SPARC induces M2 polarization of macrophages to promote proliferation, migration, and angiogenesis of cholangiocarcinoma cells

Deng, Shikang; Yun, Jimmy; Yan, Jun; Wang, Junfeng

doi:10.4149/neo_2022_220324n333

Cited by 6 publications

(5 citation statements)

References 19 publications

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“…The proportion of macrophage2 and macrophage4 was higher in CRR patients than those in NCRR patients (Figure 5A and 5B). In CRR patients, macrophage2 expressed a high level of SPARC , an anti-inflammatory 33 and angiogenesis regulator, 34 and macrophage4 expressed a high level of HSPG2 , a gene that inhibited the inflammatory response. 27 OMIHC confirmed the results of snRNA-seq (Figure 5C and 5D).…”

Section: Resultsmentioning

confidence: 99%

Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling

Xu,

Zhang,

Chang

et al. 2024

Circ: Heart Failure

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BACKGROUND: The mechanism of cardiac reverse remodeling (CRR) mediated by the left ventricular assist device remains unclear. This study aims to identify the specific cell type responsible for CRR and develop the therapeutic target that promotes CRR. METHODS: The nuclei were extracted from the left ventricular tissue of 4 normal controls, 4 CRR patients, and 4 no cardiac reverse remodeling patients and then subjected to single-nucleus RNA sequencing for identifying key cell types responsible for CRR. Gene overexpression in transverse aortic constriction and dilated cardiomyopathy heart failure mouse model (C57BL/6J background) and pathological staining were performed to validate the results of single-nucleus RNA sequencing. RESULTS: Ten cell types were identified among 126 156 nuclei. Cardiomyocytes in CRR patients expressed higher levels of ATP5F1A than the other 2 groups. The macrophages in CRR patients expressed more anti-inflammatory genes and functioned in angiogenesis. Endothelial cells that elevated in no cardiac reverse remodeling patients were involved in the inflammatory response. Echocardiography showed that overexpressing ATP5F1A through cardiomyocyte-specific adeno-associated virus 9 demonstrated an ability to improve heart function and morphology. Pathological staining showed that overexpressing ATP5F1A could reduce fibrosis and cardiomyocyte size in the heart failure mouse model. CONCLUSIONS: The present results of single-nucleus RNA sequencing and heart failure mouse model indicated that ATP5F1A could mediate CRR and supported the development of therapeutics for overexpressing ATP5F1A in promoting CRR.

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Section: Resultsmentioning

confidence: 99%

Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling

Xu,

Zhang,

Chang

et al. 2024

Circ: Heart Failure

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“…SPARC is a matricellular protein that regulates extracellular matrix (ECM) deposition and cancer cell–ECM interaction, generating a TME favorable for metastasis (Sangaletti et al, 2008). In addition, it induces M2 polarization of macrophages and facilitates the proliferation, migration, and angiogenesis of cholangiocarcinoma (Deng et al, 2022). COL4A1 and IGFBP4 can also promote EMT of multiple types of cancer and enhance their migration and invasion (Hu et al, 2022; Praveen Kumar et al, 2014; Zhang et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

FERMT2 upregulation in CAFs enhances EMT of OSCC and M2 macrophage polarization

Ma,

Zhao,

Liu

et al. 2023

Oral Diseases

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ObjectivesFERMT2 upregulation was associated with malignant tumor behaviors, including epithelial‐to‐mesenchymal (EMT). This study aimed to characterize the expression profile of FERMT2 in oral squamous cell carcinoma (OSCC) and to explore its involvement in the tumor microenvironment sculptured by oral cancer‐associated fibroblasts (OCAFs).MaterialsPrevious bulk‐seq (TCGA‐HNSC) and single‐cell RNA‐seq data sets were retrieved for bioinformatic analysis. Human OSCC lines SCC15 and CAL27, primary normal oral fibroblasts (NOFs), OCAFs, and THP‐1 cells were used for intro studies.ResultsFERMT2 expression was significantly higher in CAFs compared with OSCC tumor cells and normal fibroblasts. Higher FERMT2 expression might independently predict unfavorable disease‐specific survival (DSS) in patients with OSCC. Knockdown of FERMT2 suppressed the expression and secretion of IGFBP7, SPARC, TIMP3, COL4A1, and IGFBP4 in OCAFs. OCAFs with FERMT2 knockdown had significantly weakened capability to induce the invasion of OSCC cells and the expression of mesenchymal markers. FERMT2 knockdown impaired the inducing effect of OCAFs on the migration of M0 macrophages and the expression of M2 macrophage markers.ConclusionsFERMT2 could modulate the production and secretion of IGFBP7, SPARC, COL4A1, and IGFBP4 in OCAFs, thereby inducing the EMT of OSCC and M2 macrophage polarization.

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“…The decreased chemokine production and the subsequent reduced recruitment of macrophages may partly explain the mechanisms underlying this effect. 128 Phenotypic alteration to the M2 state is essential for TAMs to exert their protumor effects, providing new avenues for treatment. Knockdown of SPARC via si-SPARC suppresses M2 polarization by inhibiting the PI3K/AKT signaling pathway.…”

Section: Targeting Cellular Components In the Timementioning

confidence: 99%

Igniting cold tumors of intrahepatic cholangiocarcinoma: An insight into immune evasion and tumor immune microenvironment

Zhou,

Zhang,

et al. 2024

TIME

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<p>Intrahepatic cholangiocarcinoma (ICC) is a rare hepatobiliary cancer that originates from the epithelium of the intrahepatic bile duct. The various treatments for ICC, such as chemotherapy, radiotherapy, and locoregional therapy, confer only modest improvements in survival rates. Immunotherapy, although revolutionary in cancer treatment, has found limited application in the treatment of ICCs due to the ��cold�� nature of these tumors, which is marked by scant T-cell infiltration. This characteristic makes immune checkpoint inhibitors (ICIs) unsuitable for the majority of ICC patients. Therefore, comprehensively understanding the mechanisms underlying these ��cold�� tumors is crucial for harnessing the potential of immunotherapy for treating ICC patients. This paper explores immune evasion mechanisms and the complex tumor immune microenvironment of ICC. This study provides a comprehensive overview of therapeutic strategies aimed at activating cold tumors and enhancing their immunogenicity. Furthermore, potential and promising targets for cancer vaccines and adoptive cellular therapy in the context of ICC are discussed. This endeavor strives to reveal new pathways for innovative immunotherapy strategies, with a focus on overcoming the key challenge of triggering an effective immune response in ICC patients.</p>

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SPARC induces M2 polarization of macrophages to promote proliferation, migration, and angiogenesis of cholangiocarcinoma cells

Cited by 6 publications

References 19 publications

Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling

Overexpression of ATP5F1A in Cardiomyocytes Promotes Cardiac Reverse Remodeling

FERMT2 upregulation in CAFs enhances EMT of OSCC and M2 macrophage polarization

Igniting cold tumors of intrahepatic cholangiocarcinoma: An insight into immune evasion and tumor immune microenvironment

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