Correction: LncRNA MYLK-AS1 facilitates tumor progression and angiogenesis by targeting miR-424-5p/E2F7 axis and activating VEGF R-2 signaling pathway in hepatocellular carcinoma.
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ABSTRACT:
SUBMITTER: Teng F
PROVIDER: S-EPMC10542228 | biostudies-literature | 2023 Sep
REPOSITORIES: biostudies-literature
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Correction: LncRNA MYLK-AS1 facilitates tumor progression and angiogenesis by targeting miR-424-5p/E2F7 axis and activating VEGF R-2 signaling pathway in hepatocellular carcinoma.
Teng Fei F Zhang Ju-Xiang JX Chang Qi-Meng QM Wu Xu-Bo XB Tang Wei-Guo WG Wang Jian-Fa JF Feng Jin-Feng JF Zhang Zi-Ping ZP Hu Zhi-Qiu ZQ
Journal of experimental & clinical cancer research : CR 20230930 1
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Project description:BackgroundLong non-coding RNAs (lncRNAs) are crucial in the invasion, angiogenesis, progression, and metastasis of hepatocellular carcinoma (HCC). The lncRNA MYLK-AS1 promotes the growth and invasion of HCC through the EGFR/HER2-ERK1/2 signaling pathway. However, the clinical significance of MYLK-AS1 in HCC still needs to be further determined.MethodsBioinformatic analysis was performed to determine the potential relationship among MYLK-AS1, miRNAs and mRNAs. A total of 156 samples of normal liver and paired HCC tissues from HCC patients were used to evaluate MYLK-AS1 expression by qRT-PCR. Human HCC cell lines were used to evaluate the colony formation, cell proliferation, migration, invasion, cell cycle and apoptosis after transfection of lentiviral short-hairpin RNAs (shRNAs) targeting MYLK-AS1 or MYLK-AS1 vectors. The competitive endogenous RNA (ceRNA) mechanism was clarified using fluorescence in situ hybridization (FISH), Western blotting, qPCR, RNA binding protein immunoprecipitation (RIP), and dual luciferase reporter analysis.ResultsMYLK-AS1 up-regulation was detected in the HCC tumor tissues and cell lines associated with the enhancement of the angiogenesis and tumor progression. The down-regulation of MYLK-AS1 reversed the effects on angiogenesis, proliferation, invasion and metastasis in the HCC cells and in vivo. MYLK-AS1 acted as ceRNA, capable of regulating the angiogenesis in HCC, while the microRNA miR-424-5p was the direct target of MYLK-AS1. Promoting the angiogenesis and the tumor proliferation, the complex MYLK-AS1/miR-424-5p activated the VEGFR-2 signaling through E2F7, whereas the specific targeting of E2F transcription factor 7 (E2F7) by miR-424-5p, was indicated by the mechanism studies.ConclusionsMYLK-AS1 and E2F7 are closely related to some malignant clinicopathological features and prognosis of HCC, thus the MYLK-AS1/ miR-424-5p/E2F7 signaling pathway might represent a promising treatment strategy to combat HCC.
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Project description:Previous studies have indicated that long non-coding RNA (lncRNA) down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) serves an oncogenic role in numerous cancer types. However, its role in endometrial cancer (EC) remains largely unknown. In the present study, DSCAM-AS1 expression levels in EC tissues and cells and their normal counterparts were analyzed using reverse transcription-quantitative. In vitro and in vivo experiments were conducted to validate the functions of DSCAM-AS1 in EC. It was revealed that DSCAM-AS1 was expressed at a high level in EC tissues and cells after analyzing patient data and data obtained from The Cancer Genome Atlas. Notably, it was also revealed that high DSCAM-AS1 expression was associated with a less favorable overall survival in patients with EC. Knockdown of DSCAM-AS1 was able to suppress EC cell proliferation by upregulating cell apoptosis in vitro. Furthermore, it was revealed that DSCAM-AS1 acted as a microRNA (miR)-136-5p sponge to exert its oncogenic roles in EC. Collectively and to the best of our knowledge, the current results provided first evidence that DSCAM-AS1 stimulated EC progression by regulating miR-136-5p, which may improve the understanding of the roles of ncRNAs in EC, and may help identify novel targets for anticancer treatment.
