Author Correction: The necrosome promotes pancreatic oncogenesis via CXCL1 and Mincle-induced immune suppression

Seifert, Lena; Werba, Gregor; Tiwari, Shaun; Ly, Nancy Ngoc Giao; Alothman, Sara; Alqunaibit, Dalia; Avanzi, Antonina; Barilla, Rocky; Daley, Donnele; Greco, Stephanie H.; Torres‐Hernandez, Alejandro; Pergamo, Matthew; Ochi, Atsuo; Zambirinis, Constantinos P.; Pansari, Mridul; Rendon, Mauricio; Tippens, Daniel; Hundeyin, Mautin; Mani, Vishnu R.; Hajdu, Cristina; Engle, Dannielle; Miller, George

doi:10.1038/s41586-021-03322-8

Cited by 4 publications

(4 citation statements)

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“…RIPK3-dependent necroptosis of pancreatic cancer cells results in increased expression of sin3A-associated protein 130 (SAP130) and release of chemokines such as C-x-c motif chemokine ligand 1 (CXCL1) and CXCL5, leading to the recruitment of immunosuppressive cells such as MDSCs to form immunosuppressive TME mediating the migration and invasion of cancer cells. 350 , 351 Similarly, RIPK3 signaling in MDSCs increases tumor size by expanding IL17-producing T cells in tumor models. 352 In addition, RIPK1 expression was found to be upregulated and then STAT1 was inhibited in TAMs which were differentiated into immunosuppressive M2 cells.…”

Section: Necroptosis Antagonizes the Antitumor Immune Responsementioning

confidence: 99%

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Gao

Wang

Zhou

et al. 2022

Sig Transduct Target Ther

316

189

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In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly limits the application of ICIs. Converting these immune “cold” tumors into “hot” tumors that may respond to ICIs is an unsolved question in cancer immunotherapy. Since it is a general characteristic of cancers to resist apoptosis, induction of non-apoptotic regulated cell death (RCD) is emerging as a new cancer treatment strategy. Recently, several studies have revealed the interaction between non-apoptotic RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, and necroptosis exhibit synergistic antitumor immune responses while possibly exerting inhibitory effects on antitumor immune responses. Thus, targeted therapies (inducers or inhibitors) against autophagy, ferroptosis, pyroptosis, and necroptosis in combination with immunotherapy may exert potent antitumor activity, even in tumors resistant to ICIs. This review summarizes the multilevel relationship between antitumor immunity and non-apoptotic RCD, including autophagy, ferroptosis, pyroptosis, and necroptosis, and the potential targeting application of non-apoptotic RCD to improve the efficacy of immunotherapy in malignancy.

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Section: Necroptosis Antagonizes the Antitumor Immune Responsementioning

confidence: 99%

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Gao

Wang

Zhou

et al. 2022

Sig Transduct Target Ther

316

189

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“…Porphyromonas gingivalis and Aggregatibacter activate, similarly to Bifidobacterium pseudolongum [ 53 ] , the TLR signaling pathway increasing the risk of PanCa development in both animal models and humans[ 28 , 54 ]. Different studies documented that mice deficient in pattern recognition receptors signaling, including TLR 4, TLR7, TLR9, and mincle, show less PanCa progression[ 53 , 55 , 56 ].…”

Section: Cancer Developmentmentioning

confidence: 99%

Impact of microbiota-immunity axis in pancreatic cancer management

Bartolini¹,

Nannini²,

Risaliti³

et al. 2022

WJG

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The microbiota impact on human diseases is well-known, and a growing body of literature is providing evidence about the complex interplay between microbiota-immune system-human physiology/pathology, including cancers. Together with the defined risk factors ( e.g. , smoke habits, diet, diabetes, and obesity), the oral, gut, biliary, and intrapancreatic microbiota contribute to pancreatic cancer development through different pathways including the interaction with the immune system. Unfortunately, a great majority of the pancreatic cancer patients received a diagnosis in advanced stages not amenable to be radically treated and potentially cured. Given the poor pancreatic cancer prognosis, complete knowledge of these complicated relationships could help researchers better understand the disease pathogenesis and thus provide early potential non-invasive biomarkers, new therapeutic targets, and tools for risk stratification that might result in greater therapeutic possibilities and eventually in a better and longer patient survival.

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“…RIPK1 was found to be upregulated in tumor-associated macrophages (TAMs) during M2 Macrophages polarization in a PDAC mice model ( 17 ). Necroptosis mediated by RIPK3 promoted the accumulation of immunosuppressive myeloid-derived suppressor cells (MDSCs) in tumor microenvironment (TME) of pancreatic cancer through producing C-x-c motif chemokine ligand 1 (CXCL1) and CXCL5 ( 18 , 19 ). In an intestinal tumor model, RIPK3 in intermediate MDSC subpopulation was found to increase tumor size ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

Single-cell RNA-seq analyses inform necroptosis-associated myeloid lineages influence the immune landscape of pancreas cancer

Dong,

Zhao,

Xiao

et al. 2023

Front. Immunol.

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IntroductionTumor-infiltrating myeloid cells (TIMs) are key regulators in tumor progression, but the similarity and distinction of their fundamental properties in pancreatic ductal adenocarcinoma (PDAC) remain elusive.MethodIn this study, we conducted scRNA-seq data analysis of cells from 12 primary tumor (PT) tissues, 4 metastatic (Met) tumor tissues, 3 adjacent normal pancreas tissues (Para), and PBMC samples across 16 PDAC patients, and revealed a heterogeneous TIMs environment in PDAC.ResultSystematic comparisons between tumor and non-tumor samples of myeloid lineages identified 10 necroptosis-associated genes upregulated in PDAC tumors compared to 5 upregulated in paratumor or healthy peripheral blood. A novel RTM (resident tissue macrophages), GLUL-SQSTM1- RTM, was found to act as a positive regulator of immunity. Additionally, HSP90AA1+HSP90AB1+ mast cells exhibited pro-immune characteristics, and JAK3+TLR4+ CD16 monocytes were found to be anti-immune. The findings were validated through clinical outcomes and cytokines analyses. Lastly, intercellular network reconstruction supported the associations between the identified novel clusters, cancer cells, and immune cell populations.ConclusionOur analysis comprehensively characterized major myeloid cell lineages and identified three subsets of myeloid-derived cells associated with necroptosis. These findings not only provide a valuable resource for understanding the multi-dimensional characterization of the tumor microenvironment in PDAC but also offer valuable mechanistic insights that can guide the design of effective immuno-oncology treatment strategies.

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Author Correction: The necrosome promotes pancreatic oncogenesis via CXCL1 and Mincle-induced immune suppression

Cited by 4 publications

References 0 publications

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy

Impact of microbiota-immunity axis in pancreatic cancer management

Single-cell RNA-seq analyses inform necroptosis-associated myeloid lineages influence the immune landscape of pancreas cancer

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