Exosomes from BM-MSCs increase the population of CSCs via transfer of miR-142-3p

Li, Hongdan; Li, Feng

doi:10.1038/s41416-018-0254-z

Cited by 82 publications

(75 citation statements)

References 36 publications

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“…Nonetheless, other data confirm that miR-142-3p is indeed released in EVs, particularly from bone marrow-derived cells, and can affect target gene expression in recipient cells in a paracrine manner. This has been directly documented for macrophages [59,69,70], T cells [71][72][73], and bone marrow-derived mesenchymal stem/stromal cells [74], with uptake and activity in recipient endothelial and cancer cells [59,[69][70][71]74]. Additional data support the use of miR-142-3p as a biomarker due to elevation of circulating miR-142-3p levels in various pathological states .…”

Section: Discussionmentioning

confidence: 58%

Head and neck squamous cancer progression is marked by CLIC4 attenuation in tumor epithelium and reciprocal stromal upregulation of miR-142-3p, a novel post-transcriptional regulator of CLIC4

Carofino

Dinshaw

et al. 2019

Oncotarget

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Chloride intracellular channel 4 (CLIC4) is a tumor suppressor implicated in processes including growth arrest, differentiation, and apoptosis. CLIC4 protein expression is diminished in the tumor parenchyma during progression in squamous cell carcinoma (SCC) and other neoplasms, but the underlying mechanisms have not been identified. Data from The Cancer Genome Atlas suggest this is not driven by genomic alterations. However, screening and functional assays identified miR-142-3p as a regulator of CLIC4. CLIC4 and miR-142-3p expression are inversely correlated in head and neck (HN) SCC and cervical SCC, particularly in advanced stage cancers. In situ localization revealed that stromal immune cells, not tumor cells, are the predominant source of miR-142-3p in HNSCC. Furthermore, HNSCC single-cell expression data demonstrated that CLIC4 is lower in tumor epithelial cells than in stromal fibroblasts and endothelial cells. Tumor-specific downregulation of CLIC4 was confirmed in an SCC xenograft model concurrent with immune cell infiltration and miR-142-3p upregulation. These findings provide the first evidence of CLIC4 regulation by miRNA. Furthermore, the distinct localization of CLIC4 and miR-142-3p within the HNSCC tumor milieu highlight the limitations of bulk tumor analysis and provide critical considerations for both future mechanistic studies and use of miR-142-3p as a HNSCC biomarker.

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Section: Discussionmentioning

confidence: 58%

Head and neck squamous cancer progression is marked by CLIC4 attenuation in tumor epithelium and reciprocal stromal upregulation of miR-142-3p, a novel post-transcriptional regulator of CLIC4

Carofino

Dinshaw

et al. 2019

Oncotarget

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“…The combined action of MSCs, exosomes, and miRNAs has gradually appeared . Exosomes originated from BM‐MSCs increase CSCs population via transfer of miR‐142‐3p . While exosomal miR‐23b derived from BM‐MSCs promotes the dormancy of metastatic breast cancer cells .…”

Section: Introductionmentioning

confidence: 99%

Exosomal miRNA‐1231 derived from bone marrow mesenchymal stem cells inhibits the activity of pancreatic cancer

et al. 2019

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Pancreatic cancer (PC) is a highly malignant tumor with increased morbidity and mortality, which is difficult to diagnose and cure in the clinic. Through secreting exosomes containing biological molecules, including diverse RNAs and proteins, bone marrow mesenchymal stem cells (BM‐MSCs) influence the immunity, inflammation, tumor environment, and cancer metastasis. In this study, low expression of miRNA‐1231 (miR‐1231) in exosomes derived from the peripheral blood was significantly correlated with the TNM stage of PC, suggesting the potential inhibitory effect of exosomal miR‐1231 on PC occurrence and development. The proliferation, migration, invasion, and adhesion to the matrix of PC cells BxPC‐3 and PANC‐1 were negatively regulated by exosomes derived from the supernatants of BM‐MSCs that transfected with miR‐1231 oligonucleotides. Simultaneously, tumor growth in vivo was seriously restrained in BALB/C nude mice by tail vein injection with exosomes originated from BM‐MSCs that transfected with miR‐1231 mimics. The exosomes extracted from BM‐MSCs with high level of miR‐1231 inhibit the activity of PC, providing the potential application for developing new and efficient medicine for cancer therapy, especially for PC treatment. The exosomal miR‐1231 of peripheral blood may also be a potential indicator for PC diagnosis in the future.

