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MAGT1 is involved in HeLa cell proliferation through regulating p21 expression, S-phase progress and ERK/p38 MAPK MYC axis

ABSTRACT: Background: Magnesium transporter subtype 1 (MAGT1) is involved in animal development and cell differentiation. Thus far, researches on MAGT1 are mainly focused on Cardiomyocyte regulation and differentiation, but rare research has been reported on cell proliferation, especially concerning the underlying molecular mechanisms. Methods: HeLa cells were transiently knock down with different SiRNAs and processed for RNA sequencing and bioinformatics analysis, western blot, real-time PCR as well as cell cycle assays. Results: We showed that cell proliferation was significantly restricted with S-phase arrest in MAGT1 knock down cells, which was further confirmed by the up expression of p21, CCNA1 and CCNB1, while down expression of CCND1, CCNE1 and CDK4. Knocking down MAGT1 also resulted in significant transcriptional expression changes of 1599 target genes analyzed by RNA sequencing. The bioinformatics analysis showed that MAGT1 was related to MAPK signaling pathway. Western blot analysis confirmed that the phosphorylation of ERK1/2 and p38 exhibited a remarkable reduction in MAGT1 downregulated group. Conclusion: MAGT1 is critical in HeLa cell proliferation, S-phase progress and ERK/p38 MAPK signaling pathway, indicating that MAGT1 might be a novel target of anticancer research.

ORGANISM(S): Homo sapiens

PROVIDER: GSE166084 | GEO | 2022/02/02

REPOSITORIES: GEO

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FGF9 Promotes Mouse Spermatogonial Stem Cell Proliferation Mediated by p38 MAPK Signaling [bulk RNA-seq]

Project description:Objectives: Fibroblast growth factor 9 (FGF9) is expressed by somatic cells in the seminiferous tubules, yet little information exists about its role in regulating spermatogonial stem cells (SSCs). Materials and Methods: Fgf9 overexpression lentivirus was injected into mouse testes, and PLZF immunostaining was performed to investigate the effect of FGF9 on spermatogonia in vivo. Effect of FGF9 on SSCs was detected by transplanting cultured germ cells into tubules of testes. RNA-seq of bulk RNA and single-cell was performed to explore FGF9 working mechanisms. SB203580 was used to disrupt p38 MAPK pathway. p38 MAPK protein expression was detected by western blot and qPCR was performed to determine different gene expression. Small interfering RNA (siRNA) was used to knock down Etv5 gene expression in germ cells. Results: Overexpression of Fgf9 in vivo resulted in arrested spermatogenesis and accumulation of undifferentiated spermatogonia. Exposure of germ cell cultures to FGF9 resulted in larger numbers of SSCs over time. Inhibition of p38 MAPK phosphorylation negated the SSC growth advantage provided by FGF9. Etv5 and Bcl6b gene expression was enhanced by FGF9 treatment. Gene knockdown of Etv5 disrupted the growth effect of FGF9 in cultured SSCs along with downstream expression of Bcl6b. Conclusions: Taken together, this data indicates that FGF9 is an important regulator of SSC proliferation, operating through p38 MAPK phosphorylation and upregulating Etv5 and Bcl6b in turn.

2020-10-26 | GSE160062 | GEO

FGF9 Promotes Mouse Spermatogonial Stem Cell Proliferation Mediated by p38 MAPK Signaling [single-cell RNA-seq]

2020-10-26 | GSE160061 | GEO

Homo sapiens

Project description:EWS siRNA knock-down in HeLa cell line

| PRJNA127931 | ENA

Transcription profiling by array of left ventricle tissues from rat with overexpression of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38? in the heart

Project description:Mitogen-activated protein kinases (MAPKs) regulate cardiomyocyte growth and apoptosis in response to extracellular stimulation, but the downstream effectors that mediate their pathophysiological effects remain poorly understood. We determined the targets and role of p38 MAPK in the heart in vivo by using local adenovirus-mediated gene transfer of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38Î± in rats. DNA microarray analysis of animals with cardiac-specific overexpression of p38 MAPK revealed that 264 genes were upregulated more than 2-fold including multiple genes controlling cell division, cell signaling, inflammation, adhesion and transcription. Several previously unknown p38 target genes were found. Using gel mobility shift assays we identified several cardiac transcription factors that were directly activated by p38 MAPK. Finally, we determined the functional significance of the altered cardiac gene expression profile by histological analysis and echocardiographic measurements, which indicated that p38 MAPK overexpression induced gene expression results in cell proliferation, myocardial inflammation and fibrosis. In conclusion, we defined the novel target genes and transcription factors as well as the functional effects of p38 MAPK in the heart. Expression profiling of p38 MAPK overexpression identified cell cycle regulatory and inflammatory genes critical for pathological processes in the adult heart. Experiment Overall Design: Left ventricular gene expression profiles three days after MKK3bE + WT p38Î± gene transfer were compared with those of Lac Z âtreated animals by screening Affymetrix Rat Expression Set 230_2.0 Arrays (there are 5 samples in both group).

