CircRNA-0002109 promotes glioma malignant progression via modulating the miR-129-5P/EMP2 axis.
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ABSTRACT:
SUBMITTER: Xia H
PROVIDER: S-EPMC8646083 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Introduction: Circular RNAs (circRNAs) are important regulators in various cancers, especially hepatocellular carcinoma. However, the role of circ RNA PTPRM (circPTPRM) in the development of non-small-cell lung cancer (NSCLC) remains unclear. Methods: We collected 26 clinical specimens (corresponding to 26 normal lung tissues) of lung adenocarcinoma and the expression of mir-139-5p and circPTPRM were first detected. Cell proliferation was detected by EdU method, invasion/migration ability of cells was evaluated by transwell method. And the correlation between circPTPRM and mir-139-5p was detected by luciferase reporter gene and RNA pull-down assay. Finally, we verified our hypothesis with BALB/c nude mice. Results: Through bioinformatics software, we found that circPTPRM was negatively correlated with mir-139-5p, and then we used human adenocarcinoma tissue samples to further verify their relationship and get the same result. EdU method, transwell method, and luciferase assay, RNA pull-down assay were applied, and the results show that the knockdown of circPTPRM inhibit proliferation, migration, and invasion of cells can be reversed by mir-139-5p inhibitor. Next, we used Starbase v2.0 to identify the target site of miR-139-5p and focused on SET domain containing 5 (SETD5). We derive the hypothesis by verifying the relationship between miR-139-5p and SETD5 that circPTPRM may interact with miR-139-5p/SETD5 axis. At last, we evaluated the effects of circPTPRM, SETD5, and miR-139-5p on tumor growth in vivo using BALB/c nude mice to prove the hypothesis. Conclusion: We thus conclude that circPTPRM promotes the progression of NSCLC by regulating the miR-139-5p/SETD5 axis.
| S-EPMC9066640 | biostudies-literature
Project description:Circular RNAs (circRNAs) play essential roles in tumorigenesis and tumor progression. CircRNA GFRA1 (circGFRA1) was dysregulated in many cancer samples and acted as an independent marker for prediction of survivals in various cancer patients. However, the functions and molecular mechanisms of circGFRA1 in hepatocellular carcinoma (HCC) remain unclear. We collected 62 HCC tissues and normal adjacent tissues to evaluate the expression of circGFRA1 and the relationship between circGFRA1 expression and HCC patients' survival. We carried out a list of characterization experiments to investigate the roles and underling mechanisms of circGFRA1 and miR-498 in HCC progressions. CircGFRA1 was greatly increased in HCC tissues and cells, and the over-expression of circGFRA1 was intimately related with the advanced clinical stage and poor survival of HCC patients. The expression of circGFRA1 was negatively correlated with the expression of miR-498, but a positive correlation was found between circGFRA1 and NAP1L3 expression in HCC tissues. Silencing circGFRA1 inhibited the growth and invasion of hepatocellular carcinoma. Moreover, miR-498 over-expression or NAP1L3 inhibition could abrogate the oncogene role of circGFRA1 in HCC in vivo. Our findings indicated that circGFRA1 contributed to HCC progression by modulating the miR-498/NAP1L3 axis in HCC.
