MiRNA is a type of small non-coding RNA, by regulating downstream gene expression that affects the progression of multiple diseases, especially cancer. MiRNA can participate in the biological processes of tumor, including proliferation, invasion and escape, and exhibit tumor enhancement or inhibition. The tumor immune microenvironment contains numerous immune cells. These cells include lymphocytes with tumor suppressor effects such as CD8+ T cells and natural killer cells, as well as some tumor-promoting cells with immunosuppressive functions, such as regulatory T cells and myeloid-derived suppressor cells. MiRNA can affect the tumor immune microenvironment by regulating the function of immune cells, which in turn modulates the progression of tumor cells. Investigating the role of miRNA in regulating the tumor immune microenvironment will help elucidate the specific mechanisms of interaction between immune cells and tumor cells, and may facilitate the use of miRNA as a predictor of immune disorders in tumor progression. This review summarizes the multifarious roles of miRNA in tumor progression through regulation of the tumor immune microenvironment, and provides guidance for the development of miRNA drugs to treat tumors and for the use of miRNA as an auxiliary means in tumor immunotherapy.

/pdf/tumor-immune-microenvironment-and-its-related-mirnas-in-2vfsdzwv56.pdf

Tumor Immune Microenvironment and Its Related miRNAs in Tumor Progression.

Inflammation plays a decisive role in inducing tumorigenesis, promoting tumor development, tumor invasion and migration. The interaction of cancer cells with their surrounding stromal cells and inflammatory cells further forms an inflammatory tumor microenvironment (TME). The large number of cells present within the TME, such as mesenchymal stem cells (MSCs), macrophages, neutrophils, etc., play different roles in the changing TME. Exosomes, extracellular vesicles released by various types of cells, participate in a variety of inflammatory diseases and tumor-related inflammation. As an important communication medium between cells, exosomes continuously regulate the inflammatory microenvironment. In this review, we focused on the role of exosomes in inflammatory diseases and tumor-related inflammation. In addition, we also summarized the functions of exosomes released by various cells in inflammatory diseases and in the TME during the transformation of inflammatory diseases to tumors. We discussed in depth the potential of exosomes as targets and tools to treat inflammatory diseases and tumor-related inflammation.

/pdf/the-role-of-exosomes-in-inflammatory-diseases-and-tumor-2mbmt8lx.pdf

The Role of Exosomes in Inflammatory Diseases and Tumor-Related Inflammation

Integration of chemokine signaling with non-coding RNAs in tumor microenvironment and heterogeneity in different cancers.

Prostate cancer is a common male cancer with high morbidity and mortality worldwide. According to current research, the integration of long non-coding RNA (lncRNAs) and microRNA(miRNAs) can be expressed in a variety of cancers and play an important role in diagnosis. Based on this, this study explored the clinical role of lncRNA MAGI2-AS3 (MAGI2-AS3) in prostate cancer. By detecting the expression levels of MAGI2-AS3 and miR-142-3p, the correlation between the MAGI2-AS3 expression and the characteristics of clinical data was analyzed. ROC curve analysis was performed and the area under the ROC curve (AUC) was used to evaluate the diagnostic value of MAGI2-AS3 in distinguishing prostate cancer patients from healthy controls. The function of MAGI2-AS3 in prostate cancer cells was explored through CCK-8 and Transwell assays, and the relationship between MAGI2-AS3 and miR-142-3p was investigated by luciferase activity assay. MAGI2-AS3 has descended expression while miR-142-3p has an ascendant one in prostate cancer serum samples and cells. ROC curve analysis revealed that the AUC was 0.953 for MAGI2-AS3, with a sensitivity of 91.5% and specificity of 84.7%. Overexpression of MAGI2-AS3 in LNCaP and PC3 cells suppressed the biological function of the cell including proliferation capacity, migration level, and invasion. MAGI2-AS3 was considered a diagnostic biomarker for prostate cancer patients and inhibited prostate cancer progression by targeting miR-142-3p.

