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Real time PCR array for cancer inflamation and immunity and tumor metastasis on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

ABSTRACT: Real time PCR array for cancer inflamation and immunity and tumor metastasis on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

PROVIDER: PRJNA665023 | ENA |

REPOSITORIES: ENA

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Real time PCR array for cancer inflamation and immunity on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

Project description:This experiment was done to compare cancer inflamation and immunity profile between liver tissues of mice with liver metastasis which treated with miR-122 delivery compared with those treated with miRNC delivery as control.

2020-09-23 | GSE158365 | GEO

Real time PCR array for mouse tumor metastasis on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

Project description:This experiment was done to compare mouse metastasis gene profile between liver tissues of mice with liver metastasis which treated with miR-122 delivery compared with those treated with miRNC delivery as control.

2020-09-23 | GSE158366 | GEO

Real time PCR array for cancer inflamation and immunity on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

Project description:Real time PCR array for cancer inflamation and immunity on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

| PRJNA665028 | ENA

Real time PCR array for mouse tumor metastasis on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

Project description:Real time PCR array for mouse tumor metastasis on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

| PRJNA665026 | ENA

Real time PCR array for cancer inflamation and immunity and tumor metastasis on mice with liver metastasis treated with miR-122 delivery vs miRNC delivery

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-23 | GSE158368 | GEO

Hepatitis C virus functionally sequesters miR-122 [miR-122 KO vs Control CLIP]

Project description:Hepatitis C virus uniquely requires the liver specific microRNA-122 for replication, yet global effects on endogenous miRNA targets during infection are unexplored. Here, high-throughput sequencing and crosslinking immunoprecipitation (HITS-CLIP) experiments of human Argonaute (Ago) during HCV infection showed robust Ago binding on the HCV 5’UTR, at known and predicted miR-122 sites. On the human transcriptome, we observed reduced Ago binding and functional mRNA de-repression of miR-122 targets during virus infection. This miR-122 “sponge” effect could be relieved and redirected to miR-15 targets by swapping the miRNA tropism of the virus. Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and number of sites. We describe a quantitative mathematical model of HCV induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.

2015-01-06 | GSE64679 | GEO

miR-122-dependent binding of TNRC6 to HCV RNA

Project description:The liver-specific microRNA, miR-122, is an essential host factor for replication of hepatitis C virus (HCV), an important infectious cause of chronic liver disease and hepatocellular carcinoma. miR-122 stabilizes the positive-strand HCV RNA genome and promotes viral RNA synthesis by binding two closely spaced sites (S1 and S2) near the 5’ end of the genome in association with Ago2. Ago2 is essential for both host factor activities, but whether other host proteins are involved is unknown. Using a quantitative proteomics approach, we identified TNRC6A (GW182) and its paralogs (TNRC6B and TNRC6C), as functionally important components of the miR-122/Ago2 host factor complex binding HCV RNA. Depletion of any two TNRC6 proteins reduced HCV replication in Huh-7.5 cells,but did not reduce viral RNA stability or translational activity, but rather dampened miR-122 stimulation of viral RNA synthesis. However, TNRC6 depletion had no effect on replication of HCV in which S2 was mutated so that miR-122 binds only S1, whereas it significantly enhanced replication when S1 was mutated and only S2 bound by miR-122. Consistent with this, we found that TNRC6 proteins preferentially associate with the S1 site, and that the association of Ago2 with S2 is increased in TNRC6-depleted cells. Collectively, these data suggest a model in which TNRC6 proteins, which are known to interact with Ago2, preferentially direct the miR-122/Ago2 complex to S1 while restricting its association with S2, thereby fine tuning the spatial organization of miR-122/Ago2 complexes bound to the viral RNA.

2019-04-24 | PXD013054 | Pride

Hepatitis C virus functionally sequesters miR-122 [miR-122 KO vs Control CLIP]

2015-01-06 | E-GEOD-64679 | biostudies-arrayexpress

Nanoparticle Delivery of miR-122 Inhibits Colorectal Cancer Liver Metastasis.

Project description:Liver metastasis is a leading cause of cancer morbidity and mortality. Thus, there has been strong interest in the development of therapeutics that can effectively prevent liver metastasis. One potential strategy is to utilize molecules that have broad effects on the liver microenvironment, such as miR-122, a liver-specific miRNA that is a key regulator of diverse hepatic functions. Here we report the development of a nanoformulation miR-122 as a therapeutic agent for preventing liver metastasis. We engineered a galactose-targeted lipid calcium phosphate (Gal-LCP) nanoformulation of miR-122. This nanotherapeutic elicited no significant toxicity and delivered miR-122 into hepatocytes with specificity and high efficiency. Across multiple colorectal cancer liver metastasis models, treatment with Gal-LCP miR-122 treatment effectively prevented colorectal cancer liver metastasis and prolonged survival. Mechanistic studies revealed that delivery of miR-122 was associated with downregulation of key genes involved in metastatic and cancer inflammation pathways, including several proinflammatory factors, matrix metalloproteinases, and other extracellular matrix degradation enzymes. Moreover, Gal-LCP miR-122 treatment was associated with an increased CD8+/CD4+ T-cell ratio and decreased immunosuppressive cell infiltration, which makes the liver more conducive to antitumor immune response. Collectively, this work presents a strategy to improve cancer prevention and treatment with nanomedicine-based delivery of miRNA. SIGNIFICANCE: Highly specific and efficient delivery of miRNA to hepatocytes using nanomedicine has therapeutic potential for the prevention and treatment of colorectal cancer liver metastasis.

| S-EPMC8732321 | biostudies-literature

RAW246.1 cells activation by internalized synthetic miR-122

Project description:Hepatic injury is often accompanied by pulmonary inflammation and tissue damage, but the underneath mechanism is not fully elucidated. Here we identify hepatic miR-122 as a culprit of pulmonary inflammation induced by various liver injuries. Analyses of acute and chronic liver injury mouse models confirm that liver dysfunction can cause pulmonary inflammation and tissue damage. Injured livers release large amounts of miR-122 in a microvesicle-independent manner into the circulation compared to normal livers. Circulating miR-122 is then preferentially transported to mouse lungs and taken up by alveolar macrophages, in which it binds toll-like receptor 7 (TLR7) and activates inflammatory responses. Depleting plasma miR-122 largely abolishes liver injury-induced pulmonary inflammation and tissue damage. Furthermore, alveolar macrophage activation by miR-122 is blocked by mutating the TLR7-binding UG-rich sequence on miR-122 or knocking out macrophage TLR7. Our findings reveal a novel causative role of hepatic miR-122 in liver injury-induced pulmonary dysfunction.

2018-12-27 | GSE124360 | GEO

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