The matricellular protein SPARC induces inflammatory interferon-response in macrophages during aging

Ryu, Seungjin; Sidorov, Sviatoslav; Ravussin, Éric; Artyomov, Maxim N.; Iwasaki, Akiko; Wang, Andrew; Dixit, Vishwa Deep

doi:10.1016/j.immuni.2022.07.007

Cited by 59 publications

(34 citation statements)

References 86 publications

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“…Previous studies have suggested that the calcium-binding glycoprotein SPARC can transform anti-inflammatory macrophages into pro-inflammatory ones by inducing IFN-stimulated genes [15]. Consistently, our study demonstrated SPARC's impact on the balance between M1 and M2 macrophage phenotypes through co-incubation experiments with macrophages.…”

Section: Discussionsupporting

confidence: 90%

“…It has been established that SPARC is an essential Ca 2+ -binding protein involved in cell proliferation, differentiation, and migration [13]. SPARC has been associated with various pathological processes (including chronic hypoxia, pulmonary hypertension [14], cellular aging [15], inflammation, and cancer [16][17][18]) and the prognosis of neuroendocrine tumors, including triple-negative breast cancer and prostate cancer, through interactions with cathepsin D and stromal cells [16,17]. In glioblastoma, SPARC affects invasive capability by regulating the process of myelin invasion [18].…”

Section: Introductionmentioning

confidence: 99%

“…In glioblastoma, SPARC affects invasive capability by regulating the process of myelin invasion [18]. Recent studies have also indicated that SPARC polarizes anti‐inflammatory macrophages toward M1 phenotype, thereby influencing the balance between M1 and M2 macrophages, inducing proinflammatory cytokine production, and affecting the regulatory T (Treg) cell capacity [15].…”

Section: Introductionmentioning

confidence: 99%

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Citric acid promotes SPARC release in pancreatic cancer cells and inhibits the progression of pancreatic tumors in mice on a high‐fat diet

Xiao,

Wei,

Xie

et al. 2024

The FEBS Journal

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Over the years, pancreatic cancer has experienced a global surge in incidence and mortality rates, largely attributed to the influence of obesity and diabetes mellitus on disease initiation and progression. In this study, we investigated the pathogenesis of pancreatic cancer in mice subjected to a high‐fat diet (HFD) and observed an increase in citric acid expenditure. Notably, citrate treatment demonstrates significant efficacy in promoting tumor cell apoptosis, suppressing cell proliferation, and inhibiting tumor growth in vivo. Our investigations revealed that citrate achieved these effects by releasing secreted protein acidic and rich in cysteine (SPARC) proteins, repolarizing M2 macrophages into M1 macrophages, and facilitating tumor cell apoptosis. Overall, our research highlights the critical role of citric acid as a pivotal metabolite in the intricate relationship between obesity and pancreatic cancer. Furthermore, we uncovered the significant metabolic and immune checkpoint function of SPARC in pancreatic cancer, suggesting its potential as both a biomarker and therapeutic target in treating this patient population.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Citric acid promotes SPARC release in pancreatic cancer cells and inhibits the progression of pancreatic tumors in mice on a high‐fat diet

Xiao,

Wei,

Xie

et al. 2024

The FEBS Journal

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“…Single-cell sequencing findings have confirmed that MS4A7 is highly expressed in some macrophages ( 24 ), and can be used as an immune signature to predict ovarian cancer prognoses ( 25 ). SPARC, a CR-mimetic adipokine, induces inflammatory interferon response in macrophages during aging ( 26 ). SPARC is a tumor suppressor in some studies and a tumor promoter in others, depending on tissue and cell type ( 27 ).…”

Section: Discussionmentioning

confidence: 99%

“…SPARC, a CR-mimetic adipokine, induces inflammatory interferon response in macrophages during aging (26). SPARC is a tumor suppressor in some studies and a tumor promoter in others, depending on tissue and cell type (27).…”

Section: Discussionmentioning

confidence: 99%

Model for predicting immunotherapy based on M2 macrophage infiltration in TNBC

Feng

Zhong

et al. 2023

Front. Immunol.

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IntroductionCompared to other types of breast cancer, triple-negative breast cancer (TNBC) does not effectively respond to hormone therapy and HER2 targeted therapy, showing a poor prognosis. There are currently a limited number of immunotherapeutic drugs available for TNBC, a field that requires additional development.MethodsCo-expressing genes with M2 macrophages were analyzed based on the infiltration of M2 macrophages in TNBC and the sequencing data in The Cancer Genome Atlas (TCGA) database. Consequently, the influence of these genes on the prognoses of TNBC patients was analyzed. GO analysis and KEGG analysis were performed for exploring potential signal pathways. Lasso regression analysis was conducted for model construction. The TNBC patients were scored by the model, and patients were divided into high- and low-risk groups. Subsequently, the accuracy of model was further verified using GEO database and patients information from the Cancer Center of Sun Yat-sen University. On this basis, we analyzed the accuracy of prognosis prediction, correlation with immune checkpoint, and immunotherapy drug sensitivity in different groups.ResultsOur findings revealed that OLFML2B, MS4A7, SPARC, POSTN, THY1, and CD300C genes significantly influenced the prognosis of TNBC. Moreover, MS4A7, SPARC, and CD300C were finally determined for model construction, and the model showed good accuracy in prognosis prediction. And 50 immunotherapy drugs with therapeutic significance in different groups were screened, which were assessed possible immunotherapeutics that have potential application and demonstrated the high precision of our prognostic model for predictive analysis.ConclusionMS4A7, SPARC, and CD300C, the three main genes used in our prognostic model, offer good precision and clinical application potential. Fifty immune medications were assessed for their ability to predict immunotherapy drugs, providing a novel approach to immunotherapy for TNBC patients and a more reliable foundation for applying drugs in subsequent treatments.

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Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment

Zhang,

Guo,

et al. 2024

Cancer Communications

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The intrinsic oncogenic mechanisms and properties of the tumor microenvironment (TME) have been extensively investigated. Primary features of the TME include metabolic reprogramming, hypoxia, chronic inflammation, and tumor immunosuppression. Previous studies suggest that senescence‐associated secretory phenotypes that mediate intercellular information exchange play a role in the dynamic evolution of the TME. Specifically, hypoxic adaptation, metabolic dysregulation, and phenotypic shifts in immune cells regulated by cellular senescence synergistically contribute to the development of an immunosuppressive microenvironment and chronic inflammation, thereby promoting the progression of tumor events. This review provides a comprehensive summary of the processes by which cellular senescence regulates the dynamic evolution of the tumor‐adapted TME, with focus on the complex mechanisms underlying the relationship between senescence and changes in the biological functions of tumor cells. The available findings suggest that components of the TME collectively contribute to the progression of tumor events. The potential applications and challenges of targeted cellular senescence‐based and combination therapies in clinical settings are further discussed within the context of advancing cellular senescence‐related research.

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The matricellular protein SPARC induces inflammatory interferon-response in macrophages during aging

Cited by 59 publications

References 86 publications

Citric acid promotes SPARC release in pancreatic cancer cells and inhibits the progression of pancreatic tumors in mice on a high‐fat diet

Citric acid promotes SPARC release in pancreatic cancer cells and inhibits the progression of pancreatic tumors in mice on a high‐fat diet

Model for predicting immunotherapy based on M2 macrophage infiltration in TNBC

Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment

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