LncRNA MAGI2-AS3 Inhibits Prostate Cancer Progression by Targeting the miR-142-3p.

Despite significant advances in diagnostic methods and treatment strategies, the prognosis for patients with advanced colon cancer remains poor, and mortality rates are often high due to metastasis. Increasing evidence showed that it is of significant importance to investigate how the tumor microenvironment participates in the development of colorectal cancer (CRC). In this manuscript, neutrophils were sequentially stimulated with all-trans retinoic acid and transforming growth factor-β in turn to induce the neutrophil polarization. Differentially expressed miRNA in neutrophil exosomes have been sequenced by microarray profile, and the effect of N2-like neutrophil-derived exosomal miR-4780 on epithelial-mesenchymal transition (EMT) and angiogenesis was investigated. In our results, we found that neutrophils were enriched in CRC tumor tissue and that CD11b expression correlated with tumor site and serous membrane invasion. At the same time, we demonstrated that internalization of N2 exosomes exacerbated the viability, migration, and invasion of CRC cell lines and inhibited apoptosis. To further investigate the molecular mechanism, we analyzed the miRNA expression profile in the N2-like neutrophils, which led to the selection of hsa-miR-4780 for the subsequent experiment. The overexpression of miR-4780 from N2-like neutrophil-derived exosomes exacerbated EMT and angiogenesis. Moreover, miR-4780 can regulate its target gene SOX11 to effect EMT and angiogenesis in CRC cell lines. CRC with liver metastasis model also validated that aberrant expression of miR-4780 in N2-like neutrophil exosomes exacerbated tumor metastasis and development of tumor via EMT and angiogenesis. In conclusion, our current findings reveal an important mechanism by which mR-4780 from N2-like neutrophil exosomes exacerbates tumor metastasis and progression via EMT and angiogenesis. 

miR-4780 Derived from N2-Like Neutrophil Exosome Aggravates Epithelial-Mesenchymal Transition and Angiogenesis in Colorectal Cancer

Decreased expression of miR-142-3p was observed in human cancers. However, the function and mechanism of miR-142-3p in human colorectal cancer remain obscure. The expressions of miR-142-3p in human colorectal cancer tissues and cell lines were measured by RT-qPCR. The effects of miR-142-3p on cell invasion and migration were detected by transwell assays. The efficiency of aerobic glycolysis was determined by glucose consumption and lactate production. Dual-luciferase reporter assays were performed to confirm the correlation between miR-142-3p and pyruvate kinase isozyme M2 (PKM2). The level of PKM2 was assessed by western blotting. Our results showed that the expression of miR-142-3p was decreased both in human colorectal cancer tissues and in cells. Overexpression of miR-142-3p in cell line attenuated colorectal cancer cell invasion and migration. About the underlying mechanism, we found that miR-142-3p modulated aerobic glycolysis via targeting pyruvate kinase M2 (PKM2). In addition, we demonstrated PKM2 and PKM2-mediated aerobic glycolysis contributes to miR-142-3p-mediated colorectal cancer cell invasion and migration. Hence, these data suggested that miR-142-3p was a potential therapeutic target for the treatment of human colorectal cancer.

/pdf/mir-142-3p-modulates-cell-invasion-and-migration-via-pkm2-5nm62yozhz.pdf

miR-142-3p Modulates Cell Invasion and Migration via PKM2-Mediated Aerobic Glycolysis in Colorectal Cancer

