Home > Publications database > Chronic chromosome instability induced by Plk1 results in immune suppression in breast cancer. > print |
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100 | 1 | _ | |a Kandala, Sridhar |0 P:(DE-He78)d8285822e4aff9a18b05b78084ed3f09 |b 0 |e First author |
245 | _ | _ | |a Chronic chromosome instability induced by Plk1 results in immune suppression in breast cancer. |
260 | _ | _ | |a [New York, NY] |c 2023 |b Elsevier |
336 | 7 | _ | |a article |2 DRIVER |
336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1700481848_7062 |2 PUB:(DE-HGF) |
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520 | _ | _ | |a Chromosome instability (CIN) contributes to resistance to therapies and tumor evolution. Although natural killer (NK) cells can eliminate cells with complex karyotypes, high-CIN human tumors have an immunosuppressive phenotype. To understand which CIN-associated molecular features alter immune recognition during tumor evolution, we overexpress Polo-like kinase 1 (Plk1) in a Her2+ breast cancer model. These high-CIN tumors activate a senescence-associated secretory phenotype (SASP), upregulate PD-L1 and CD206, and induce non-cell-autonomous nuclear factor κB (NF-κβ) signaling, facilitating immune evasion. Single-cell RNA sequencing from pre-neoplastic mammary glands unveiled the presence of Arg1+ macrophages, NK cells with reduced effector functions, and increased resting regulatory T cell infiltration. We further show that high PLK1-expressing human breast tumors display gene expression patterns associated with SASP, NF-κβ signaling, and immune suppression. These findings underscore the need to understand the immune landscape in CIN tumors to identify more effective therapies, potentially combining immune checkpoint or NF-κβ inhibitors with current treatments. |
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650 | _ | 7 | |a CP: Cancer |2 Other |
650 | _ | 7 | |a CP: Cell biology |2 Other |
650 | _ | 7 | |a Her2(+) breast cancer |2 Other |
650 | _ | 7 | |a NF-κβ signaling |2 Other |
650 | _ | 7 | |a chromosomal instability |2 Other |
650 | _ | 7 | |a immune evasion |2 Other |
650 | _ | 7 | |a senescence-associated secretory phenotype, SASP |2 Other |
650 | _ | 7 | |a single-cell sequencing |2 Other |
700 | 1 | _ | |a Ramos, Maria |0 P:(DE-HGF)0 |b 1 |e First author |
700 | 1 | _ | |a Voith von Voithenberg, Lena |0 P:(DE-He78)065afb554417f5acd8ea579fc0d13d0b |b 2 |e First author |
700 | 1 | _ | |a Diaz-Jimenez, Alberto |0 P:(DE-HGF)0 |b 3 |
700 | 1 | _ | |a Chocarro, Sara |0 P:(DE-HGF)0 |b 4 |
700 | 1 | _ | |a Keding, Sigrun Johanna Elisabeth |0 P:(DE-He78)4009b389a34f8d3f41368959e7fd8e6a |b 5 |
700 | 1 | _ | |a Brors, Benedikt |0 P:(DE-He78)fc949170377b58098e46141d95c72661 |b 6 |
700 | 1 | _ | |a Imbusch, Charles D |0 P:(DE-HGF)0 |b 7 |
700 | 1 | _ | |a Sotillo, Rocio |0 P:(DE-HGF)0 |b 8 |e Last author |
773 | _ | _ | |a 10.1016/j.celrep.2023.113266 |g Vol. 42, no. 12, p. 113266 - |0 PERI:(DE-600)2649101-1 |n 12 |p 113266 |t Cell reports |v 42 |y 2023 |x 2211-1247 |
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