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“…A recent study provides a novel notion that miR-200c and miR-141 contain in exosomes of mesenteric vein plasma could predict colon cancer patients with poor prognosis [15]. Exosomes derived from bone marrow-derived mesenchymal stem/stromal cells also enlarge the population of colon cancer stem cells by treating colon cancer cells (HCT-116, HT-29 and SW480) [16]. Therefore, it is important to explore the mechanisms by which exosomes derived from CRC cells regulate CRC progression, especially the metastatic process.…”

mentioning

confidence: 99%

Exosomal MALAT1 sponges miR-26a/26b to promote the invasion and metastasis of colorectal cancer via FUT4 enhanced fucosylation and PI3K/Akt pathway

Xiao

Liu

et al. 2020

J Exp Clin Cancer Res

100

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Background: Exosomes are vesicles of endocytic origin released by various cell types and emerging as important mediators in tumor cells. Human metastases-associated lung adenocarcinoma transcript 1 (MALAT1) is a long noncoding RNA known to promote cell proliferation, metastasis, and invasion in colorectal cancer (CRC).Methods: The expression of MALAT1 was analyzed in CRC using qRT-PCR. FUT4 and fucosylation levels were detected in CRC clinical samples and CRC cell lines by immunofluorescent staining, western blot and lectin blot analysis. CRC derived exosomes were isolated and used to examine their tumor-promoting effects in vitro and in vivo. Results:The invasive and metastatic abilities of primary CRC cells were enhanced after exposure to exosomes derived from highly metastatic CRC cells, which increased the fucosyltransferase 4 (FUT4) levels and fucosylation not by directly transmitting FUT4 mRNA. Exosomal MALAT1 increased FUT4 expresssion via sponging miR-26a/26b. Furthermore, MALAT1/miR-26a/26b/FUT4 axis played an important role in exosome-mediated CRC progression. Exosomal MALAT1 also mediated FUT4-associated fucosylation and activated the PI3K/AKT/mTOR pathway.Conclusions: These data indicated that exosomal MALAT1 promoted the malignant behavior of CRC cells by sponging miR-26a/26b via regulating FUT4 and activating PI3K/Akt/mTOR pathway.Keywords: CRC, Exosomal MALAT1, FUT4, miR-26a/26b, PI3K/Akt/mTOR pathway Background Colorectal cancer (CRC) is one of the leading causes of cancer-related morbidity and mortality [1,2]. More than 60% of CRC patients have initiated the metastatic process by the time of diagnosis [3]. Although there are multiple tests available for CRC screening, each method has its own limitations in terms of sensitivity and specificity. To the best of our knowledge, carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) are well established tumor markers with low sensitivity and specificity for early detection of CRC [4]. Hence, ideal CRC-specific biomarkers are urgently required to improve the current CRC diagnostic strategies.Exosomes, membrane vesicles of endocytic origin ranging in size from 30 to 150 nm approximately, are emerging as key players in intercellular communication between cancer cells and their microenvironment [5]. A distinct feature of exosomes is that they efficiently carry and deliver molecular signatures (proteins, lipids, RNA

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Exosomes from BM-MSCs increase the population of CSCs via transfer of miR-142-3p

Abstract: Our findings indicate that BM-MSC-derived exosomes promote colon cancer stem cell-like traits via miR-142-3p.

Cited by 82 publications

References 36 publications

Head and neck squamous cancer progression is marked by CLIC4 attenuation in tumor epithelium and reciprocal stromal upregulation of miR-142-3p, a novel post-transcriptional regulator of CLIC4

Head and neck squamous cancer progression is marked by CLIC4 attenuation in tumor epithelium and reciprocal stromal upregulation of miR-142-3p, a novel post-transcriptional regulator of CLIC4

Exosomal miRNA‐1231 derived from bone marrow mesenchymal stem cells inhibits the activity of pancreatic cancer

Exosomal MALAT1 sponges miR-26a/26b to promote the invasion and metastasis of colorectal cancer via FUT4 enhanced fucosylation and PI3K/Akt pathway

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