Homo sapiens
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PROVIDER: PRJNA103659 | ENA |
REPOSITORIES: ENA
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Project description:The microRNAs miR-373 and miR-520c promote tumor migration, invasion and metastasis
| PRJNA103659 | ENA
Project description:MicroRNAs (miRNAs) are single-stranded noncoding RNAs that play important roles in many biological processes. Although the oncogenic and tumor suppressive functions of several miRNAs have been characterized, the role of miRNAs in mediating tumor metastasis was only recently addressed and still remain largely unexplored. To identify potential metastasis-promoting miRNAs, we set up a genetic screen using a non-metastatic human breast tumor cell line that was transduced with a miRNA expression library and subjected to a trans-well migration assay. We found human miR-373 and 520c to stimulate cancer cell migration as well as tumor cell invasion in vitro and in vivo, and that certain cancer cell lines depend on endogenous miR-373 activity to migrate efficiently. Mechanistically, the migration phenotype of miR-373 and miR-520c can be explained by their suppression of CD44 expression. Finally, we found significant up-regulation of miR-373 expression in clinical breast cancer primary and metastasis samples that inversely correlated with CD44 expression. Taken together, our study indicates that miRNAs are involved in tumor migration and invasion and implicates miR-373 and conceivably miR-520c as metastasis-promoting miRNAs. Keywords: human breast cancer cell MCF7 vs MCF7 expressing miR-373 vs MCF7 expressing miR-520c
2007-12-04 | GSE9742 | GEO
Project description:To metastasize, a tumor cell must acquire abilities such as the capacity to colonize new tissue and evade immune surveillance. Recent evidence suggests that microRNAs can promote the evolution of malignant behaviors by regulating multiple targets simultaneously. We performed a microRNA analysis of human melanoma, an aggressively invasive cancer, and found that miR-30b/30d upregulation correlates with stage, metastatic potential of primary tumors, shorter time to recurrence and reduced overall survival. Ectopic expression of miR-30b/30d promoted the metastatic behavior of melanoma cells by directly targeting the GalNAc transferase GALNT7, resulted in increased synthesis of the immunosuppressive cytokine IL-10, and reduced immune cell activation and recruitment. These data point to a key role of miR-30b/30d and GalNAc transferases in metastasis, by simultaneously promoting cellular invasion and immune suppression. MicroRNAs are emerging as key contributors to tumor metastasis because of their ability to regulate multiple targets, and thereby alter several functions, simultaneously. We found a miRNA cluster that promotes metastasis by concurrently enhancing invasive capabilities of melanoma cells and suppressing immune surveillance mechanisms, allowing the tumor cells to migrate and invade foreign tissue. Both these effects of miR-30b/30d are mediated by direct suppression of GalNAc transferases. Aberrant glycosylation has previously been connected to tumor progression, but the underlying molecular mechanisms and their impact on specific cellular pathways are poorly understood. Our work places the control of glycosylation as a novel molecular link between tumor cell migration and immune evasion, two processes that act synergistically during metastasis. 2 different melanoma cell line, 2 biological duplicates for each cell line Differentially expressed genes (mRNAs) in response to miRNA over-expression
2011-03-08 | E-GEOD-27718 | biostudies-arrayexpress
Project description:Tumor-associated macrophages (TAMs)，the main part of immune cells in tumor microenvironment (TME)，play a potent role in promoting tumorigenesis through mechanisms such as stimulating angiogenesis, enhancing tumor migration and suppressing antitumor immunity. MicroRNAs (miRNAs) are considered as crucial regulators in multiple biological processes. The relationship between miRNAs and macrophages function has been extensively reported, but the roles that miRNAs play in regulating TAMs phenotype remains unclear. In this study, we screened highly-expressed microRNAs in TAMs, and first identified that miR-100 represented a TAMs-high expression pattern and maintained TAMs phenotype by targeting mTOR signaling pathway. Moreover, miR-100 expression level in TAMs was positively related to IL-1ra secretion, a traditional immune-suppressive cytokine, which was determined to promote tumor cells stemness via stimulating Hedgehog pathway. Mechanism study suggested that mTOR/Stat5a pathway was involved in IL-1ra transcriptional regulation process mediated by miR-100. More importantly, tumor metastasis and invasion capacity were significantly decreased in a 4T1 mouse breast cancer model injected intratumorally with miR-100 antagomir, and combination therapy with cisplatin showed much better benefit. In this study, we confirmed that highly expressed miR-100 maintains the phenotype of TAMs and promotes tumor metastasis via enhancing IL-1ra secretion. Interfering miR-100 expression of TAMs in mouse breast cancer model could inhibit TAMs pro-tumor function and reduce tumor metastasis, which suggested that miR-100 could serve as a potential therapy target to remodel tumor microenvironment in breast cancer.
