruidong-
dc.contributor.authorLing, Guang Sheng-
dc.date.accessioned2025-08-07T00:31:45Z-
dc.date.available2025-08-07T00:31:45Z-
dc.date.issued2024-12-05-
dc.identifier.citationJournal of Experimental Medicine, 2025, v. 222, n. 1-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/358361-
dc.description.abstractTumor-associated neutrophils (TANs) are heterogeneous; thus, their roles in tumor development could vary depending on the cancer type. Here, we showed that TANs affect metabolic dysfunction-associated steatohepatitis hepatocellular carcinoma (MASH-related HCC) more than viral-associated HCC. We attributed this difference to the predominance of SiglecFhi TANs in MASH-related HCC tumors. Linoleic acid and GM-CSF, which are commonly elevated in the MASH-related HCC microenvironment, fostered the development of this c-Myc-driven TAN subset. Through TGFβ secretion, SiglecFhi TANs promoted HCC stemness, proliferation, and migration. Importantly, SiglecFhi TANs supported immune evasion by directly suppressing the antigen presentation machinery of tumor cells. SiglecFhi TAN removal increased the immunogenicity of a MASH-related HCC model and sensitized it to immunotherapy. Likewise, a high SiglecFhi TAN signature was associated with poor prognosis and immunotherapy resistance in HCC patients. Overall, our study highlights the importance of understanding TAN heterogeneity in cancer to improve therapeutic development.-
dc.languageeng-
dc.publisherRockefeller University Press-
dc.relation.ispartofJournal of Experimental Medicine-
dc.titleTumor-associated neutrophils attenuate the immunosensitivity of hepatocellular carcinoma-
dc.typeArticle-
dc.identifier.doi10.1084/jem.20241442-
dc.identifier.pmid39636298-
dc.identifier.scopuseid_2-s2.0-85211830660-
dc.identifier.volume222-
dc.identifier.issue1-
dc.identifier.eissn1540-9538-
dc.identifier.issnl0022-1007-

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