D(+)-Raffinose pentahydrate targeting PI3K/AKT pathway inducing apoptosis to inhibit pancreatic carcinoma proliferation
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ABSTRACT:
PROVIDER: PRJNA765607 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16022010_1.fastq.gz | Fastqsanger.gz | |||
| SRR16022010_2.fastq.gz | Fastqsanger.gz | |||
| SRR16022011_1.fastq.gz | Fastqsanger.gz | |||
| SRR16022011_2.fastq.gz | Fastqsanger.gz | |||
| SRR16022012_1.fastq.gz | Fastqsanger.gz |
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Project description: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.
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Project description:The fat tail of sheep is an important organ that has evolved to adapt to extreme environmental conditions. Mesenchyme homeobox 2 (MEOX2) can inhibit adipogenic differentiation of stromal vascular fractions (SVFs) isolated from ovine tail adipose tissue. However, the underlying mechanism through which MEOX2 regulates ovine adipogenesis remains unclear. Therefore, this study aims to employ RNA sequencing (RNA-seq) to explore the downstream genes regulated by MEOX2 during the adipogenic differentiation of ovine SVFs. Based on RNA sequencing, several differentially expressed genes (DEGs) were identified in response to MEOX2 overexpression. The PI3K/AKT signaling pathway was significantly enriched in DEGs, indicating its importance in mediating fat accumulation regulated by MEOX2. Additionally, the PI3K/AKT signaling pathway activation was found to be crucial for ovine SVF adipogenic differentiation. Mechanistically, MEOX2 inhibited the PI3K/AKT pathway. These findings highlight the significance of the PI3K/AKT signaling pathway during ovine SVF adipogenic differentiation. Furthermore, they shed light on the involvement of MEOX2 in this differentiation via the PI3K/AKT pathway. Our findings provide novel insights into the critical role of MEOX2 as an adipogenetic differentiation regulator, potentially enhancing our understanding of ovine fat development and its regulatory processes.
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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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