Colorectal cancer tumor cell-derived exosomal miR-203a-3p promotes CRC metastasis by targeting PTEN-induced macrophage polarization

Pei, Wenhao; Wei, Ke; Wu, Yulun; Qiu, Quanwei; Zhu, Haitao; Mao, Lingyu; Shi, Xiuru; Zhang, Shiwen; Shi, Yingxiang; Tao, Shuang; Mao, Huilan; Pang, Siyan; Wang, Jing; Liu, Mulin; Wang, Wenrui; Yang, Qingling; Chen, Changjie

doi:10.1016/j.gene.2023.147692

Cited by 7 publications

(8 citation statements)

References 35 publications

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“…found that miR-203a-3p in sEVs from CRC cells act similarly to what was mentioned earlier by targeting PTEN to promote M2 polarization and assist in CRC hepatic metastasis. Additionally, they performed plasma analysis and discovered that CRC cell-derived sEVs containing miR-203a-3p might be used as a non-invasive fluid marker to identify liver metastasis ( 87 ). Therefore, we found that miRNAs in sEVs can strongly indicate diagnostic markers and trigger the onset of CRC, which could help with the subsequent CRC diagnosis and treatment.…”

Section: Extracellular Vesicles Induce M2 Polarization In Macrophagesmentioning

confidence: 99%

Tumor-derived extracellular vesicles regulate macrophage polarization: role and therapeutic perspectives

Wang,

et al. 2024

Front. Immunol.

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Extracellular vesicles (EVs) are important cell-to-cell communication mediators. This paper focuses on the regulatory role of tumor-derived EVs on macrophages. It aims to investigate the causes of tumor progression and therapeutic directions. Tumor-derived EVs can cause macrophages to shift to M1 or M2 phenotypes. This indicates they can alter the M1/M2 cell ratio and have pro-tumor and anti-inflammatory effects. This paper discusses several key points: first, the factors that stimulate macrophage polarization and the cytokines released as a result; second, an overview of EVs and the methods used to isolate them; third, how EVs from various cancer cell sources, such as hepatocellular carcinoma, colorectal carcinoma, lung carcinoma, breast carcinoma, and glioblastoma cell sources carcinoma, promote tumor development by inducing M2 polarization in macrophages; and fourth, how EVs from breast carcinoma, pancreatic carcinoma, lungs carcinoma, and glioblastoma cell sources carcinoma also contribute to tumor development by promoting M2 polarization in macrophages. Modified or sourced EVs from breast, pancreatic, and colorectal cancer can repolarize M2 to M1 macrophages. This exhibits anti-tumor activities and offers novel approaches for tumor treatment. Therefore, we discovered that macrophage polarization to either M1 or M2 phenotypes can regulate tumor development. This is based on the description of altering macrophage phenotypes by vesicle contents.

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Section: Extracellular Vesicles Induce M2 Polarization In Macrophagesmentioning

confidence: 99%

Tumor-derived extracellular vesicles regulate macrophage polarization: role and therapeutic perspectives

Wang,

et al. 2024

Front. Immunol.

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“…It could induce M2 polarization through downregulation of PTEN expression and activation of the PI3K/AKT signaling pathway. Polarized M2 macrophages secrete CXCL12, which promotes tumor metastasis through the CXCL12/CXCR4/NF-κB axis and mediates the formation of PMN for colorectal cancer liver metastasis [ 68 ]. Cooks et al found that CRC cells containing the TP53 mutant (mutp53) secrete exosomal miR-1246, which is phagocytosed by macrophages, inducing macrophage reprogramming and polarization into M2 macrophages.…”

Section: Exosomes Promote the Development Of The Microenvironment Bef...mentioning

confidence: 99%

Exosomes promote pre-metastatic niche formation in colorectal cancer

Si,

Chen,

et al. 2024

Heliyon

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“…M2 polarized macrophages secreted CXCL12, which promoted tumor metastasis through the CXCL12/CXCR4/NF-κB signaling pathway. 95 Sun et al. demonstrated that exosomes derived from CRC stem cells delivered miR-17-5p to HCT116 cells, thereby suppressing anti-tumor immunity and promoting their malignant behavior.…”

Section: Colorectal Cancer-derived Exosomesmentioning

confidence: 99%

“… Immune escape Pei et al. 95 CRC lncRNA RPPH1 Up-regulated Interacte with TUBB3 to prevent its ubiquitination Immune escape Liang et al. 100 CRC miR-106b-5p Up-regulated Activate the PI3Kγ/AKT/mTOR signaling cascade by directly suppressing PDCD4 Immune escape Yang et al.…”

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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Colorectal cancer tumor cell-derived exosomal miR-203a-3p promotes CRC metastasis by targeting PTEN-induced macrophage polarization

Cited by 7 publications

References 35 publications

Tumor-derived extracellular vesicles regulate macrophage polarization: role and therapeutic perspectives

Tumor-derived extracellular vesicles regulate macrophage polarization: role and therapeutic perspectives

Exosomes promote pre-metastatic niche formation in colorectal cancer

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

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