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Targeting Smyd3 by antisense oligonucleotides attenuates liver tumor growth

ABSTRACT: Targeting Smyd3 by antisense oligonucleotides attenuates liver tumor growth

PROVIDER: PRJNA641395 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12075800.fastq.gz	Fastqsanger.gz
	SRR12075801.fastq.gz	Fastqsanger.gz
	SRR12075802.fastq.gz	Fastqsanger.gz
	SRR12075803.fastq.gz	Fastqsanger.gz
	SRR12075804.fastq.gz	Fastqsanger.gz

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Targeting Smyd3 by antisense oligonucleotides attenuates liver tumor growth

Project description:We investigated whether pharamacological inhibition of Smyd3 by antisense oligonucleotides (ASOs) can influence diethylnitrosamine (DEN)-induced liver cancer development. Our phenotypic analyses, among others, included gene expression profiling.

2020-06-24 | GSE153077 | GEO

Targeting Smyd3 by next-generation antisense oligonucleotides suppresses liver tumor growth.

Project description:The oncogenic function of suppressor of variegation, enhancer of zeste and MYeloid-Nervy-DEAF1-domain family methyltransferase Smyd3 has been implicated in various malignancies, including hepatocellular carcinoma (HCC). Here, we show that targeting Smyd3 by next-generation antisense oligonucleotides (Smyd3-ASO) is an efficient approach to modulate its mRNA levels in vivo and to halt the growth of already initiated liver tumors. Smyd3-ASO treatment dramatically decreased tumor burden in a mouse model of chemically induced HCC and negatively affected the growth rates, migration, oncosphere formation, and xenograft growth capacity of a panel of human hepatic cancer cell lines. Smyd3-ASOs prevented the activation of oncofetal genes and the development of cancer-specific gene expression program. The results point to a mechanism by which Smyd3-ASO treatment blocks cellular de-differentiation, a hallmark feature of HCC development, and, as a result, it inhibits the expansion of hepatic cancer stem cells, a population that has been presumed to resist chemotherapy.

| S-EPMC8169948 | biostudies-literature

Hemophilia mice treated with antisense oligonucleotides targeting either Upf1 or Upf3b

Project description:Hemophilia mice treated with antisense oligonucleotides targeting either Upf1 or Upf3b

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Expression data from dosing four different antisense oligonucleotides in mice II

Project description:We used microarrays to globally profile the gene expression changes observed in liver after 3 days when dosing antisense oligonucleotides in mice

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Expression data from transfection of two different antisense oligonucleotides in HuH7 cells

Project description:We used microarrays to globally profile the gene expression changes observed after 24h when transfecting antisense oligonucleotides in HuH77 cells

2017-04-21 | GSE93245 | GEO

Transcriptome profiling of primary human aortic Vascular Smooth Muscle cells abrogated of NEIL3 mRNA via antisense oligonucleotides targeting NEIL3 exon 4

Project description:We performed high-throughput RNA sequencing to characterize possible differences in the transcriptome of primary human aortic Vascular Smooth Muscle cells abrogated of NEIL3 mRNA via antisense oligonucleotides targeting NEIL3 exon 4, compared with control cells treated with a scramble version of the same antisense oligonucleotide

2021-03-15 | GSE140789 | GEO

Expression data from transfection of 14 different antisense oligonucleotides in HuH7 cells

Project description:We used microarrays to globally profile the gene expression changes observed after 10h and 24h when transfecting antisense oligonucleotides in HuH7 cells

2017-04-21 | GSE93244 | GEO

Knockdown of circular RNAs using LNA-modified antisense oligonucleotides

Project description:Knockdown of circular RNAs using LNA-modified antisense oligonucleotides

| PRJNA607690 | ENA

Phospholamban Antisense Oligonucleotides Improve Cardiac Function in Murine Cardiomyopathy

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Antisense oligonucleotides targeting nuclear RNA for in vivo correction of myotonic dystrophy

Project description:This study examined the effects of antisense oligonucleotides (ASOs) on the muscle transcriptome in a transgenic mouse model of myotonic dystrophy. Two ASOs were tested in HSALR transgenic mice. Both of the ASOs targeted mRNA from a human skeletal actin (hACTA1) transgene. This transgene contains an expanded CTG repeat in the 3M-bM-^@M-^Y untranslated region (UTR) (Mankodi et al M-bM-^@M-^\Myotonic dystrophy in transgenic mice expressing an expanded CUG repeatM-bM-^@M-^] Science 2000; 289:1769-72). ASO 445235 targeted the hACTA1 transcript in the 3M-bM-^@M-^Y UTR, downstream from the expanded repeat. ASO 190401 targeted the hACTA1 transcript in the coding region. The HSALR mice received 4 weeks of biweekly subcutaneous injections of vehicle (saline), ASO 190401, or ASO 445236 (n = 4 per group), at a dose of 25 mg/kg per injection. Wild-type mice of the same strain background received saline injections (n = 4). One week after the final injection, quadriceps muscle was harvested for RNA analysis. Four conditions, four arrays per condition, to compare WT and HSALR trangenic mice without treatment (saline) and to examine the effect of two oligos (vs. saline) in the HSALR transgenic mice.

2012-06-27 | E-GEOD-38962 | biostudies-arrayexpress

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