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Next Generation Sequencing Analysis of Gene expression of Min6 insulinoma cell line transfected with siNC, siSRSF1 or siSRSF2

ABSTRACT: Assessment of the impact of SRSF1 or SRSF2 silencing in Min6 cell lines

ORGANISM(S): Mus musculus

PROVIDER: GSE178357 | GEO | 2024/04/28

REPOSITORIES: GEO

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Next Generation Sequencing Analysis of Gene expression of Min6 insulinoma cell line transfected with siNC, siSRSF1 or siSRSF2

Project description:Next Generation Sequencing Analysis of Gene expression of Min6 insulinoma cell line transfected with siNC, siSRSF1 or siSRSF2

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Selenomethionine Modulates Insulin Secretion in the MIN6-K8 Mouse Insulinoma Cell Line

Project description:Selenium is an essential trace element that has gained interest for its potential role in glucose homeostasis. The purpose of the present study was to investigate the impact of selenium supplementation as selenomethionine (SeMet) on insulin secretion in MIN6-K8 cells, a model of pancreatic -cells. We found that 40 μM and 80 μM SeMet significantly enhanced percent insulin secretion at low (2.8 mM), intermediate (11.7 mM), and high (16.7 mM) glucose stimulation. SeMet also increased tolbutamide- or KCl-induced percent insulin secretion at 40 μM and 80 μM. Ca2+ influx was only reduced with 80 μM SeMet. RNA-sequencing showed that 40 μM SeMet supplementation upregulated expression of selenoprotein H (SelH) and thioredoxin reductase 1 (Txnrd 1) and downregulated expression of glutathione peroxidase 3 (Gpx3), selenoprotein O (SelO), and selenoprotein P (SelP). Gpx3 knockdown increased both percent and total insulin release with high glucose stimulation. SelP knockdown increased insulin release at high glucose. In conclusion, high SeMet supplementation augments insulin secretion, while reductions in Gpx3 and SelP expression, from SeMet supplementation or via silencing, augment -cell function in the MIN6-K8 cell line. These studies support a putative role for selenium and selenoproteins in the regulation of glucose homeostasis and diabetes risk.

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Transcriptome analysis of the D3 mouse embryonic stem cell line in comparison to the MIN6 pancreatic beta-cell insulinoma cell line

Project description:Analysis of the transcriptional differences between mouse ES cells from the D3 cell line and transformed beta-cells (MIN6 cell line) as determined by a direct comparative analysis of their transcriptome. The results show that 40% of transcripts were differentially expressed between D3 and MIN6 cells. There is thus a marked difference in the pattern of transcription between the ES cell and beta-cell genomes. Total RNA was extracted from three independent replicates of passage 21 D3 cells and passage 23 MIN6 cells. A whole mouse genome comparison between D3 and MIN6 cells was performed using the Mouse WG-6 v2.0 Expression Beadchip from Illumina.

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Transcriptome analysis of the D3 mouse embryonic stem cell line in comparison to the MIN6 pancreatic beta-cell insulinoma cell line

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Expression data from mouse insulinoma cells

Project description:We previously isolated a subclone, MIN6 clone 4, from the parental MIN6 cells, that shows well-regulated insulin secretion in response to glucose, glybenclamide, and KCl, even after prolonged culture. To investigate the molecular mechanisms responsible for preserving GSIS in this subclone, we compared four groups of MIN6 cells: Pr-LP (parental MIN6, low passage number), Pr-HP (parental MIN6, high passage number), C4-LP (MIN6 clone 4, low passage number), and C4-HP (MIN6 clone 4, high passage number). Based on their capacity for GSIS, we designated the Pr-LP, C4-LP, and C4-HP cells as “responder cells.” In a DNA microarray analysis, we identified a group of genes with high expression in responder cells (“responder genes”), but extremely low expression in the Pr-HP cells.

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Transcription profiling by array of mouse pancreatic beta cells of MIN6 insulinoma cell line transfected with siRNA directed against murine Meis3 or non targeting control.

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m6A-seq of Min6 cells were transfected with the GR cDNA expression vector or control vector

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Project description:SRSFs are a subset of RNA binding proteins that exert precise control over RNA splicing, including cancer-associated AS events. Serine/arginine-rich splicing factors 2 (SRSF2), a member of SRSF family, plays a crucial role in regulating splicing events. We profiled gene expression and splicing changes in AGS cells silencing SRSF2. Our study unveils that SRSF2 binds to the exon 4 region of YTHDF1 pre-mRNA, inducing YTHDF1Δexon 4 skipping and resulting in elevation levels of the oncogenic YTHDF1-S in GC. Overall, we provide evidence that YTHDF1 is an AS target of SRSF2.

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