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Gene expression profiling of LNCaP cells following short term shRNA-mediated knockdown of TMEFF2 and growth in presence and absence of dihydrotestosterone

ABSTRACT: Analysis of RNA expression in LNCaP cells expressing shTMEFF2 to define its trancriptome. We report global changes in the AR-signaling transcriptome in response to shRNA targeted to TMEFF2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE165246 | GEO | 2021/02/01

REPOSITORIES: GEO

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Gene expression profiling of LNCaP cells following shRNA-mediated knockdown of TMEFF2 and growth in presence and absence of dihydrotestosterone

Project description:TMEFF2 is an androgen regulated transmembrane protein mainly restricted to brain and prostate, that functions as a tumor suppressor in prostate cancer (PCa). Studies using publically available prostate cancer (PCa) datasets, reveal changes in the expression of TMEFF2 with disease stage, supporting an important role of TMEFF2 in this disease. However, the role of TMEFF2 in the biology and pathogenesis of PCa is still unknown. Using a transgenic TMEFF2 mouse, we have demonstrated that TMEFF2 overexpression modulates prostate branching morphogenesis, and androgen regulated process, during prostate regeneration. We hypothesized that TMEFF2 may have a regulatory function within androgen signaling that could explain its role in PCa. To better understand its function in androgen signaling and PCa, we compared the transcriptome of LNCaP prostate cancer cells transduced with control shRNA and shRNA targeting TMEFF2 in the presence and absence of dihydrotestosterone (DHT). The results indicated that globally, there is a significant interaction between the effects of DHT and shTMEFF2. Of the 519 genes with significant gene expression changes after DHT treatment of Scramble control cells, 208 (40%) had significant differential expression when the shTMEFF2 +DHT group was compared to Scramble +DHT group, including numerous androgen activated and androgen repressed genes.

2019-04-01 | GSE117180 | GEO

Gene expression profiling of LNCaP cells following short term shRNA-mediated knockdown of TMEFF2 and growth in presence and absence of dihydrotestosterone

Project description:Gene expression profiling of LNCaP cells following short term shRNA-mediated knockdown of TMEFF2 and growth in presence and absence of dihydrotestosterone

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Gene expression profiling of LNCaP cells following shRNA-mediated knockdown of TMEFF2 and growth in presence and absence of dihydrotestosterone

Project description:Gene expression profiling of LNCaP cells following shRNA-mediated knockdown of TMEFF2 and growth in presence and absence of dihydrotestosterone

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TMEFF2 isoform detection in LNCaP prostate cancer cells

Project description:TMEFF2 isoform detection in LNCaP prostate cancer cells

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TMEFF2 isoform detection in LNCaP prostate cancer cells

Project description:Deep sequencing was performed in LNCaP cells

2021-02-01 | GSE165248 | GEO

LNCaP cells: shRNA library with bicalutamide

Project description:Short hairpin RNA library-based functional screening identified ribosomal protein L31 that modulates prostate cancer cell growth Vehicle vs. bicalutamide treated LNCaP cells infected with lentiviral shRNA library. Biological replicates: 2 vehicle treatments, 2 bicalutamide treatments.

2015-05-15 | E-GEOD-60382 | biostudies-arrayexpress

Expression data of LNCaP and MDA PCa 2b cells in absence or presence of IL6

Project description:Prostate cancer (PCa) development and progression are associated with chronic inflammation. The cytokine interleukin (IL)-6 can influence progression, differentiation, survival, and angiogenesis of PCa. To identify novel pathways that are triggered by IL-6, we performed a gene expression profiling of two PCa cell lines, LNCaP and MDA PCa 2b, under treatment with 5 ng/ml IL-6. Interferon regulatory factor (IRF)9 was identified as one of the most prevalent IL-6 regulated genes in both cell lines. IRF9 is a mediator of type I interferon signaling and acts together with signal transduction and activator of transcription (STAT)1 and 2 to activate transcription of interferon responsive genes. The IL-6 regulation of IRF9 was confirmed at mRNA and protein levels by quantitative real-time PCR and Western blot, respectively, in both cell lines and could be blocked by the anti-IL-6 antibody Siltuximab. Three PCa cell lines with an autocrine IL-6 loop, PC3, DU145, and LNCaP-IL-6+, showed a high expression of IRF9. A tissue microarray with 36 malignant and adjacent 36 benign areas from prostate cancer specimens showed that IRF9 protein expression is moderately elevated in malignant areas and positively correlates with the tissue expression of IL-6. Downregulation and overexpression of IRF9 provided evidence for an interferon-independent role of IRF9 on cellular proliferation of different PCa cell lines. Furthermore, expression of IRF9 was essential to mediate the antiproliferative effects of IFN-α2. We concluded that IL-6 is an inducer of IRF9 expression in prostate cancer and a sensitizer for the antiproliferative effects of IFNα2.