Objective Colorectal cancer (CRC) is one of the most common malignant tumors in the digestive tract, which accounts for 10% of all the malignant tumors in the world The aim of this study was to identify key genes and miRNAs in CRC diagnosis, prognosis, and therapy and to further explore the potential molecular mechanisms of CRC Methods The infiltration and metastasis of neutrophils in primary colorectal cancer tissue and paracancerous tissue were observed by immunohistochemical staining After inducing N2 neutrophils with TGF-β1 in vitro, exosomes were extracted and sequenced, and then the expression differences of miRNAs were screened by using Agilent miRNA microarrays The data were imported to the Web CARMA for differential expression analysis The GO and KEGG enrichment analysis were performed using DIANA-MirPath v30 using TargetScan database And the corresponding targets were imported into Gephi for network analysis The expression level of differentially expressed miRNA using quantitative real-time polymerase chain reaction (RT-PCR) was validated Results A total of 2 miRNAs were found to be associated with N2 neutrophils, in which the expression of hsa-miR-4780 was upregulated and the expression of hsa-miR-3938 was downregulated in N2 neutrophils, compared with the neutrophils In addition, the results of miRNA-targets networks showed that the hsa-mir-3938 and hsa-mir-4780 could regulate TUSC1 and ZNF197 The expression level of hsa-miR-4780 and hsa-miR-3938 wase validated in accordance with the results of RT-PCR Conclusion The hsa-mir-3938 and hsa-mir-4780 were differentially expressed between N2 neutrophils and neutrophils Moreover, the regulation of TUSC1 and ZNF197 by these DEmiRNA established the theoretical basis for the mechanism of N2 type neutrophils regulating the invasion and metastasis of CRC cells and provided the potential biomarker for prognosis for clinical treatment of CRC

/pdf/mirna-expression-profile-in-the-n2-phenotype-neutrophils-of-1u1h8om4z3.pdf

miRNA Expression Profile in the N2 Phenotype Neutrophils of Colorectal Cancer and Screen of Putative Key miRNAs.

Long non-coding RNAs (lncRNAs) emerge as vital modulators and tissue-specific biomarkers of multiple cancers, including gastric cancer (GC). Instead, the expression characteristics, biological function and molecular mechanism of lncRNA PCED1B antisense RNA 1 (PCED1B-AS1) in GC await more elaboration. In this study, 48 cases of GC tissues and matched non-cancerous tissues were collected, and PCED1B-AS1, microRNA-215-3p (miR-215-3p) and C-X-C motif chemokine receptor 1 (CXCR1) expression levels were detected by qRT-PCR. Besides, CCK-8, EdU, Transwell and Western blot assays were conducted to assess the impact of PCED1B-AS1 or miR-215-3p on cell growth, migration, invasion and epithelial-mesenchymal transition (EMT). The interaction between genes was verified by bioinformatics analysis, rna immunoprecitipation (RIP) and dual-luciferase reporter gene assays. We demonstrated that, PCED1B-AS1 expression level was raised in GC tissues and cell lines, and increased expression of PCED1B-AS1 was in association with tumor size, TNM stage and lymph node metastasis in GC patients. Additionally, PCED1B-AS1 overexpression promoted GC cells proliferation, migration, invasion and EMT, and miR-215-3p overexpression counteracted the biological effects of PCED1B-AS1. Mechanistically, PCED1B-AS1 specifically inhibited miR-215-3p expressions, thus up-regulating CXCR1 expressions. In conclusion, PCED1B-AS1 accelerates GC progression via adsorbing miR-215-3p and up-regulating CXCR1, indicating that PCED1B-AS1 is a novel therapeutic target for treating GC.

Long non-coding RNA PCED1B antisense RNA 1 promotes gastric cancer progression via modulating microRNA-215-3p / C-X-C motif chemokine receptor 1 axis.

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miR-142-3p Modulates Cell Invasion and Migration via PKM2-Mediated Aerobic Glycolysis in Colorectal Cancer

miRNA Expression Profile in the N2 Phenotype Neutrophils of Colorectal Cancer and Screen of Putative Key miRNAs.

Long non-coding RNA PCED1B antisense RNA 1 promotes gastric cancer progression via modulating microRNA-215-3p / C-X-C motif chemokine receptor 1 axis.