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D(+)-Raffinose pentahydrate targeting PI3K/AKT pathway inducing apoptosis to inhibit pancreatic carcinoma proliferation

ABSTRACT: Our study confirmed the D(+)-Raffinose pentahydrate have the inhibitory effect on pancreatic cancer cells from different methods. By RNA-seq and q-PCR, we detected that D(+)-Raffinose pentahydrate could induce apoptosis via PI3K/Akt signaling pathway. Together, our findings presented a potential therapeutic effect of D(+)-Raffinose pentahydrate for human pancreatic cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184668 | GEO | 2024/09/23

REPOSITORIES: GEO

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D(+)-Raffinose pentahydrate targeting PI3K/AKT pathway inducing apoptosis to inhibit pancreatic carcinoma proliferation

Project description:D(+)-Raffinose pentahydrate targeting PI3K/AKT pathway inducing apoptosis to inhibit pancreatic carcinoma proliferation

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PI3K/AKT/mTOR and Sonic hedgehog pathways cooperate together to inhibit human pancreatic cancer stem cell characteristics and tumor growth

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Global transcriptomic analysis of the Raffinose Utilization in Lactobacillus salivarius Ren

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Thioguanine suppresses growth in triple-negative breast cancer by inhibiting PI3K-AKT pathway and inducing apoptosis

Project description:Triple-negative breast cancer (TNBC) is difficult to treat due to the lack of biological targets and poor sensitivity to conventional therapies. Chemotherapy is the main treatment in the clinic, but there is still no effective screening strategy for chemotherapy drugs. Several studies have attempted to find the pathogenesis through sequencing, but the integration of transcriptome maps of various tumors for drug discovery has been slow. Drug repurposing has attracted increasing attention in recent years. We first found there were common features between leukemia and TNBC. Therefore, we chose a classic leukemia drug thioguanine (6-TG) as a candidate drug. We utilized RNA-seq and DNA methylation arrays to evaluate its role in MDA-MB-231 cells. Our results demonstrated that 6-TG inhibited cell proliferation by suppressing PI3K-AKT pathway via downregulating the DNA methylation level of PTEN. Moreover, apoptosis was induced via the activation of PI3K-AKT downstream molecular TSC1 and the downregulation of methylation levels of DAXX, TNF, FADD and CASP8 etc., these genes involved in apoptosis pathways. 6-TG presents anti-tumor effects in vitro and vivo by regulating the DNA methylation levels of PI3K-AKT pathway and apoptosis pathway. Meanwhile, we proved transcriptome-based drug screening has potential implications for breast cancer therapy and drug selection.

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Kanglaite reverses multidrug resistance of HCC by inducing apoptosis and cell cycle arrest via PI3K/AKT pathway.

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| S-EPMC5833758 | biostudies-literature

RNA sequencing analysis of transcriptomics to study the growth of Lactobacillus salivarius Ren in raffinose

Project description:Purpose: To understand the metabolic mechanism of Lactobacillus salivarius Ren in raffinose Methods: Samples of Lactobacillus salivarius Ren grown in glucose and raffinose were sequenced on the Illumina Hiseq platform. Three independent biological replicates were generated, including a total of six samples. Results: Raw data were firstly processed through in-house perl scripts to generate clean data, and then clean date were mapped to the reference genome, getting about 8-10 million total mapped reads per sample.

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Transcription profiling of yeast after a shift from media containing raffinose to one containg galactose

Project description:expression profile from a shift from raffinose to galatose. This serves as a control expirement.

2009-09-19 | E-TABM-693 | biostudies-arrayexpress

microRNA-29b prevents liver fibrosis by attenuating hepatic stellate cell activation and inducing apoptosis through targeting PI3K/AKT pathway.

Project description:microRNA-29b (miR-29b) is known to be associated with TGF-?-mediated fibrosis, but the mechanistic action of miR-29b in liver fibrosis remains unclear and is warranted for investigation. We found that miR-29b was significantly downregulated in human and mice fibrotic liver tissues and in primary activated HSCs. miR-29b downregulation was directly mediated by Smad3 through binding to the promoter of miR-29b in hepatic stellate cell (HSC) line LX1, whilst miR-29b could in turn suppress Smad3 expression. miR-29b transduction in the liver of mice prevented CCl4 induced-fibrogenesis, concomitant with decreased expression of ?-SMA, collagen I and TIMP-1. Ectopic expression of miR-29b in activated HSCs (LX-1, HSC-T6) inhibited cell viability and colony formation, and caused cell cycle arrest in G1 phase by downregulating cyclin D1 and p21cip1. Further, miR-29b induced apoptosis in HSCs mediated by caspase-9 and PARP. miR-29b inhibited its downstream effectors of PIK3R1 and AKT3 through direct targeting their 3'UTR regions. Moreover, knockdown of PIK3R1 or AKT3 suppressed ?-SMA and collagen I and induced apoptosis in both HSCs and in mice. In conclusion, miR-29b prevents liver fibrogenesis by inhibiting HSC activation and inducing HSC apoptosis through inhibiting PI3K/AKT pathway. These results provide novel mechanistic insights for the anti-fibrotic effect of miR-29b.

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