Whole gene expression profiling after overexpression of Evl or miR-342 in murine hematopoietic LSK cells
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ABSTRACT:
PROVIDER: PRJNA431454 | ENA |
REPOSITORIES: ENA
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Project description:Analyzing the influence of the protein-coding gene Evl or it's intronic miR-342 on hematopoietic stem and progenitor cells on gene expression level. Evl drives lymphopoiesis, whereas miR-342 deregulates myeloid signaling pathways.
2021-06-08 | GSE109600 | GEO
Project description:LncRNAs play a crucial role in regulating the progression of NSCLC, making them potential targets for cancer diagnosis and treatment. Therefore, identifying new lncRNAs as therapeutic target and comprehending their underlying regulatory mechanisms are crucial for treating NSCLC. In this study, we found that glioblastoma down-regulated RNA (GLIDR) was increased in non-response NSCLC patients with the primary treatment, and GLIDR was also highly expressed in NSCLC patients. We used bioinformatic analysis and luciferase assays to identify that microRNA-342-5p (miR-342-5p) directly targets GLIDR. MiR-342-5p overexpression inhibits NSCLC cell proliferation, migration, and invasion, whereas miR-342-5p inhibition promotes NSCLC malignancy, which can be rescued by suppressing GLIDR. Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PPARGC1A) was identified as a downstream target of miR-342-5p. PPARGC1A inhibition significantly suppresses NSCLC malignancy, whereas overexpression promotes it. The results also revealed that GLIDR overexpression reduced PPARGC1A inhibition by miR-342-5p, and increased PPARGC1A expression reversed the inhibition of NSCLC malignancies caused by decreased GLIDR. To the best of our knowledge, we are the first to discover that GLIDR promotes NSCLC progression by sponging miR-342-5p to regulate PPARGC1A expression, presenting that GLIDR act as a potential therapeutic target in NSCLC.
2023-11-16 | GSE243455 | GEO
Project description:In this experiment, we want to assess the effect of a lentiviral miR-10a and miR-335 overexpression on the transcriptome of murine LSK (Lin-,Sca-1+,c-Kit+) cells. Primary LSK cells were transduced with lentiviral miRNA overexpression constructs (control: GFP overexpression) and sorted for transduced cells (GFP+) after five days of in vitro culture (Flt-3, TPO, IL-3, SCF containing media).
2018-06-01 | E-MTAB-6496 | biostudies-arrayexpress
Project description:RAW264.7 mouse macrophages were transfected with negative control and miR-342-3p mimics and subjected to microarray analysis 18 hours after the transfection. We used microarray to obtain global mRNA expression data of negative control and miR-342-3p mimics-transfected RAW264.7 cells.
2016-04-29 | GSE71642 | GEO
Project description:Background: Characterized by high incidence, mutilation, and death rate, acute ischemic stroke (AIS) has threatened people’s health seriously. Therefore, there is an urge need for early diagnosis and effective treatment of AIS. The purpose of this study was to clarify the regulatory role and potential molecular mechanism of miR-342-5p and circRNA_0008146 in AIS. Materials and Methods: Small RNA sequencing analysis was performed to screen differentially expressed miRNAs between the AIS and control group. Middle cerebral artery occlusion/reperfusion (MCAO/R) models were constructed in C57BL/6J mice. The circRNA_0008146 and miRNA expression levels were detected by quantitative real-time PCR. Assay kits were used to determine Fe2+ levels and assess a battery of oxidative stress indicators, including ROS, MDA, LPO, SOD, and GSH/GSSG. The content of ACSL4 was measured by Western blot. The neurobehavioral manifestation was evaluated using the modified Neurological Severity (mNSS) Score, rotarod test, and corner test. TTC staining was employed to detect cerebral infarction volume. Nissl staining was adapted to detect histological change and neuronal damage. Results: RNA sequencing analysis revealed miR-342-5p was significantly downregulated in the plasma of AIS patients. MiR-342-5p inhibited oxidative stress and RSL3-induced ferroptosis after cerebral ischemic-reperfusion injury in vivo by targeting ferroptosis-related gene ACSL4. CircRNA_0008146 acted as a sponge of miR-342-5p, and overexpression of circRNA_0008146 increased brain damage in stroke mice. CircRNA_0008146 contributed to ferroptosis in cerebral infraction via sponging miR-342-5p to regulate ACSL4. Conclusion: CircRNA_0008146/miR-342-5p/ACSL4 axis regulate ferroptosis after cerebral ischemia-reperfusion, which may be a potential therapeutic target for ischemic stroke.
2024-08-08 | GSE254322 | GEO
Project description:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274045 | GEO
Project description:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274044 | GEO
Project description:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274046 | GEO
Project description:Liver macrophages are crucial to maintain liver homeostasis. However, upon metastatic seeding, cancer cells co-opt these macrophages to act as tumor-associated macrophages (TAMs), facilitating tumor growth and invasiveness. MicroRNAs (miRNAs) are key regulators of TAM pro-tumoral functions, thus modulating their expression in liver macrophages may constitute a novel approach for liver metastasis immunotherapy. In this study, we identify a myeloid specific miRNA, miR-342-3p, and investigate its anti-tumoral function in liver macrophages in the context of colorectal cancer liver metastasis (CRLM). To this aim, we harnessed lentiviral vectors (LV) to infer and modulate miRNA activity in liver macrophages in vitro and in vivo. We found that miR-342-3p was highly active in macrophages in the healthy liver, but downregulated in proximity to CRLM. Rescuing miR-342-3p activity through enforced miRNA expression induced a pro-inflammatory phenotype in liver macrophages, which was associated to reduced CRLM growth. Transcriptomic analysis revealed Slc7a11, a cysteine-glutamate antiporter associated with TAM pro-tumoral functions, as a major miR-342-3p target. Overall, our findings highlight the potential of miR-342-3p in TAM reprogramming to enhance anti-tumoral immunity.
2025-03-11 | GSE274043 | GEO
Project description:The molecular mechanisms behind the miR-342-5p-induced HER2 pathway regulation are not known. Here, we aimed to further investigate the role of miR-342-5p in HER2 driven breast cancer cells. Transfected cells were incubated for 24 hours, and total RNA were run on mRNA arrays.
2017-12-21 | GSE108324 | GEO