2019-06-03 | GSE115295 | GEO
Project description:To metastasize, a tumor cell must acquire abilities such as the capacity to colonize new tissue and evade immune surveillance. Recent evidence suggests that microRNAs can promote the evolution of malignant behaviors by regulating multiple targets simultaneously. We performed a microRNA analysis of human melanoma, an aggressively invasive cancer, and found that miR-30b/30d upregulation correlates with stage, metastatic potential of primary tumors, shorter time to recurrence and reduced overall survival. Ectopic expression of miR-30b/30d promoted the metastatic behavior of melanoma cells by directly targeting the GalNAc transferase GALNT7, resulted in increased synthesis of the immunosuppressive cytokine IL-10, and reduced immune cell activation and recruitment. These data point to a key role of miR-30b/30d and GalNAc transferases in metastasis, by simultaneously promoting cellular invasion and immune suppression. MicroRNAs are emerging as key contributors to tumor metastasis because of their ability to regulate multiple targets, and thereby alter several functions, simultaneously. We found a miRNA cluster that promotes metastasis by concurrently enhancing invasive capabilities of melanoma cells and suppressing immune surveillance mechanisms, allowing the tumor cells to migrate and invade foreign tissue. Both these effects of miR-30b/30d are mediated by direct suppression of GalNAc transferases. Aberrant glycosylation has previously been connected to tumor progression, but the underlying molecular mechanisms and their impact on specific cellular pathways are poorly understood. Our work places the control of glycosylation as a novel molecular link between tumor cell migration and immune evasion, two processes that act synergistically during metastasis.
2011-03-08 | GSE27718 | GEO
Project description:The chromosome 8q21 locus, which contains NKX3.1 and microRNA (miR)-3622 family (miR-3622a/b), is a frequently deleted region in human prostate cancer. Thus, miR-3622 is proposed as a tumor suppressor in various cancers, including prostate cancer, but its role remains debatable. In the present study, we found that mature miR-3622b-3p expression was higher in human prostate cancer than in normal prostate, while expression of miR-3622a was downregulated in human prostate cancer. Also, miR-3622b-3p facelifted cell proliferation, migration and invasion, whereas miR-3622a-3p inhibited cell migration and invasion but not proliferation in human prostate cancer cells. To address the role of miR-3622 locus, we knockout (KO) endogenous miR-3622, including both miR-3622a/b, in various human prostate cancer cell lines. Our data showed that miR-3622 KO reduced cell proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo. Functional analysis revealed that miR-3622 regulated p53 downstream gene network, including p21, c-MYC, and AIFM2, to control the cell cycle and apoptosis. Furthermore, using CRISPR interference, miRNA/mRNA immunoprecipitation assay, and dual-luciferase assay, we identified AIFM2, a direct target gene of miR-3622b-3p, that is responsible for miR-3622 KO-induced apoptosis. Also, we established a miR-3622-AIFM2 axis that contributes to oncogenic function during tumor progression. In addition, miR-3622 KO inhibited the epithelial-mesenchymal transition via upregulation of vimentin involved in prostate cancer metastasis. Our results suggest that miR-3622b-3p is overexpressed in human prostate cancer and plays an oncogenic role in tumor progression and metastasis via repression of p53 signaling, especially through a miR-3622-AIFM2 axis. On the other hand, deletion of miR-3622 at 8q21 locus in human prostate cancer may reduce oncogenic effects on tumor progression and metastasis.