| S-EPMC7801409 | biostudies-literature
Project description:BackgroundNon-small cell lung cancer (NSCLC) is the most common tumor with severe morbidity and high mortality. Long non-coding RNAs (lncRNAs) as crucial regulators participate in multiple cancer progressions. However, the role of lncRNA MEG8 in the development of NSCLC remains unclear. Here, we aimed to investigate the effect of lncRNA MEG8 on the progression of NSCLC and the underlying mechanism.MethodsCell proliferation was analyzed by EdU assays. The impacts of lncRNA MEG8, miR-15a-5p, and miR-15b-5p on cell invasion and migration of NSCLC were assessed by transwell assay. The luciferase reporter gene assay was performed using the Dual-luciferase Reporter Assay System. The effect of lncRNA MEG8, miR-15a-5p, and miR-15b-5p on tumor growth was evaluated in nude mice of Balb/c in vivo.ResultsWe revealed that the expression levels of MEG8 were elevated in the NSCLC patient tissues compared to that in adjacent normal tissues. The expression of MEG8 was negatively relative to that of miR-15a-5p and miR-15b-5p in the NSCLC patient tissues. The expression of MEG8 was upregulated, while miR-15a-5p and miR-15b-5p were downregulated in NSCLC cell lines. The depletion of MEG8 inhibited NSCLC cell proliferation, migration, and invasion in vitro. MEG8 contributed to NSCLC progression by targeting miR-15a-5p/miR-15b-5p in vitro. LncRNA MEG8 contributes to tumor growth of NSCLC via the miR-15a/b-5p/PSAT1 axis in vivo. Thus, we concluded that lncRNA MEG8 promotes NSCLC progression by modulating the miR-15a/b-5p/PSAT1 axis.ConclusionsOur findings demonstrated that lncRNA MEG8 plays a critical role in NSCLC development. LncRNA MEG8, miR-15a-5p, miR-15b-5p, and PSAT1 may serve as potential targets for NSCLC therapy.
| S-EPMC7852147 | biostudies-literature
Project description:IntroductionAccumulating evidence highlights the critical roles of circular RNAs (circRNAs) in the malignant progression of cancers. In this study, we investigated the expression pattern of a newly identified circRNA (hsa_circ_0017109) in non-small cell lung cancer (NSCLC), and examined its downstream molecular targets.MethodsQuantitative real-time PCR (qRT-PCR) and Western blotting (WB) were conducted to quantify gene and protein expression. In vitro functional assays such as colony formation assay, cell counting kit-8 (CCK-8) and flow cytometry were used to study cell proliferation and apoptosis. RNA pull-down assay, luciferase reporter assay and RNA immunoprecipitation were performed to validate molecular interaction. Mouse xenograft model of NSCLC cells was used to assess the role of circ_0017109 in tumorigenesis.ResultsCirc_0017109 was upregulated in NSCLC tumor samples and cells. Silencing circ_0017109 impaired cell proliferation and promoted apoptosis in NSCLC cells, and circ_0017109 knockdown suppressed in vivo tumorigenesis of NSCLC cells in mouse xenograft model. MiR-671-5p was identified as a target of circ_0017109, and circ_0017109 negatively impacted on miR-671-5p expression. MiR-671-5p downregulated FZD4 and dampened the activity of Wnt/β-catenin signaling pathway. Circ_0017109 modulated FZD4 expression by suppressing miR-671-5p activity.ConclusionsElevated circ_0017109 expression promotes tumor progression of NSCLC by modulating miR-671-5p/FZD4/β-catenin axis.
| S-EPMC9700975 | biostudies-literature
Project description:BackgroundCircular RNA RHOT1 (circRHOT1) plays crucial roles in tumorigenesis by competing with microRNAs. It is largely abundant in tumor cell-derived exosomes. Meanwhile, cancer-derived exosomes participate in diverse biological processes. However, the expression patterns and functions of exosomal circRHOT1 in breast cancer remain unknown. This study is aimed to investigate and elucidate the exosomal circRHOT1/miR-204-5p/PRMT5 axis in breast cancer.MethodsThe exosomes derived from serum samples of breast cancer patients and breast cancer cell lines were characterized using transmission electron microscopy and Western blot. MTT, colony formation, wound healing, and transwell assays were utilized to analyze cell proliferation, migration, and invasion of breast cancer cells. Flow cytometry was used for apoptosis analysis. The bioinformatics method was employed to screen differentially expressed novel circRNAs and predict the microRNA targets of circRHOT1. Dual-luciferase reporter gene assays were performed to verify their direct interaction. Finally, Xenograft experiments were used to investigate the effect of exosomal circRHOT1 on tumor growth in vivo.ResultsCircRHOT1 exhibited significantly high expression in exosomes derived from the serum of breast cancer patients and breast cancer cell lines, which suggested its potential diagnostic value. Breast cancer-derived exosomes promoted the cell proliferation, migration, invasion, and epithelial-mesenchymal transition of breast cancer cells while inhibiting apoptosis. However, exosomes with downregulated circRHOT1 inhibited the growth of co-cultured cells. Mechanistically, circRHOT1 acted as a sponge of miR-204-5p and promoted protein arginine methyltransferase 5 (PRMT5) expression. Moreover, miR-204-5p inhibitor and pcPRMT5 could reverse the tumor suppressive effects mediated by circRHOT1-knockdown. Furthermore, treatment with exosomes derived from breast cancer cells with circRHOT1 knockdown attenuated tumor growth in tumor-bearing nude mice, which was accompanied by a reduction in PRMT5 expression and an enhancement of miR-204-5p expression.ConclusionThe exosomal circRHOT1 may promote breast cancer progression by regulating the miR-204-5p/PRMT5 axis. The current study strengthens the role of circRHOT1, miR-204-5p, and PRMT5 in breast cancer development and provides a potential treatment strategy for breast cancer.
