Exosomal transfer of miR-126 promotes the anti-tumour response in malignant mesothelioma: Role of miR-126 in cancer-stroma communication

Monaco, Francesca Roversi; Gaetani, Simona; Alessandrini, Federica; Tagliabracci, Adriano; Bracci, Massimo; Valentino, Matteo; Neužil, Jiřı́; Amati, Monica; Bovenzi, Massimo; Tomasetti, Marco; Santarelli, Lory

doi:10.1016/j.canlet.2019.08.001

Cited by 45 publications

(29 citation statements)

References 31 publications

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“…Recently, many studies have found that tumor cell-derived exosomes can be secreted out of the cells, then migrate away from the primary positions for transferring all types of functional effectors (RNAs, miRNAs, and proteins, etc. ) into receptors, thereby resulting in the changes of the tumor microenvironment and consequently affecting the tumor development (Mathivanan et al, 2010;Bai et al, 2019;Monaco et al, 2019). Some serum exosome-derived miRNAs or lncRNAs have been identified to have the potential serving as biomarkers for tumor diagnosis and prognosis.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Exosome-Derived miR-486-5p Regulates Cell Cycle, Proliferation and Metastasis in Lung Adenocarcinoma via Targeting NEK2

et al. 2020

Front. Bioeng. Biotechnol.

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Objective: This study aimed to describe the mechanism of exosome-derived miR-486-5p underlying the cell cycle and progression in lung adenocarcinoma (LUAD). Methods: Bioinformatics methods were applied for identifying the differentially expressed genes (DEGs) in the GEO-LUAD dataset, predicting where the potential target miRNA was expressed and exploring the corresponding downstream target mRNA. qRT-PCR was conducted to detect the levels of the target genes in cancer cells. Thereafter, a series of in vitro experiments were performed for cell activities evaluation, including CCK-8, EdU, colony formation assay and transwell. Besides, Western blot was applied to determine the protein levels of the migration and invasion-related factors (NEK2, E-cadherin, N-cadherin, Vimentin, MMP-2, and MMP-9). Dual-luciferase reporter gene assay was employed for validating the targeted relationship between the target genes. Furthermore, nude mouse transplantation tumor experiment was conducted to further validate the role of the target miRNA in tumor development, and immunohistochemistry was used for Ki67 detection and TUNEL was applied for cell apoptosis assay. Results: miR-486-5p was observed to be enriched in serum exosomes, and seen to be significantly down-regulated in cancer tissues as well as in cancer serum exosomes. It was proven that exosomes could release miR-486-5p, thus regulating LUAD progression and affecting cell cycle. Moreover, NEK2 was identified as a target of miR-486-5p both in vivo and in vitro. Enrichment analysis revealed that NEK2 was mainly activated in cell cycle and mitosis-related pathways. Meanwhile, NEK2 was found to present significant difference in different TNM stages. Furthermore, rescue experiments indicated that the inhibitory effect of miR-486-5p overexpression on LUAD progression could be abrogated when miR-486-5p and NEK2 were simultaneously up-regulated. Conclusion: Exosome-derived miR-486-5p is responsible for cell cycle arrest as well as the inhibition of cell proliferation and metastasis in LUAD via targeting NEK2.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Exosome-Derived miR-486-5p Regulates Cell Cycle, Proliferation and Metastasis in Lung Adenocarcinoma via Targeting NEK2

et al. 2020

Front. Bioeng. Biotechnol.