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Project description:The antisense transcript of SATB2 protein (SATB2-AS1) is a novel long non-coding RNA (lncRNA) which is involved in the development of colorectal cancer, breast cancer and hepatocellular carcinoma. In the present study, it was aimed to investigate the consequent situation of SATB2-AS1 in tissue and cell lines of glioma. The expression of SATB2-AS1 in glioma cases was analyzed in The Cancer Genome Atlas datasets. The glycolytic metabolism was determined in glioma cells by detection of extracellular glucose level, oxygen consumption rate and extracellular acidification rate. Cell Counting Kit-8 assay and flow cytometry were used to assess cell proliferation and apoptosis in glioma cells. The interaction between SATB2-AS1 and microRNA (miR)-671-5p was verified by bioinformatic analysis, reverse transcription-quantitative PCR, dual luciferase reporter assay and RNA immunoprecipitation assay. The expression levels of the downstream targets of SATB2-AS1 were studied by western blotting. Results demonstrated that SATB2-AS1 was a downregulated lncRNA in low grade glioma and glioblastoma. Gain-of-function assay demonstrated that SATB2-AS1 inhibited cell proliferation, and glycolytic metabolism, while induced cell apoptosis in glioma cells. SATB2-AS1 sponged and suppressed the expression of an oncogenic miRNA miR-671-5p. By regulation of miR-671-5p, SATB2-AS1 upregulated cerebellar degeneration related protein 1 (CDR1) and Visinin-like 1 (VSNL1) expression in glioma cells. miR-671-5p overexpression partially reversed the antitumor effect of SATB2-AS1 in glioma. In conclusion, the current study demonstrated that there was a downregulation of SATB2-AS1 in glioma, and SATB2-AS1 regulated miR-671-5p/CDR1 axis and miR-671-5p/VSNL1 axis in glioma.
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Project description:ObjectiveThis study aims to explore the mechanism of the miR-424-5p/E2F7 axis in hepatocellular carcinoma (HCC) and provide new ideas for targeted therapy of HCC.MethodsBioinformatics analysis was used to identify the target differentially expressed miRNA in HCC and predict its target gene. qRT-PCR was employed to verify the expression of miR-424-5p and E2F7 mRNA in HCC cells. Western blot was performed to detect the effect of miR-424-5p ectopic expression on the protein expression of E2F7. CCK-8 was used to detect proliferative activity of HCC cells and flow cytometry was carried out for analyzing cell cycle distribution. Dual luciferase reporter assay was conducted to verify the direct targeting relationship between miR-424-5p and E2F7.ResultsWe observed that miR-424-5p was down-regulated in HCC cells. CCK-8 showed that overexpression of miR-424-5p inhibited cell proliferation, and flow cytometry showed that miR-424-5p could block cells in G0/G1 phase. E2F7 was up-regulated in HCC cells, and E2F7 overexpression could facilitate the proliferative ability of HCC cells and promote the cell cycle progressing from G0/G1 to S phase. Furthermore, dual-luciferase reporter assay indicated that miR-424-5p could directly down-regulate E2F7 expression. Analysis on cell function demonstrated that miR-424-5p inhibited the proliferation of HCC cells and blocked cell cycle at G0/G1 phase by targeting E2F7.ConclusionOur results proved that E2F7 was a direct target of miR-424-5p, and miR-424-5p could regulate cell cycle and further inhibit the proliferation of HCC cells by targeting E2F7.
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Project description:Long non-coding RNAs (lncRNAs) take various effects in cancer mostly through sponging with microRNAs (miRNAs). lncRNA NR2F1-AS1 is found to promote tumour progression in hepatocellular carcinoma, endometrial cancer and thyroid cancer. However, the role of lncRNA NR2F1-AS1 in breast cancer angiogenesis remains unknown. In this study, we found lncRNA NR2F1-AS1 was positively related with CD31 and CD34 in breast cancer through Pearson's correlation analysis, while lncRNA NR2F1-AS1 transfection promoted human umbilical vascular endothelial cell (HUVEC) tube formation. In breast cancer cells, lncRNA NR2F1-AS1 enhanced the HUVEC proliferation, tube formation and migration ability through tumour-conditioned medium (TCM). In zebrafish model, lncRNA NR2F1-AS1 increased the breast cancer cell-related neo-vasculature and subsequently promoted the breast cancer cell metastasis. In mouse model, lncRNA NR2F1-AS1 promoted the tumour vessel formation, increased the micro vessel density (MVD) and then induced the growth of primary tumour. Mechanically, lncRNA NR2F1-AS1 increased insulin-like growth factor-1 (IGF-1) expression through sponging miRNA-338-3p in breast cancer cells and then activated the receptor of IGF-1 (IGF-1R) and extracellular signal-regulated kinase (ERK) pathway in HUVECs. These results indicated that lncRNA NR2F1-AS1 could promote breast cancer angiogenesis through IGF-1/IGF-1R/ERK pathway.