2009-04-25 | E-GEOD-3866 | biostudies-arrayexpress

Effects of Ars2 or DGCR8 siRNA on gene expression

Project description:Ars2 is a component of the nuclear cap-binding complex that is required for cellular proliferation and contributes to microRNA biogenesis. Arrays were performed to determine the repertoire of genes that change following knock-down of Ars2. Knock-down of DGCR8 was also performed to determine which changes in Ars2 knock-down cells resulted from defects in microRNA expression. 9 samples were analyzed including: three biological replicates of control siRNA-transfected HeLa cells, HeLa cells transfected with three independent siRNAs targeting Ars2, or HeLa cells transfected with three independent siRNAs targeting DGCR8.

2012-02-01 | E-GEOD-34679 | biostudies-arrayexpress

FGF9 Promotes Mouse Spermatogonial Stem Cell Proliferation Mediated by p38 MAPK Signaling

Project description:FGF9 Promotes Mouse Spermatogonial Stem Cell Proliferation Mediated by p38 MAPK Signaling

| PRJNA671712 | ENA

p38 MAPK overexpression in heart in vivo.

Project description:Mitogen-activated protein kinases (MAPKs) regulate cardiomyocyte growth and apoptosis in response to extracellular stimulation, but the downstream effectors that mediate their pathophysiological effects remain poorly understood. We determined the targets and role of p38 MAPK in the heart in vivo by using local adenovirus-mediated gene transfer of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38α in rats. DNA microarray analysis of animals with cardiac-specific overexpression of p38 MAPK revealed that 264 genes were upregulated more than 2-fold including multiple genes controlling cell division, cell signaling, inflammation, adhesion and transcription. Several previously unknown p38 target genes were found. Using gel mobility shift assays we identified several cardiac transcription factors that were directly activated by p38 MAPK. Finally, we determined the functional significance of the altered cardiac gene expression profile by histological analysis and echocardiographic measurements, which indicated that p38 MAPK overexpression induced gene expression results in cell proliferation, myocardial inflammation and fibrosis. In conclusion, we defined the novel target genes and transcription factors as well as the functional effects of p38 MAPK in the heart. Expression profiling of p38 MAPK overexpression identified cell cycle regulatory and inflammatory genes critical for pathological processes in the adult heart. Keywords: Gene transfer

2006-12-19 | GSE3866 | GEO

MAGT1 is involved in HeLa cell proliferation through regulating p21 expression, S-phase progress and ERK/p38 MAPK MYC axis

Project description:MAGT1 is involved in HeLa cell proliferation through regulating p21 expression, S-phase progress and ERK/p38 MAPK MYC axis

| PRJNA699234 | ENA

Knockdown of the transcription factor PAX6 by short hairpin RNA in the adenocarcinoma cell line HPAFII reveal changes in gene expression of several cancer relevant genes

Project description:PAX6 is an evolutionary conserved transcription factor important for normal development of the CNS, eye and pancreas. Its role in cancer is however poorly understood as both tumor suppressive- and oncogenic properties have been reported. We generated a pancreatic adenocarcinoma cell line (HPAFII) were PAX6 was knocked down by the use of short hairpin RNA. To generate a control cell line scrambled short hairpin RNA was used. Successful knock down of PAX6 was confirmed by RT-qPCR and Western blot. RNA were harvested from shPAX6, shControl and untransfected HPAFII cells, and used in gene expression microarray to look for differences in gene expression when PAX6 was knocked down.

2020-07-01 | E-MTAB-5416 | biostudies-arrayexpress

Gene expression profiling in mouse livers after administration of both hydrogen-rich water and hydrogen gas

Project description:Molecular hydrogen is a hopeful agent for oxidative stress-related and/or inflammatory disorders. However, the molecular mechanism for these therapeutic effects of hydrogen still remains to be fully elucidated. We examined whether molecular hydrogen alters gene expression levels in normal mouse livers by DNA microarray analysis. We identified 140 mouse genes that were upregulated (31 genes) or downregulated (109 genes) after three weeks of the inhalation of 2% hydrogen-containing air with oral intake of hydrogen-rich water. Ingenuity Pathway Analysis revealed that hydrogen influenced expression of NF-kB- and NFAT-regulated genes. Western blot analysis showed that hydrogen attenuated Erk, p38 MAPK, and NF-kB signaling in mouse livers.

2014-08-01 | GSE48826 | GEO

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