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“…In normal cells, KO mouse model showed that plasmacytoid dendritic cell apoptosis rate is increased in Mir126 −/− mice, and miR-126 regulates the expression of innate response genes (e.g., Tlr7, Tlr9, Nfkb1, and Vegfr2) and directly targets the mammalian target of rapamycin pathway 49 . In pathological cells, miR-126 widely regulated cell apoptosis of various cancer cells, such as mesothelioma cells 50 and cervical cancer cells 51 .…”

Section: Discussionmentioning

confidence: 99%

NORFA, long intergenic noncoding RNA, maintains sow fertility by inhibiting granulosa cell death

Liu

Zhang

et al. 2020

Commun Biol

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Long intergenic non-coding RNAs (lincRNAs) have been proved to be involved in regulating female reproduction. However, to what extent lincRNAs are involved in ovarian functions and fertility is incompletely understood. Here we show that a lincRNA, NORFA is involved in granulosa cell apoptosis, follicular atresia and sow fertility. We found that NORFA was downregulated during follicular atresia, and inhibited granulosa cell apoptosis. NORFA directly interacted with miR-126 and thereby preventing it from binding to TGFBR2 3′-UTR. miR-126 enhanced granulosa cell apoptosis by attenuating NORFA-induced TGF-β signaling pathway. Importantly, a breed-specific 19-bp duplication was detected in NORFA promoter, which proved association with sow fertility through enhancing transcription activity of NORFA by recruiting transcription factor NFIX. In summary, our findings identified a candidate lincRNA for sow prolificacy, and provided insights into the mechanism of follicular atresia and female fertility.

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“…miRNAs play an independent role in the pathogenesis and progression of almost all types of cancers, such as non-small cell lung cancer , breast cancer , gastric carcinoma, bladder tumors and may other known tumor types. They are responsible for modulation of their cellular differentiation, as well as in regulating the transcription of their downstream targets [22][23][24][25][26][27][28][29].…”

Section: Ivyspringmentioning

confidence: 99%

High-matrix-stiffness induces promotion of hepatocellular carcinoma proliferation and suppression of apoptosis via miR-3682-3p-PHLDA1-FAS pathway

Yao

Niu

et al. 2020

J. Cancer

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Hepatocellular carcinoma (HCC) with malignant behaviors related to death causes distant metastasis and is the fourth primary cancer in the whole world, which has taken millions lives in Asian countries such as China. The novel miR-3682-3p involving high-expression-related poor prognosis in HCC tissues and cell lines indicate oncogenesis functions in vitro and in vivo. According to TCGA database, our group find several none-coding RNAs showing abnormal expression including miR-3682-3p, thus we originally confirmed the inhibition of proliferation and acceleration of apoptosis are enhanced in miR-3682-3p knock-down cell lines. Then, in nude mice transplantation assays, we found the suppressor behaviors, smaller nodules and lower speed of tumor expansion in model of injection of cell cultured and transfected shRNA-miR-3682-3p. A combination of databases (Starbase, Targetscan and MiRgator) illustrates miR-3682-3p targets PHLDA1, which shows negative correlation demonstrated by dual-luciferase reporter system. To make functional verification of PHLDA1, we upregulate the gene and rescue tests are established to confirm that miR-3682-3p suppresses PHLDA1 to promotion of cell growth. Rescue experiments finish making confirmation of relation of miR-3682-3p and PHLDA1 subsequently. Cirrhotic tissues illustrate strong correlation to higher miR-3682-3p and clinical features make the hint that high-extracellular-matrix-stiffness environment promotes such miRNA. Functional tests on different stiffness provide the proof of underlying mechanism. In conclusion, the overexpression of miR-3682-3p mediates PHLDA1 inhibition could impede apoptosis and elevate proliferation of HCC through high-extracellular-matrix-stiffness environment potentially.

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Exosomal transfer of miR-126 promotes the anti-tumour response in malignant mesothelioma: Role of miR-126 in cancer-stroma communication

Cited by 45 publications

References 31 publications

RETRACTED: Exosome-Derived miR-486-5p Regulates Cell Cycle, Proliferation and Metastasis in Lung Adenocarcinoma via Targeting NEK2

RETRACTED: Exosome-Derived miR-486-5p Regulates Cell Cycle, Proliferation and Metastasis in Lung Adenocarcinoma via Targeting NEK2

NORFA, long intergenic noncoding RNA, maintains sow fertility by inhibiting granulosa cell death

High-matrix-stiffness induces promotion of hepatocellular carcinoma proliferation and suppression of apoptosis via miR-3682-3p-PHLDA1-FAS pathway

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