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Inhibition of proliferation and induction of autophagy by atorvastatin in PC3 prostate cancer cells correlate with downregulation of Bcl2 and upregulation of miR-182 and p21

NIAID Data Ecosystem2026-03-10 收录

前列腺癌药物机制

阿托伐他汀抗肿瘤

数据链接：

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE46376 数据链接链接失效反馈

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资源简介：

This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

应用场景：

创建时间：

2018-01-09

前列腺癌药物机制

BET溴结构域靶向

RNA-Sequencing data for DU145 and PC3 cell lines treated with two concentrations of JQ1 in combination with IFN-y to determine effects of BET Bromodomain inhibition on prostate cancer cell lines RNA-S

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"Drug-seq": An Approach to Identify the Genomic Targets of Chemicals Identified by Functional Phenotypic Screens [Drug-seq]. Homo sapiens

药物基因组靶点识别

前列腺癌药物机制

Here we report an approach that has permitted us to uncover the sites and mechanisms of action of a drug, referred to as SD70, initially identified by phenotypic screening for inhibitors of ligand and

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The HDAC Inhibitor LBH589 Induces ERK-Dependent Prometaphase Arrest in Prostate Cancer via HDAC6 Inactivation and Down-Regulation

前列腺癌药物机制

HDAC6信号通路

Histone deacetylase inhibitors (HDACIs) have potent anti-cancer activity in a variety of cancer models. Understanding the molecular mechanisms involved in the therapeutic responsiveness of HDACI is ne

NIAID Data Ecosystem40

Human prostate cancer cell lines treated with BET Bromodomain inhibitor JQ1. Human prostate cancer cell lines treated with BET Bromodomain inhibitor JQ1

前列腺癌药物机制

RNA测序表达分析

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Effect of AZD1208 on gene expression in recurrent resistant Myc-CaP tumors grown in castrated mice.

前列腺癌药物机制

基因表达谱分析

AZD1208 is a novel PIM kinase inhibitor that we have shown inhibits tumorigenesis in tissue recombination models, Myc-CaP allograft models, and human prostate cancer xenografts. We sought to determine

NIAID Data Ecosystem40

Inhibition of proliferation and induction of autophagy by atorvastatin in PC3 prostate cancer cells correlate with downregulation of Bcl2 and upregulation of miR-182 and p21

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