The Role of Exosomal microRNA in Cancer Drug Resistance

Guo, Qiao Ru; Wang, Hui; Yan, Yaping; Liu, Yun; Su, Chao; Chen, Hubiao; Yan, Yan Yan; Adhikari, Rameshwar; Wu, Qiang; Zhang, Jian Ye

doi:10.3389/fonc.2020.00472

Cited by 37 publications

(25 citation statements)

References 176 publications

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“…It is currently known that tumor drug resistance mechanisms include drug efflux, altered drug metabolism, altered energy programming, DNA damage repair, cancer stem cells, and epigenetic alterations. 116 …”

Section: Exosome-mediated Metabolic Reprogramming In Cancer Progressimentioning

confidence: 99%

Exosome-mediated metabolic reprogramming: the emerging role in tumor microenvironment remodeling and its influence on cancer progression

Yang

Wang

Gong

et al. 2020

Sig Transduct Target Ther

201

147

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Metabolic reprogramming is reported to be one of the hallmarks of cancer, which is an adaptive mechanism by which fast-growing cancer cells adapt to their increasing energy demands. Recently, extracellular vesicles (EVs) known as exosomes have been recognized as crucial signaling mediators in regulating the tumor microenvironment (TME). Meanwhile, the TME is a highly heterogeneous ecosystem incorporating cancer cells, fibroblasts, adipocytes, endothelial cells, mesenchymal stem cells, and extracellular matrix. Accumulated evidence indicates that exosomes may transfer biologically functional molecules to the recipient cells, which facilitate cancer progression, angiogenesis, metastasis, drug resistance, and immunosuppression by reprogramming the metabolism of cancer cells and their surrounding stromal cells. In this review, we present the role of exosomes in the TME and the underlying mechanism of how exosomes exacerbate tumor development through metabolic reprogramming. In addition, we will also discuss the potential role of exosomes targeting metabolic process as biomarkers for tumor diagnosis and prognosis, and exosomes-mediated metabolic reprogramming as potential targets for cancer therapy. Furthermore, a better understanding of the link between exosomes and metabolic reprogramming, and their impact on cancer progression, would provide novel insights for cancer prevention and treatment in the future.

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Section: Exosome-mediated Metabolic Reprogramming In Cancer Progressimentioning

confidence: 99%

Exosome-mediated metabolic reprogramming: the emerging role in tumor microenvironment remodeling and its influence on cancer progression

Yang

Wang

Gong

et al. 2020

Sig Transduct Target Ther

201

147

View full text Add to dashboard Cite

show abstract

“…They are secreted by various cell types and can promote intercellular communication by transferring varieties of cargos, such as nucleic acid, proteins, and metabolites. 6,7 MicroRNAs (miRNAs), a family of small non-coding RNA molecules of approximately 19-25 nucleotides in length, are essential cargos delivered by exosomes. 7 We have previously identified miRNAs associated with EGFR-mutant NSCLC, such as miR-21 and miR-134/487b/655 clusters.…”

Section: Introductionmentioning

confidence: 99%

“…6,7 MicroRNAs (miRNAs), a family of small non-coding RNA molecules of approximately 19-25 nucleotides in length, are essential cargos delivered by exosomes. 7 We have previously identified miRNAs associated with EGFR-mutant NSCLC, such as miR-21 and miR-134/487b/655 clusters. 8,9 Epithelial-mesenchymal transition (EMT) induces tumor progression and drug resistance to various cytotoxic and targeted drugs, including EGFR-TKIs.…”

Section: Introductionmentioning

confidence: 99%

Exosome‐derived miR‐210 involved in resistance to osimertinib and epithelial–mesenchymal transition in EGFR mutant non‐small cell lung cancer cells

et al. 2021

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Background: Osimertinib is a third-generation epidermal growth factor receptortyrosine kinase inhibitor (EGFR-TKI) approved for the treatment of patients with EGFR-mutant non-small cell lung cancer (NSCLC). However, the mechanisms of acquired drug resistance to osimertinib have not as yet been clarified. Exosomes and microRNAs (miRNAs) are involved in carcinogenesis and drug resistance in human cancers. Methods: We used previously established osimertinib-resistant HCC827 (HCC827-OR) and PC-9 (PC-9-OR) cells. We evaluated the profiles of exosomal miRNA associated with resistance to osimertinib in EGFR-mutant NSCLC cells. Results: Epithelial-mesenchymal transition (EMT) phenomenon was observed in HCC827-OR and PC-9-OR cells. Microarray and quantitative reverse transcriptionpolymerase chain reaction analysis revealed that miR-210-3p was co-upregulated in exosomes isolated from HCC827-OR and PC-9-OR cells compared with those isolated from parental HCC827 and PC-9 cells. HCC827-OR cell-derived exosomes induced EMT changes and resistance to osimertinib in HCC827 cells. Subsequently, the induction of miR-210-3p directly promoted the EMT phenomenon and resistance to osimertinib in HCC827 cells. Conclusions: Exosomal miR-210-3p may play a crucial role in resistance to osimertinib in the tumor microenvironment of EGFR-mutant NSCLC.

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“…Dysregulation of miRNAs in CAFs and the transfer of exosomal miRNAs between cancer cells and the microenvironment are associated with chemoresistance in multiple cancer types (Tanaka et al, 2015;Qin et al, 2019;Guo et al, 2020). In pancreatic cancer, gemcitabine (GEM) treatment induced resistant CAFs that released exosomes containing SNAI1 and miRNA 164a.…”

Section: Delivering Exosomesmentioning

confidence: 99%

The Role of Tumor-Stroma Interactions in Drug Resistance Within Tumor Microenvironment

Zhou

Yang

et al. 2021

Front. Cell Dev. Biol.

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Cancer cells resistance to various therapies remains to be a key challenge nowadays. For a long time, scientists focused on tumor cells themselves for the mechanisms of acquired drug resistance. However, recent evidence showed that tumor microenvironment (TME) is essential for regulating immune escape, drug resistance, progression and metastasis of malignant cells. Reciprocal interactions between cancer cells and non-malignant cells within this milieu often reshape the TME and promote drug resistance. Therefore, advanced knowledge about these sophisticated interactions is significant for the design of effective therapeutic approaches. In this review, we highlight cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), tumor-associated neutrophils (TANs), myeloid-derived suppressor cells (MDSCs), T-regulatory lymphocytes (Tregs), mesenchymal stem cells (MSCs), cancer-associated adipocytes (CAAs), and tumor endothelial cells (TECs) existing in TME, as well as their multiple cross-talk with tumor cells, which eventually endows tumor cells with therapeutic resistance.

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The Role of Exosomal microRNA in Cancer Drug Resistance

Cited by 37 publications

References 176 publications

Exosome-mediated metabolic reprogramming: the emerging role in tumor microenvironment remodeling and its influence on cancer progression

Exosome-mediated metabolic reprogramming: the emerging role in tumor microenvironment remodeling and its influence on cancer progression

Exosome‐derived miR‐210 involved in resistance to osimertinib and epithelial–mesenchymal transition in EGFR mutant non‐small cell lung cancer cells

The Role of Tumor-Stroma Interactions in Drug Resistance Within Tumor Microenvironment

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