{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T11:09:39Z","timestamp":1791544179717,"version":"4.3.4"},"reference-count":54,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"11","license":[{"start":{"date-parts":[[2024,9,2]],"date-time":"2024-09-02T00:00:00Z","timestamp":1725235200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"name":"National Key Projects of Ministry of Science and Technology of China","award":["MOST2018YFE0113700"],"award-info":[{"award-number":["MOST2018YFE0113700"]}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["NSFC81874199"],"award-info":[{"award-number":["NSFC81874199"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["NSFC82173155"],"award-info":[{"award-number":["NSFC82173155"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Commun"],"published-print":{"date-parts":[[2024,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Tumor metastasis is a major threat to cancer patient survival. The organ\u2010specific niche plays a pivotal role in tumor organotropic metastasis. Fibroblasts serve as a vital component of the metastatic microenvironment, but how heterogeneous metastasis\u2010associated fibroblasts (MAFs) promote organotropic metastasis is poorly characterized. Here, we aimed to decipher the heterogeneity of MAFs and elucidate the distinct roles of these fibroblasts in pulmonary metastasis formation in breast cancer.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Mouse models of breast cancer pulmonary metastasis were established using an in vivo selection method of repeated injections of metastatic cells purified from the mouse lung. Single\u2010cell RNA\u2010sequencing (scRNA\u2010seq) was employed to investigate the heterogeneity of MAFs. Transgenic mice were used to examine the contribution of tryptophan 2,3\u2010dioxygenase\u2010positive matrix fibroblasts (TDO2\n                      <jats:sup>+<\/jats:sup>\n                      MFs) in lung metastasis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      We uncovered 3 subtypes of MAFs in the lung metastatic microenvironment, and their transcriptome profiles changed dynamically as lung metastasis evolved. As the predominant subtype, MFs were exclusively marked by platelet\u2010derived growth factor receptor alpha (PDGFRA) and mainly located on the edge of the metastasis, and T cells were enriched around MFs. Notably, high MF signatures were significantly associated with poor survival in breast cancer patients. Lung metastases were markedly diminished, and the suppression of T cells was dramatically attenuated in MF\u2010depleted experimental metastatic mouse models. We found that TDO2\n                      <jats:sup>+<\/jats:sup>\n                      MFs controlled pulmonary metastasis by producing kynurenine (KYN), which upregulated ferritin heavy chain 1 (FTH1) level in disseminated tumor cells (DTCs), enabling DTCs to resist ferroptosis. Moreover, TDO2\n                      <jats:sup>+<\/jats:sup>\n                      MF\u2010secreted chemokines C\u2010C motif chemokine ligand 8 (CCL8) and C\u2010C motif chemokine ligand 11 (CCL11) recruited T cells. TDO2\n                      <jats:sup>+<\/jats:sup>\n                      MF\u2010derived KYN induced T cell dysfunction. Conditional knockout of\n                      <jats:italic toggle=\"yes\">Tdo2<\/jats:italic>\n                      in MFs diminished lung metastasis and enhanced immune activation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Our study reveals crucial roles of TDO2\n                      <jats:sup>+<\/jats:sup>\n                      MFs in promoting lung metastasis and DTCs\u2019 immune evasion in the metastatic niche. It suggests that targeting the metabolism of lung\u2010specific stromal cells may be an effective treatment strategy for breast cancer patients with lung metastasis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cac2.12608","type":"journal-article","created":{"date-parts":[[2024,9,2]],"date-time":"2024-09-02T09:22:33Z","timestamp":1725268953000},"page":"1261-1286","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["Tryptophan 2,3\u2010dioxygenase\u2010positive matrix fibroblasts fuel breast cancer lung metastasis via kynurenine\u2010mediated ferroptosis resistance of metastatic cells and T cell dysfunction"],"prefix":"10.34133","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-6698-5282","authenticated-orcid":false,"given":"Yongcan","family":"Liu","sequence":"first","affiliation":[{"name":"Chinese Ministry of Education","place":["Chongqing, P. R. 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