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Effects of kockouts of EGR1, FOS and their combination on the MAPK induced transcriptome [RNA_KO_clones]

ABSTRACT: In this study we used CRISPR/Cas9 to generate KO clones of the HEK-RAF-ER cell line that lack expression of EGR1, FOS and profiled the transcriptome after inducing RAF/MAPK signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE250532 | GEO | 2024/01/13

REPOSITORIES: GEO

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c-Fos mediates cell proliferation, invasion and drug-resistance of lung adenocarcinoma through MAPK signal pathway

Project description:Lung cancer is the main cause of cancer-related death in men and women all over the world. Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer, with the overall 5-year survival rate is less than 20% . We found the mRNA expression of c-Fos in LUAD clinical samples was decreased significantly compared to adjacent normal control. Overexpression of c-Fos inhibited LUAD cell proliferation, colony formation, and induced cell apoptosis while c-Fos knockdown promoted cell proliferation, colony formation, and suppressed cell apoptosis. Cell cycle showed little difference after c-Fos knockdown but overexpression of c-Fos increased the distribution of G1 phase when decreased G2 phase cells. Knockdown of c-Fos reduced the sensitivity of LUAD cells to cisplatin but overexpression of c-Fos increased the efficacy of cisplatin both in vitro and in vivo. MAPK signaling pathway was enriched after c-Fos was overexpressed in LUAD cells. The expression of c-Jun, c-Myc and DUSP1 was greatly inhibited after c-Fos overexpression but incresed after c-Fos knockdown, which suggests c-Fos regulated MAPK signaling pathway in LUAD. Furthermore, c-Fos was shown to interact with c-Jun and overexpression of c-Jun partially recovered the expression of c-Jun, c-Myc and DUSP1 caused by c-Fos overexpression. Cell proliferation was also rescued when apoptosis was decreased followed by c-Jun overexpression. In contrast, knockdown of c-Jun inhibited cell proliferation and promoted cell apoptosis in LUAD cells when reduced the level of c-Jun, c-Myc and DUSP1. In summary, c-Fos inhibits cell proliferation, promotes apoptosis and increses cisplatin-sensitivity of lung adenocarcinoma cells via regulating MAPK signaling by interacting with c-Jun in certain LUADs.

2023-09-20 | GSE213590 | GEO

Glucocorticoids delay RAF-induced senescence promoted by EGR1

Project description:Glucocorticoids delay RAF-induced senescence promoted by EGR1

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Transcriptome analysis of pulsed activation of MAPK signaling in HEK-RAF-ER cells [RNA_seq_pulse_time_series]

Project description:In this study we performed pulsed activation of MAPK signalling by inducing RAF activity of the RAF-ER constract by tamoxifen, and subsequently blocking MAPK activity using MEK inhibitor at different times. Transcriptomes were sampled 0.5 h to 8h after induction

2024-01-13 | GSE250533 | GEO

ChIP-seq of CSF-1R in THP-1 cell lines deleted for EGR1 gene by CRISPR-Cas9 and ChIP-seq of CSF-1R in 2 CMML patients

Project description:CSF-1R is recruited on EGR1 motifs in monocytes where it colocalizes with EGR1. To address if EGR1 required for CSF-1R recruitment on chromatin, THP-1 monocytic cell line has been deleted for EGR1 by CRISPR-Cas9 approach. 3 clones were generated by single cell cloning and CSF-1R localization on chromatin was compared to two unmodified THP-1 clones by ChIP-sequencing. Since the read number was strongly decreased in the EGR1-deleted clones, the three clones were pooled for the comparison with wild-type clones. ChIPseq of CSF-1R (Nter Antibody) in monocytes of two CMML patients (CMML2130 and CMML2609)

2019-03-28 | E-MTAB-7756 | biostudies-arrayexpress

Glucocorticoids delay RAF-induced senescence promoted by EGR1 [ChIP-seq]

Project description:Glucocorticoids delay RAF-induced senescence promoted by EGR1 [ChIP-seq]

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Targeted Perturb-seq of regulators of the transcriptional network downstream of RAF-MAPK signaling [perturb_seq]

Project description:In this study we use a (targeted) perturb seq experiment in which we knock out 22 transcription factors downstream of MAPK signalling in order to reconstruct the transcriptional network downstream of RAF/MAPK signaling.

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IFN-kappa Suppresses the Replication of Influenza A Virus through IFNAR-MAPK-Fos-CHD6 Axis

Project description:IFN-kappa Suppresses the Replication of Influenza A Virus through IFNAR-MAPK-Fos-CHD6 Axis

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EGR1 regulation in human bone marrow stromal cells

Project description:Human bone marrow stromal cells (BMSCs) are key elements of the hematopoietic environment and they play a central role in bone and bone marrow physiology. However, how key BMSC functions are regulated is largely unknown. We analyzed the role of the immediate early response transcription factor EGR1 as key BMSC regulator and found that EGR1 was highly expressed in prospectively-isolated primary BMSCs, downregulated upon culture, and lower in non-CFU-F-containing CD45neg BM cells. Furthermore, EGR1 expression was lower in proliferative regenerating adult and fetal primary cells compared to adult steady-state BMSCs. Accordingly, EGR1 overexpression markedly decreased BMSC proliferation but considerably improved hematopoietic stroma support function as indicated by an increased production of transplantable CD34+CD90+ hematopoietic stem cells in expansion co-cultures. The improvement of BMSC stroma support function was mediated by increased expression of hematopoietic supporting genes, such as VCAM1 and CCL28. On the other hand, EGR1 knockdown increased ROS-mediated BMSC proliferation, and clearly reduced BMSC hematopoietic stroma support potential. These findings thus show that EGR1 is a key BMSC transcription factor with a dual role in regulating proliferation and hematopoietic stroma support function that is controlling a genetic program to coordinate the specific functions of BMSC in their different biological contexts.

2019-06-27 | PXD011767 | Pride

Chromatin accessibility changes in experimentally-induced basal to squamous cell carcinoma transition (BST) upon EGFR/MAPK inhibitor treatments [ASZ_ATACseq_inhibitor]

Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST. Alternatively we drive c-FOS to induce BST. Here, we analyze chromatin accessibility profiles upon c-FOS activation

2021-10-20 | GSE178914 | GEO

DNA binding profile of c-FOS in experimentally-induced basal to squamous cell carcinoma transition (BST)

Project description:Basal cell carcinoma may undergo BST spontaneously or upon Hedgehog targeting therapy. We identified that modulation of Ras/MAPK or TGFb signaling drive BST. Here, we induce Ras/MAPK and/or abrogate TGFb signaling to induce BST and examine the DNA binding profile of the AP-1 transcription factor c-FOS.

2021-10-20 | GSE168374 | GEO

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