microRNA-let-7e in serum-derived exosomes inhibits the metastasis of non-small-cell lung cancer in a SUV39H2/LSD1/CDH1-dependent manner

Xu, Shufeng; Zheng, Lei; Kang, Liying; Xu, Hongmei; Gao, Lian

doi:10.1038/s41417-020-00216-1

Cited by 18 publications

(8 citation statements)

References 29 publications

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“…They represent potential use as biomarkers in a variety of cancers including HCC. 56 , 57 It has been demonstrated that exosomes can promote the occurrence and development of tumours and make a significant contribution to tumour invasion and metastasis. 58 Exosomes can be divided into tumour and stromal cell secretions based on their origin in the tumour microenvironment.…”

Section: Introductionmentioning

confidence: 99%

Non‐coding RNA‐associated competitive endogenous RNA regulatory networks: Novel diagnostic and therapeutic opportunities for hepatocellular carcinoma

Moghadam

Bakhshinejad

Khalafizadeh

et al. 2021

J Cellular Molecular Medi

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Hepatocellular carcinoma (HCC), as the most prevalent liver malignancy, is annually diagnosed in more than half a million people worldwide. HCC is strongly associated with hepatitis B and C viral infections as well as alcohol abuse. Obesity and nonalcoholic fatty liver disease (NAFLD) also significantly enhance the risk of liver cancer. Despite recent improvements in therapeutic approaches, patients diagnosed in advanced stages show poor prognosis. Accumulating evidence provides support for the regulatory role of non‐coding RNAs (ncRNAs) in cancer. There are a variety of reports indicating the regulatory role of microRNAs (miRNAs) in different stages of HCC. Long non‐coding RNAs (LncRNAs) exert their effects by sponging miRNAs and controlling the expression of miRNA‐targeted genes. Circular RNAs (circRNAs) perform their biological functions by acting as transcriptional regulators, miRNA sponges and protein templates. Diverse studies have illustrated that dysregulation of competing endogenous RNA networks (ceRNETs) is remarkably correlated with HCC‐causing diseases such as chronic viral infections, nonalcoholic steatohepatitis and liver fibrosis/cirrhosis. The aim of the current article was to provide an overview of the role and molecular mechanisms underlying the function of ceRNETs that modulate the characteristics of HCC such as uncontrolled cell proliferation, resistance to cell death, metabolic reprogramming, immune escape, angiogenesis and metastasis. The current knowledge highlights the potential of these regulatory RNA molecules as novel diagnostic biomarkers and therapeutic targets in HCC.

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Section: Introductionmentioning

confidence: 99%

Non‐coding RNA‐associated competitive endogenous RNA regulatory networks: Novel diagnostic and therapeutic opportunities for hepatocellular carcinoma

Moghadam

Bakhshinejad

Khalafizadeh

et al. 2021

J Cellular Molecular Medi

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“…12 Xu et al reported that exosomal miR-let-7e from serum inhibited cell proliferation, migration and invasion in vitro as well as delayed tumor growth in vivo by downregulating the expression of SUV39H2. 13 A current study indicated that the role of exogenous miRNAs in tumors was similar to that of endogenous miRNAs transported by exosomal. 14 Moreover, due to the double-layer structure of exosomes, exosomal miRNAs are remarkably stable compared to miRNAs that are not contained in exosomes.…”

Section: Introductionmentioning

confidence: 68%

Exosome-derived miR-2682-5p suppresses cell viability and migration by HDAC1-silence-mediated upregulation of ADH1A in non-small cell lung cancer