2013-08-02 | GSE47973 | GEO

Expression data of LNCaP and MDA PCa 2b cells in absence or presence of IL6

Project description:Prostate cancer (PCa) development and progression are associated with chronic inflammation. The cytokine interleukin (IL)-6 can influence progression, differentiation, survival, and angiogenesis of PCa. To identify novel pathways that are triggered by IL-6, we performed a gene expression profiling of two PCa cell lines, LNCaP and MDA PCa 2b, under treatment with 5 ng/ml IL-6. Interferon regulatory factor (IRF)9 was identified as one of the most prevalent IL-6 regulated genes in both cell lines. IRF9 is a mediator of type I interferon signaling and acts together with signal transduction and activator of transcription (STAT)1 and 2 to activate transcription of interferon responsive genes. The IL-6 regulation of IRF9 was confirmed at mRNA and protein levels by quantitative real-time PCR and Western blot, respectively, in both cell lines and could be blocked by the anti-IL-6 antibody Siltuximab. Three PCa cell lines with an autocrine IL-6 loop, PC3, DU145, and LNCaP-IL-6+, showed a high expression of IRF9. A tissue microarray with 36 malignant and adjacent 36 benign areas from prostate cancer specimens showed that IRF9 protein expression is moderately elevated in malignant areas and positively correlates with the tissue expression of IL-6. Downregulation and overexpression of IRF9 provided evidence for an interferon-independent role of IRF9 on cellular proliferation of different PCa cell lines. Furthermore, expression of IRF9 was essential to mediate the antiproliferative effects of IFN-M-NM-12. We concluded that IL-6 is an inducer of IRF9 expression in prostate cancer and a sensitizer for the antiproliferative effects of IFNM-NM-12. LNCaP and MDA PCa 2b cells were seeded in 12 wells each. The cells were starved for 24 h and half were treated with 5 ng/ml IL-6 for 18 h. Two biological replicates were performed, each in three replicates, resulting in 12 samples per cell line.

2013-08-02 | E-GEOD-47973 | biostudies-arrayexpress

TMEFF2 and CD95L derived shRNAs promote prostate cancer cell death by targeting the essential androgen receptor pathway

Project description:A novel mechanism, Death Induced by Survival gene Elimination (DISE), has recently been described as a potential cancer therapy. DISE kills cancer cells through an RNA interference (RNAi) mechanism. We show that expression of certain shRNAs developed to target TMEFF2 promotes prostate cancer (PCa) cell death similar to DISE, and independently of TMEFF2 targeting/expression. In PCa cells, these shRNAs downregulate the androgen receptor (AR) and AR coregulatory genes, an effect that correlates with the presence of short seed matches in their 3’UTRs and which results in global androgen signaling inhibition and cell death. We have termed this mechanism Androgen Network DISE (AN-DISE). shL3, an shRNA to CD95L known to promote DISE in non-PCa cells, promotes AN-DISE in PCa cells by targeting the AR-signaling pathway.

2021-02-01 | GSE165247 | GEO

Stable overexpression of either mutant- or wild type SPOP in presence/absence of ΔERG in LNCaP prostate cancer cells

Project description:Purpose: Little is known about the interplay of driver mutations that never co-occur within the same cancer cells. The latter scenario has been identified in prostate cancer where recurrent gene fusions involving the oncogenic ERG transcription factor and point mutations in the ubiquitin ligase adaptor SPOP are strictly mutually exclusive. We show that ERG and mutant SPOP – even though oncogenic on their own – are together synthetic sick. Description: LNCaP cells in presence/absence of stable ΔERG overexpression, were infected with lentivirus to overexpress either wild-type or mutant SPOP (Y87C, F102C, W131G, F133S).

2020-12-10 | E-MTAB-7170 | biostudies-arrayexpress

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