2022-06-15 | GSE179399 | GEO
Project description:Lung cancer is an intrinsically highly metastatic disease and the leading cause of cancer-related deaths worldwide. Although discovery of molecular aberrations in lung adenocarcinomas has led to development of effective targeted therapies, corresponding “drivers” in lung squamous carcinomas (LUSC) have not materialized. Extensive molecular profiling has revealed LUSC tumors have non-recurrent somatic mutations and are largely driven by copy number alterations. Because microRNAs (miRs) play increasingly important roles in regulating metastasis-relevant pathways, we evaluated whether miRs can regulate LUSC progression. By integrating bioinformatics of the Cancer Genome Atlas (TCGA) with novel, highly metastatic LUSC models, we found that miR-671-5p is a key inhibitor of LUSC metastasis. Surprisingly, miR-671-5p regulates LUSC metastasis by inhibiting a circular RNA (circRNA), CDR1as. Although the putative function of CDR1as is through miR-7 sponging, we found miR-671-5p more potently silences an axis of CDR1as and its anti-sense transcript, cerebellar degeneration related antigen 1 (CDR1). To our knowledge, no function of CDR1 has ever been described. We found loss of CDR1as and CDR1 significantly inhibited LUSC metastases. Intriguingly, CDR1 was strongly associated with an epithelial-mesenchymal transition (EMT) program in LUSC tumors, and was sufficient to promote metastases, increased migration and substrate-independent survival, known as anoikis-resistance. CDR1, which directly interacts with AP1 and COPI subunits, no longer promoted migration and anoikis-resistance upon blockade of Golgi trafficking. Our findings reveal a miR/circRNA axis that regulates LUSC metastases through an enigmatic protein, CDR1.
2021-09-08 | PXD012286 | Pride
Project description:MicroRNAs are important cellular regulators and their dysfunctions are associated with various disease. miR-371/372/373 was found co-regulated in HBV-producing HepG2.2.15 cells when compared to its non-HBV producing maternal HepG2 cells. To obtain a glimpse of the potential influence of the enforced miR-371-372-373 cluster in HepG2 gene expression, a two-color Capitalbio 70-mer oligo microarray platform, which contained 21,329 well-characterized human gene probes, was used to identify the differentially expressed genes between miR-371-372-373-HepG2 and mock-HepG2 in two independent biological replicate. miR-371-372-373-HepG2 vs. mock-HepG2
2012-01-15 | E-GEOD-19981 | biostudies-arrayexpress
Project description:Metastasis accounts for almost 90% of breast cancer-related fatalities, making it frequent malignancy and the main reason of tumor mortality globally among women. A key player in breast cancer is the histone demethylase lysine-specific demethylase 1 (LSD1). We used LSD1 knockdown MCF7 and T47D cell exosomes to treat breast cancer cells for greatly increasing the invasion and migration of breast cancer cells for evaluating the impact of LSD1 on breast cancer invasion and migration. miR-1290 expression was downregulated in LSD1 knockdown MCF7 exosomes. Furthermore, miR-1290 could control NAT1 expression by looking through the database of miR-1290 target genes. These data provide fresh insights into the biology of breast cancer therapy by demonstrating how the epigenetic factor LSD1 stimulates the breast cancer cells’ invasion and migration via controlling exosomal miRNA.
2024-07-31 | GSE266982 | GEO
Project description:To identify tumor suppressive microRNAs repressed by DNA hypermethylation in gastric cancer (GC), we analyzed methylome and miRNome of EpCAM+/CD44+ GC cells. Among a set of microRNAs hypermethylated and downregulated in GC, mir-1271 was uncovered as a microRNA repressed by DNA hypermethylation in GC. Forced expression of mir-1271 significantly suppressed growth, migration, and invasion of GC cells both in vitro and in vivo. To identify target genes and cancer signaling pathways regulated by mir-1271, we examined differentially-expressed genes responsive to mir-1271 by performing RNA-sequencing.
2018-06-12 | GSE87785 | GEO