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Project description:Resistin is an adipokine that is associated with obesity, inflammation, and various cancers. Chondrosarcomas are primary malignant bone tumors that have a poor prognosis. VEGF-A is a critical angiogenic factor that is known to promote angiogenesis and metastasis in chondrosarcoma. It is unknown as to whether resistin affects human chondrosarcoma angiogenesis. In this study, we show how resistin promotes VEGF-A expression and subsequently induces angiogenesis of endothelial progenitor cells (EPCs). Resistin treatment activated the phosphatidylinositol-3-kinase (PI3K) and Akt signaling pathways, while PI3K and Akt inhibitors or siRNA diminished resistin-induced VEGF-A expression. In vitro and in vivo studies revealed the downregulation of micro RNA (miR)-16-5p in resistin-induced VEGF-A expression and EPCs angiogenesis. We also found a positive correlation between resistin and VEGF-A expression, and a negative correlation between resistin and VEGF-A with miR-16-5p in chondrosarcoma patients. These findings reveal that resistin facilitates VEGF-A expression and angiogenesis through the inhibition of miR-16-5p expression via PI3K/Akt signaling cascades. Resistin may be a promising target in chondrosarcoma angiogenesis.
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Project description:Long non-coding RNAs (lncRNAs) play a crucial role in tumor generation and progression. However, the exact functional significance and underlying molecular mechanism by which lncRNA CERS6-AS1 operates in the context of lung adenocarcinoma (LUAD) remain unknown. We aimed to evaluate the potential role of the CERS6-AS1/miR-424-5p/ANLN axis in the progression of LUAD through bioinformatics and cytobehavioral experiments, and to provide a new insight into the combined treatment of LUAD. Based on the TCGA database, the expression of CERS6-AS1 in pan-cancer was evaluated, and its prognostic performance in LUAD was evaluated by ROC curve, survival curve and COX analysis. In addition, quantification of CERS6-AS1 expression levels in LUAD patients and lung cancer cells using quantitative real-time polymerase chain reaction (RT-qPCR), and further validate the functional significance of CERS6-AS1 in promoting the proliferation, migration, and invasion abilities of lung cancer cells. The competitive endogenous RNA (ceRNA) network was constructed, and miR-424-5p inhibitors were applied to CERS6-AS1 knockdown cells. The potential downstream genes associated with the regulatory axis of CERS6-AS1/miR-424-5p were analyzed by PPI network and gene enrichment analysis (KEGG). Finally, we evaluated the prognostic value of high expression of ANLN in LUAD and its effects on immune cell infiltration, tumor mutation burden, chemotherapy response, and immunotherapy. CERS6-AS1 expression was significantly elevated in both LUAD patients and lung cancer cells. In the CERS6-AS1 knockdown assay, the proliferation, invasion, migration and epithelial-mesenchymal transformation (EMT) of cancer cells were significantly inhibited. Notably, there was a prominent upregulation of miR-424-5p expression in cells where CERS6-AS1 was knocked down. Co-transfection of siRNA and miR-424-5p inhibitors into lung cancer cells restored the restriction on lung cancer cells. Anillin (ANLN) has been identified as a potential target gene for miR-424-5p and as a prognostic and immune biomarker associated with immune cell infiltration and tumor mutational burden in LUAD. Additionally, ANLN impacts the efficacy of chemotherapy and immunotherapy in LUAD patients. This study reveals a novel regulatory mechanism in which CERS6-AS1 may contribute to the progression of LUAD by influencing the expression of ANLN as a competitive sponge for miR-424-5p.
| S-EPMC10716711 | biostudies-literature
Project description:BackgroundDelayed fracture healing (DFH) is a significant burden for patients. Therefore, early diagnosis and detection are important for the treatment of DFH. The long non-coding RNA (LncRNA) MYLK-AS1 is abnormally expressed in patients with DFH and has the potential to be used as a diagnostic marker.Methods40 patients with DFH and 87 patients with normal fracture healing were included. The levels of MYLK-AS1, miR-146a-5p and several mRNA markers of osteogenic differentiation were assessed by RT-qPCR. The diagnostic value of MYLK-AS1, miR-146a-5p was assessed using ROC curves. Cell proliferation ability was assessed by CCK-8, and apoptosis rate was detected by flow cytometry. DLR, RIP and RNA pull down assays demonstrated the targeting relationship between MYLK-AS1 and miR-146a-5p.ResultsMYLK-AS1 levels were significantly lower and miR-146a-5p levels were significantly up-regulated in DFH compared to normal healing patients. MYLK-AS1 was found to target miR-146a-5p, and the levels were negatively correlated with each other. MYLK-AS1 with miR-146a-5p is of high value for the diagnosis of DFH. High expression of MYLK-AS1 could inhibit miR-146a-5p levels, support cell proliferation, reduce apoptosis, and increase the levels of osteogenesis-specific matrix proteins and osteogenesis-related regulatory factors.ConclusionMYLK-AS1 has potential as a diagnostic marker for DFH. By increasing the expression level of MYLK-AS1 in cells can reduce the level of miR-146a-5p, increase the activity of osteoblasts and reduce their apoptosis rate, thus affecting the process of fracture healing.
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