Tumor cells-derived exosomal circVCP promoted the progression of colorectal cancer by regulating macrophage M1/M2 polarization

Tang, Yuncheng; Hu, Sheng; Li, Tian; Qiu, Xiaoqing

doi:10.1016/j.gene.2023.147413

Cited by 10 publications

(11 citation statements)

References 54 publications

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“…For instance, highly accumulated circVCP in exosomes from the plasma of colorectal cancer (CRC) patients and CRC cells promotes the proliferation, migration, and invasion of cancer cells, stimulating macrophage M2 polarization. 36 Besides, lung adenocarcinoma (LUAD) cell-derived exosomes induce M2 macrophage polarization by activating the JNK signaling pathway and further promoting LUAD progression. 37 However, there are few studies on the roles of esophageal cancer-derived exosomes in TAMs polarization and cancer progression.…”

Section: Discussionmentioning

confidence: 99%

Exosome-Delivered EGFR Induced by Acidic Bile Salts Regulates Macrophage M2 Polarization to Promote Esophageal Adenocarcinoma Cell Proliferation

Chen,

Ding,

et al. 2024

OTT

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Purpose Chronic gastroesophageal reflux disease (GERD) causes the abnormal reflux of acid and bile salts, which would induce Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC). EGFR, as one of main components of the exosome, plays an important role in cancer progression. Here, we investigated the role of acidic bile salts (ABS)-induced exosomal EGFR in EAC cell proliferation. Methods Electronic microscopic examination and Western blot were used to identify exosomes. Western blot, siRNA transfection, enzyme-linked immunosorbent assay, qRT-PCR, cell viability detection, mouse xenograft tumor models, and immunohistochemical staining were performed to study the function of ABS-induced exosomal EGFR in cell proliferation. Results We found that ABS improved the exosomal EGFR level of normal human esophageal epithelial cells, BE cells, and BE-associated adenocarcinoma cells. The results were confirmed in the serum-derived exosomes from healthy persons and patients suffering from GERD, BE with or without GERD, and EAC with or without GERD. Moreover, cell line-derived exosomal EGFR was found to promote macrophage M2 polarization through the PI3K-AKT pathway. The co-incubation medium of macrophages and exosomes improved cell proliferation and tumor growth, which depended on the exosomal EGFR level. CCL18 was identified as the most effective component of the co-incubation medium to promote EAC cell proliferation by binding to its receptor PITPNM3 in vitro and in vivo. Conclusion Our findings demonstrate that ABS-induced exosomal EGFR regulates macrophage M2 polarization to promote EAC proliferation. This study provides an important insight into the role of ABS in EAC development.

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Section: Discussionmentioning

confidence: 99%

Exosome-Delivered EGFR Induced by Acidic Bile Salts Regulates Macrophage M2 Polarization to Promote Esophageal Adenocarcinoma Cell Proliferation

Chen,

Ding,

et al. 2024

OTT

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“…113 More recent studies have reported that CRC cell-derived exosomes can carry circRNA to induce M2 macrophage polarization and participate in tumor diagnosis and therapy. 114 M2-polarized macrophage-derived exosomes also play an essential role in CRC progression, especially in metastasis. The metastasis of CRC cells can be facilitated by exosomes derived from M2-polarized macrophages.…”

Section: Macrophages-derived Exosomesmentioning

confidence: 99%

Exosomes in tumor‐stroma crosstalk: Shaping the immune microenvironment in colorectal cancer

Zhang,

Huo,

et al. 2024

The FASEB Journal

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Colorectal cancer (CRC) is a multifaceted disease characterized by a complex interaction between tumor cells and the surrounding microenvironment. Within this intricate landscape, exosomes have emerged as pivotal players in the tumor‐stroma crosstalk, influencing the immune microenvironment of CRC. These nano‐sized vesicles, secreted by both tumoral and stromal cells, serve as molecular transporters, delivering a heterogeneous mix of biomolecules such as RNAs, proteins, and lipids. In the CRC context, exosomes exert dual roles: they promote tumor growth, metastasis, and immune escape by altering immune cell functions and activating oncogenic signaling pathways and offer potential as biomarkers for early CRC detection and treatment targets. This review delves into the multifunctional roles of exosomes in the CRC immune microenvironment, highlighting their potential implications for future therapeutic strategies and clinical outcomes.

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“… 102 Moreover, the upregulation of exosomal circVCP can potentially enhance M1/M2 macrophage polarization through modulation of the miR-9-5p/NRP1 axis, thereby contributing to the progression of CRC. 103 CRC cells induced T cell apoptosis in vitro and in vivo by releasing EVs carrying Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand. 104 …”

Section: Colorectal Cancer-derived Exosomesmentioning

confidence: 99%

“… 96 CRC circVCP Up-regulated Regulate the miR-9-5p/NRP1 axis Immune escape Tang et al. 103 CRC lncRNA BANCR Up-regulated Activate RhoA/Rock pathway by recruiting IGF2BP2 Immune escape Ding et al. 102 CRC miR-203a-3p Up-regulated Regulate PTEN and activate the PI3K/Akt pathway.…”

Section: Current Challenges and Future Prospectsmentioning

confidence: 99%

Function and mechanism of exosomes derived from different cells as communication mediators in colorectal cancer metastasis

Yimin E,

Lu,

Zhu

et al. 2024

iScience

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Tumor cells-derived exosomal circVCP promoted the progression of colorectal cancer by regulating macrophage M1/M2 polarization

Cited by 10 publications

References 54 publications

Exosome-Delivered EGFR Induced by Acidic Bile Salts Regulates Macrophage M2 Polarization to Promote Esophageal Adenocarcinoma Cell Proliferation

Exosome-Delivered EGFR Induced by Acidic Bile Salts Regulates Macrophage M2 Polarization to Promote Esophageal Adenocarcinoma Cell Proliferation

Exosomes in tumor‐stroma crosstalk: Shaping the immune microenvironment in colorectal cancer

Function and mechanism of exosomes derived from different cells as communication mediators in colorectal cancer metastasis

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