Mao

2021

Hum Exp Toxicol

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Introduction: Increasing evidence indicated that miR-2682-5p acted as a tumor suppressor in various cancers. The current study aimed to investigate the biological function of exosomal miR-2682-5p in non-small cell lung cancer (NSCLC). Methods: The expression of miR-2682-5p in NSCLC tissues and adjacent non-tumor tissues, NSCLC cell lines and human embryonic lung fibroblast, as well as serum and serum exosomes of NSCLC patients and healthy donors was detected by RT-qPCR. The effects of miR-2682-5p on the viability, migration, and apoptosis of NSCLC cells were detected by CCK-8, Transwell, and flow cytometry assays. Dual-luciferase reporter gene and RNA immunoprecipitation assays were used to evalutate the relationship between miR-2682-5p and HDAC1. Results: Low expressed miR-2682-5p was found in tumor tissues, cell lines, serum, and serum exosomes of NSCLC patients. MiR-2682-5p overexpression suppressed NSCLC cell viability and migration and promoted apoptosis, while miR-2682-5p knockdown showed the opposite results. Furthermore, exosomes from healthy donor serum inhibited NSCLC cell viability and migration and promoted apoptosis. Dual-luciferase reporter gene and RNA immunoprecipitation assays verified that HDAC1 was a target of miR-2682-5p. HDAC1 overexpression abolished the effects of miR-2682-5p mimic on NSCLC cell viability, migration, and apoptosis. Chromatin immunoprecipitation assay indicated that HDAC1 bound to the promoter region of ADH1A. Upregulation of ADH1A counteracted the effects of HDAC1 overexpression on NSCLC cell viability, migration, and apoptosis. Conclusion: Taken together, exosomal miR-2682-5p inhibited NSCLC cell viability and migration and promoted apoptosis by the HDAC1/ADH1A axis, and this result might provide a novel therapeutic target for NSCLC.

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“…A study by Li et al 103 depicted that miR‐21 was overexpressed in the EGFR‐TKI‐resistant cell line PC9R, and inhibition of miR‐21 induced tumor cell apoptosis in vitro and suppressed tumor growth in vivo. Downregulation of miR‐let‐7e was found in serum‐derived exosomes from NSCLC patients, and miR‐let‐7e overexpression in serum‐derived exosomes inhibited metastasis of NSCLC nude mice 124 . These findings imply a potential application of the exosomal miRNAs.…”

Section: The Potential Application Of Tdes In the Personalized Therap...mentioning

confidence: 74%

Tumor‐derived exosomes: Key players in non‐small cell lung cancer metastasis and their implication for targeted therapy

Rizwan

Nenkov

et al. 2021

Molecular Carcinogenesis

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Exosomes represent extracellular vesicles of endocytic origin ranging from 30 to 100 nm that are released by most of eukaryotic cells and can be found in body fluids. These vesicles in carrying DNA, RNA, microRNA (miRNA), Long noncoding RNA, proteins, and lipids serve as intercellular communicators. Due to their role in crosstalk between tumor cells and mesenchymal stroma cells, they are vital for tumor growth, progression, and anticancer drug resistance. Lung cancer is a global leading cause of cancer‐related deaths with 5‐year survival rates of about 7% in patients with distant metastasis. Although the implementation of targeted therapy has improved the clinical outcome of nonsmall cell lung cancer, drug resistance remains a major obstacle. Lung tumor‐derived exosomes (TDEs) conveying molecular information from tumor cells to their neighbor cells or cells at distant sites of the body activate the tumor microenvironment (TME) and facilitate tumor metastasis. Exosomal miRNAs are also considered as noninvasive biomarkers for early diagnosis of lung cancer. This review summarizes the influence of lung TDEs on the TME and metastasis. Their involvement in targeted therapy resistance and potential clinical applications are discussed. Additionally, challenges encountered in the development of exosome‐based therapeutic strategies are addressed.

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microRNA-let-7e in serum-derived exosomes inhibits the metastasis of non-small-cell lung cancer in a SUV39H2/LSD1/CDH1-dependent manner

Cited by 18 publications

References 29 publications

Non‐coding RNA‐associated competitive endogenous RNA regulatory networks: Novel diagnostic and therapeutic opportunities for hepatocellular carcinoma

Non‐coding RNA‐associated competitive endogenous RNA regulatory networks: Novel diagnostic and therapeutic opportunities for hepatocellular carcinoma

Exosome-derived miR-2682-5p suppresses cell viability and migration by HDAC1-silence-mediated upregulation of ADH1A in non-small cell lung cancer

Tumor‐derived exosomes: Key players in non‐small cell lung cancer metastasis and their implication for targeted therapy

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