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Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib

ABSTRACT: Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage) during 5 consecutive days PML plays a role in the senescence tumor suppressor response of normal cells to oncogenic stress. PML also mediates therapy-induced senescence in acute promyelocytic leukemia cells after treatment with retinoic acid. However, many tumor cell lines fail to engage a complete senescence response to PML activation. Interestingly, in vivo and in vitro combination of PML overexpression with CDK inhibition induce senescence in PC3 prostate cancer cells. We used microarray to characterize the gene expression profile of PC3 stably expressing PML or a control vector after subcutaneous injection in BALB/c 6-wk-old nude mice and treatment of the mice with palbociclib (100mg/kg/day) during 5 consecutive days..

ORGANISM(S): Homo sapiens

PROVIDER: GSE70923 | GEO | 2016/01/01

SECONDARY ACCESSION(S): PRJNA289931

REPOSITORIES: GEO

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Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib

Project description:Expression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage) during 5 consecutive days PML plays a role in the senescence tumor suppressor response of normal cells to oncogenic stress. PML also mediates therapy-induced senescence in acute promyelocytic leukemia cells after treatment with retinoic acid. However, many tumor cell lines fail to engage a complete senescence response to PML activation. Interestingly, in vivo and in vitro combination of PML overexpression with CDK inhibition induce senescence in PC3 prostate cancer cells. We used microarray to characterize the gene expression profile of PC3 stably expressing PML or a control vector after subcutaneous injection in BALB/c 6-wk-old nude mice and treatment of the mice with palbociclib (100mg/kg/day) during 5 consecutive days.. PC3 cells were infected with a retroviral vector that express PML or an empty vector before subcutaneous injection of 10^6 cells in both flanks of BALB/c 6-wk-old nude mice. Then, mice were treated for 5 consecutive days with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage)

2016-07-03 | E-GEOD-70923 | biostudies-arrayexpress

Homo sapiens

| PRJNA289931 | ENA

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Gene expression profiling of Pml wt and Pml KO mice liver after fasted 6h

Project description:The Pml gene is essential to the formation of PML nuclear bodies, domains which have been associated with various functions such as apoptosis/senescence, DNA repair and cell proliferation( Lallemand-Breitenbach 2010). PML-NBs formation is regulated by cellular stress including oxidative stress(Jeanne 2010, de The 2012). To investigate the role of PML in ROS response in vivo, we analyse the expression difference betweem Pml wt and Pml KO under fasted condition, which easily up-regulate ROS in BALB/cByJ background

2017-09-22 | GSE100615 | GEO

Effect of Palbociclib on gene expression of two gastric cancer cell lines(including AGS and SNU1)

Project description:Palbociclib, a kind of CDK4/6 inhibitor, was proved to be able to induce senescence in several cancer cell lines. After treated with Palbociclib, two GC cell lines (including AGS and SNU1) exhibited senescence-associated features, such as enlarged cell size, formation of heterochromatin foci in the nucleus, and increased activity of SA-β-Gal.Many senescence-related genes, such as CDKN1A, CDKN2A and TP53, were evaluated in the Palbociclib-treated GC cells, while proliferation-related genes, such as TOP2A and MKI67, were decreased. Moreover, GSEA demonstrated the senescence-related pathways, such as p53 and the nuclear factor-kappaB (NF-κB) pathways, were most significantly enriched in Palbociclib-treated group . In contrast, several cell cycle-related pathways were enriched in the control group. Together, these results indicated that Palbociclib could effectively induce senescence in GC cells and the senescent GC cells harbored higher GSSS.

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Silenced LINC01963 enhanced the chemosensitivity of prostate cancer cells to docetaxel by sponging miR-216b-5p to inhibit TrkB protein level

Project description:Long noncoding RNAs (lncRNAs) affect docetaxel chemosensitivity. However, the biological role and regulatory mechanisms of lncRNAs in docetaxel-resistant prostate cancer remain unclear. Differences in lncRNAs were evaluated by lncRNA sequencing and evaluated using quantitative real-time polymerase chain reaction, and TrkB expression was measured through Western blot analysis. Proliferation was measured using the MTS, while apoptosis and cell cycle were measured using flow cytometry. Additionally, migration and invasion were measured using transwell assays. Forty-eight female BALB/c nude mice were used for subcutaneous tumorigenicity and lung metastasis assays. We found that LINC01963 was overexpressed in the PC3-DR cells. LINC01963 silencing enhanced the chemosensitivity of PC3-DR to docetaxel and inhibited tumorigenicity and lung metastasis, while LINC01963 overexpression enhanced the chemoresistance of PC3 cells to docetaxel. It was found that LINC01963 sponges miR-216b-5p. The miR-216b-5p inhibitor reversed the suppressive effect of sh-LINC01963 on PC3-DR cell proliferation, migration, and invasion. Furthermore, miR-216b-5p can bind to the 3’-UTR of NTRK2 and inhibit TrkB protein levels. TrkB enhances docetaxel resistance in prostate cancer and reverses the effects of LINC01963 silencing and miR-216b-5p overexpression. In conclusion, silencing LINC01963 enhanced the chemosensitivity of PC3-DR to docetaxel by sponging miR-216b-5p to inhibit TrkB protein levels.

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Project description:Human prostate carcinoma cell line PC3 was treated with 10mg/ml or 100mg/ml of Abacavir. Gene expression was analyzed on total RNA extracted 48h after treatement. For each condition, 5 indipendent biological replicates were performed

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PML2‐mediated thread‐like nuclear bodies mark late senescence in Hutchinson–Gilford progeria syndrome [ChIP-seq]

Project description:Regular nuclear structure is critical for genome maintenance and proper gene expression, disorder of which has a causal role in aging. Accumulation of Progerin in Hutchinson-Gilford progeria syndrome (HGPS) disrupts the integrity of nuclear lamina and causes nuclear structure abnormalities, leading to premature aging. However, the nuclear structure/function relationships in HGPS cells have not been well addressed, and roles of nuclear sub-compartments for HGPS pathogenesis are rarely reported. Here, evidence reveals that classical dot-like PML nuclear bodies (PML NBs) are reorganized into thread-like morphology in HGPS cells, and these irregular NBs are strongly associated with cell senescence. We demonstrate that farnesylated Progerin interacts with PML isoform 2 specifically, which accounts for the formation of thread-like PML NBs. Moreover, our findings uncover that irregular PML NBs perturb NBs-associated DNA repair and gene transcription, thereby promoting HGPS cell senescence. Thus, our work helps to clarify the roles of nuclear structure and sub-compartments such as PML NBs in cell aging, and evidence presented in this study strongly support that thread-like PML NBs could be a novel biomarker of human cell senescence.

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PML2‐mediated thread‐like nuclear bodies mark late senescence in Hutchinson–Gilford progeria syndrome [RNA-seq]

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