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P53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells [RNA-seq]

ABSTRACT: To identify p53-regulated lncRNAs responsive to DNA damage in human hepatocellular carcinoma (HCC) cells, we conducted paired-end and strand-specific RNA-seq using HepG2 wild-type and p53-knockout (HepG2-KO-p53) cells, which were devoid of p53 protein, using the CRISPR-Cas9 system treated with or without the DNA-damaging agent adriamycin (ADR)

ORGANISM(S): Homo sapiens

PROVIDER: GSE125756 | GEO | 2020/07/18

REPOSITORIES: GEO

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p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells [Ribo-seq]

Project description:To globally analyse the lncRNAs with potential coding ability upon DNA damage, we performed Ribo-seq using ADR-treated HepG2 cells. The HepG2 cells were treated with 500 ng/mL ADR for 24 h, and cycloheximide (CHX) was added to inhibit the translational elongation of ribosomes.Furthermore,we identified the candidate ORFs with the selected RPF reads using the RiboCode software.

2020-07-18 | GSE125757 | GEO

Expression data from treatment-induced senescence in mouse Emu-myc B-cell lymphoma model

Project description:Treatment induced senescence (TIS) is a terminal cell cycle arrest program, increasingly recognized as a tumor suppressor mechanism complementing apoptosis in response to standard chemotherapy regimens. In particular cells with blocked apoptotic pathways rely on senescence as the only remaining failsafe mechanism to keep the neoplastic growth in check. However, little is known about biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment. We used global gene expression profiling by microarrays to gain insight in the molecular programme underlying the treatment-induced senescence in Emu-myc transgenic B-cell lymphomas (apoptosis protected by Bcl2 overexpression), which robustly enter senescence in response to DNA-damaging anticancer agents such as Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc transgenic mice were used. In this model the the c-Myc oncogene is constitutively expressed in the cells of B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas, resembling Burkitt lymphoma in humans. In order to bring up the senescence as the main failsafe mechanism, primary lymphoma cells are protected from apoptosis by retroviral over-expression of a strong antiapoptotic protein Bcl2. These cells (Myc;Bcl2) massively undergo senescence upon DNA-damaging treatment. Adriamycin (ADR) is a cytostatic drug, used as a standard part of several lymphoma treatment regimens. In this study, transcriptional profiles of matched pairs of untreated vs. 5 days ADR treated Myc;Bcl2 lymphomas were analysed.

2011-11-21 | E-GEOD-31099 | biostudies-arrayexpress

p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells

Project description:p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells

| PRJNA517455 | ENA

p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-07-18 | GSE125758 | GEO

p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells [Ribo-seq]

Project description:p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells [Ribo-seq]

| PRJNA517458 | ENA

p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells [RNA-seq]

Project description:p53-inducible long non-coding RNAs encode functional peptides in hepatocellular carcinoma cells [RNA-seq]

| PRJNA517459 | ENA

Global expression profiling of treatment-induced senescence in mouse Emu-myc B-cell lymphomas

Project description:Therapy-induced senescence (TIS) is a DNA damage-triggered irreversible cell-cycle block that terminates further expansion of (pre-)malignant lesions. Utilizing the Eµ-myc transgenic mouse lymphoma model (apoptosis protected by retroviral Bcl2-overexpression), we sought to elucidate the biological properties, long-term fate of senescent tumor cells and their impact on the microenvironment. We used global gene expression profiling by microarrays to gain insight into the molecular program underlying the treatment-induced senescence in Emu-myc transgenic B-cell lymphomas (apoptosis protected by Bcl2 overexpression), which robustly enter senescence in response to DNA-damaging anticancer agents such as Adriamycin (ADR).

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