| S-EPMC10623849 | biostudies-literature
Project description:BackgroundMultiple myeloma (MM) accounts for 10% of all hematological malignancies. Dysregulation of microRNAs (miRNAs) or long non-coding RNAs (lncRNAs) has important impacts on progression of MM. Circular RNAs (circRNAs) are correlated with malignancy in the modulation of tumor progression. This study aims to investigate the effect of circ_0000190 on regulating the progression of MM.MethodMicroscopic examination via single molecule fluorescent in situ hybridization indicates the location of circ_0000190. qRT-PCR and Western blot were used to evaluate the expression of RNAs and proteins. Potential target of circ_0000190 was searched as miRNA, and examined by luciferase reporter assay. A computational screen was also conducted to search the potential target of miRNA. In vitro cell viability, proliferation, apoptosis assays and flow cytometric were performed to assess the effects of circ_0000190 and its target on MM. Mice model of human MM was established with subcutaneous xenograft tumor, qRT-PCR and western blot were performed to detect the underlying mechanisms of circ_0000190 on MM.ResultsCirc_0000190 was located in the cytoplasm, and down-regulated in both bone marrow tissue and peripheral blood, while the target of circ_0000190, miR-767-5p, was up-regulated, suggesting a negative correlation between them. The binding ability between circ_0000190 and miR-767-5p was confirmed by luciferase reporter assay. Moreover, circ_0000190 inhibited cell viability, proliferation and induced apoptosis of MM thus inhibiting cell progression, which is partially through the negative regulation of miR-767-5p. Mitogen-activated protein kinase 4 (MAPK4) is a direct target of miR-767-5p. In addition, over-expression of miR-767-5p promoted cell progression by directly targeting and regulating MAPK4. The MM model mice with administration of circ_0000190 suppressed tumor growth and progression.ConclusionOur results revealed that the ability of circ_0000190 to protect against MM was inherited through repression of miR-767-5p, and miR-767-5p might be a tumor drive through targeting MAPK4. Therefore, a novel role of circ_0000190 on regulating the progression of MM was found, and the clinical application of circRNAs might represent a strategy in MM.
| S-EPMC6364482 | biostudies-literature
Project description:BackgroundAs one of the most common gynaecological malignant tumors, cervical cancer (CC) has become an important public health issue. Emerging evidence has revealed long non-coding RNAs (lncRNAs) are crucial regulators of biological functions in cancers, including CC. And the oncogenic role of LINC00441 has been verified in hepatocellular carcinoma (HCC). But the molecular mechanism and biological functions of LINC00441 in CC remain unknown.MethodsqRT-PCR analysis detected the expression of genes in CC tissues or cells. CCK-8, colony formation, flow cytometry, transwell, western blot assays as well as animal studies were conducted to analyze the function of LINC00441 in CC. Luciferase reporter, RIP and RNA pull down assays were applied to verify the binding relations among the indicated genes.ResultsLINC00441 was upregulated in CC tissues and cells. Further, LINC00441 depletion repressed cell proliferation and motility in vitro as well as tumor growth in vivo. LINC00441 could sponge miR-450b-5p to upregulate RAB10 expression. Finally, miR-450b-5p inhibitor or RAB10 upregulation counteracted LINC00441 knockdown-mediated function on the development of CC.ConclusionsLINC00441 drives CC progression by targeting miR-450b-5p/RAB10 axis, which might provide new idea for researching CC-related molecular mechanism.
