M2 macrophage-derived extracellular vesicles augment immune evasion and development of colorectal cancer via a circRNA_CCDC66/microRNA-342-3p/metadherin axis

Fan, Linfeng; Xu, Guofeng; Zeng, Xiangfu

doi:10.1007/s10616-023-00577-z

Cited by 3 publications

(1 citation statement)

References 40 publications

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“…Increasing evidence reveals that non-coding RNA overexpression or depletion accelerates CRC development and growth, representing potential molecular prognostic and therapeutic biomarkers [8]. Indeed, aberrant expression of several miR-NAs, including miR-21, miR-146b, miR-342-3p, miR-185-5p, miR-675-5p, miR-128-1-5p, miR-138-5p, and miR-451, is frequently found in CRC [9][10][11][12][13][14][15][16]. Moreover, the miR-148a-3p gene, located on the 7p15.2 region of human chromosomes, also plays a critical role in the carcinogenesis and progression of many cancer types, including CRC [17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

MiR-148a-3p Promotes Colorectal Cancer Cell Ferroptosis by Targeting SLC7A11

Martino,

Balestrieri,

Aragona

et al. 2023

Cancers

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Ferroptosis, an iron-dependent form of cell death, and dysregulated microRNA (miRNA) expression correlate with colorectal cancer (CRC) development and progression. The tumor suppressor ability of miR-148a-3p has been reported for several cancers. Nevertheless, the role of miR-148a-3p in CRC remains largely undetermined. Here, we aim at investigating the molecular mechanisms and regulatory targets of miR-148a-3p in the CRC cell death mechanism(s). To this end, miR-148a-3p expression was evaluated in SW480 and SW620 cells and normal colon epithelial CCD 841 CoN cells with quantitative real-time polymerase chain reaction (qRT-PCR). Data reported a reduction of miR-148a-3p expression in SW480 and SW620 cells compared to non-tumor cells (p < 0.05). Overexpression of miR-148a selectively inhibited CRC cell viability (p < 0.001), while weakly affecting normal CCD 841 CoN cell survival (p < 0.05). At the cellular level, miR-148a-3p mimics promoted apoptotic cell death via caspase-3 activation (p < 0.001), accumulation of mitochondrial reactive oxygen species (ROS) (p < 0.001), and membrane depolarization (p < 0.001). Moreover, miR-148a-3p overexpression induced lipid peroxidation (p < 0.01), GPX4 downregulation (p < 0.01), and ferroptosis (p < 0.01), as revealed by intracellular and mitochondrial iron accumulation and ACSL4/TFRC/Ferritin modulation. In addition, levels of SLC7A11 mRNA and protein, the cellular targets of miR-148a-3p predicted by bioinformatic tools, were suppressed by miR-148a-3p’s overexpression. On the contrary, the downregulation of miR-148a-3p boosted SLC7A11 gene expression and suppressed ferroptosis. Together, these in vitro findings reveal that miR-148a-3p can function as a tumor suppressor in CRC by targeting SLC7A11 and activating ferroptosis, opening new perspectives for the rationale of therapeutic strategies through targeting the miR-148a-3p/SLC7A11 pathway.

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Section: Introductionmentioning

confidence: 99%

MiR-148a-3p Promotes Colorectal Cancer Cell Ferroptosis by Targeting SLC7A11

Martino,

Balestrieri,

Aragona

et al. 2023

Cancers

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MicroRNAs in extracellular vesicles: A potential role in cancer progression

Parashar,

Mukherjee,

Gupta

et al. 2024

Cellular Signalling

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PET microplastics increase the risk of insulin resistance and pancreatitis

Mierzejewski,

Kurzyńska,

Golubska

et al. 2024

Preprint

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Microplastics and their effects on the body have recently been of great concern. Today it is clear that they are not indifferent to human health, but the full spectrum of their impact has not yet been fully described. Pancreatic diseases are becoming increasingly common worldwide, and their etiology is not well understood. Worryingly, these diseases have been increasingly diagnosed in children over the last 20 years, which was previously considered unusual. The aim of the study was therefore to determine the changes in the pancreas caused by PET microplastics in young organisms. For this purpose, the global metabolomic profile of the pancreas of piglets treated with a low (0.1 g/day) or high dose (1 g/day) of PET microplastics for 4 weeks was determined by UPLC-MS analysis. In addition, insulin levels and various biochemical parameters in the blood were analyzed. The study showed that PET microplastics affected the physiological processes in the pancreas at both low and high doses. We found that PET microplastics increased the tissue levels of important metabolites such as glucose, γ-aminobutyric acid, lysophosphatidylcholine or lysophosphatidylethanolamine. In addition, PET microplastics increased blood insulin concentrations and dose-dependently regulated lipase, cholesterol and calcium levels. These results suggest that PET microplastics increase the risk of insulin resistance and pancreatitis.

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M2 macrophage-derived extracellular vesicles augment immune evasion and development of colorectal cancer via a circRNA_CCDC66/microRNA-342-3p/metadherin axis

Cited by 3 publications

References 40 publications

MiR-148a-3p Promotes Colorectal Cancer Cell Ferroptosis by Targeting SLC7A11

MiR-148a-3p Promotes Colorectal Cancer Cell Ferroptosis by Targeting SLC7A11

MicroRNAs in extracellular vesicles: A potential role in cancer progression

PET microplastics increase the risk of insulin resistance and pancreatitis

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