| S-EPMC7409438 | biostudies-literature
Project description:Circular RNAs (circRNAs) are a group of noncoding RNAs derived from back-splicing events. CircRNA is reported to be involved in various tumor progressions, including glioma. Although there are a few reports of circular RNAs participating in gliomas, it is still unclear whether circular RNAs regulate the occurrence of gliomas. In our research, we found that the expression of circITGA7 in glioma tissues and glioma cells increased significantly. Knocking down circITGA7 can significantly inhibit the proliferation of glioma cells and reduce cell metastasis. Through analysis and dual-luciferase report assay, we found that circITGA7 acts as a sponge for miR-34a-5p targeting VEGFA in glioma. Our study showed that circITGA7 regulates the proliferation and metastasis of glioma cell lines (SW1783&U373) by regulating the miR-34a-5p/VEGFA pathway. In conclusion, our study revealed a regulatory loop for the circITGA7/miR-34a-5p/VEGFA axis to regulate glioma development.
| S-EPMC8148479 | biostudies-literature
Project description:BackgroundIncreasing evidence has indicated that circular RNAs (circRNAs) play vital roles in modulating tumor progression. However, regulatory roles and underlying mechanisms of circRNA circ_0072995 in epithelial ovarian cancer (EOC) are not well characterized.ResultsCirc_0072995 was up regulated in EOC afflicted tissues and cell lines (HO8910 and A2780), and was mainly located in the cytoplasm. The expression of circ_0072995 was associated with the pathological grade of EOC for respective patients. Functional experiments revealed that circ_0072995 promoted EOC cell proliferation, migration, induced apoptosis, as well as enhanced tumorigenesis in vivo. Mechanistic analyses indicated that circ_0072995 may have acted as a sponge of miR-147a such as to relieve repressive effects of miR-147a upon its target CDK6.ConclusionsOur results revealed that circ_0072995 promoted EOC progression through the circ_0072995/miR-147a/CDK6 axis and may represent a strategy for treatment of EOC afflicted patients.MethodsExpression of circ_0072995 was evaluated in 40 EOC tissue samples and cell lines by qRT-PCR. The location of circ_0072995 was determined via nuclear-cytoplasmic fractionation. A series of functional experiments facilitated determinations of effects of circ_0072995 on EOC progression in vitro, and in vivo. Underlying mechanisms and influence of circ_0072995 on EOC were confirmed by bioinformatic analyses, luciferase reporter assays, qRT-PCR, and Western blotting.
| S-EPMC7521494 | biostudies-literature
Project description:Nasopharyngeal carcinoma is a tumor with high malignancy and poor prognosis, which severely affects the health of the patients. LncRNAs and microRNAs are crucial for the occurrence and development of nasopharyngeal carcinoma, which regulate the progression of nasopharyngeal carcinoma through the ceRNA network. SCARB1 plays an essential role in nasopharyngeal carcinoma. However, the mechanism underlying the regulation of SCARB1 in nasopharyngeal carcinoma through non-coding RNAs remains unclear. Our findings indicated that the SCAT8/miR-125b-5p axis promoted the malignant progression of nasopharyngeal carcinoma by driving the expression of SCARB1. Mechanistically, the expression of SCARB1 could be regulated by the lncRNA, SCAT8 and the microRNA, miR-125b-5p. Moreover, as a ceRNA of miR-125b-5p, SCAT8 can not only regulate the expression of SCARB1, but also regulate the malignant progression of nasopharyngeal carcinoma. Notably, our results reveal a novel ceRNA regulatory network in nasopharyngeal carcinoma, which could serve as a potential target for the diagnosis and treatment of nasopharyngeal carcinoma.
| S-EPMC10069050 | biostudies-literature