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Silcening RAC1 expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

ABSTRACT: In this study,RAC1 expression was silenced by RNA interference in colon cancer cell lines, and investigate the correlation between RAC1 expression and colon cancer proliferation,and differential expressed genes were analized by gene assay and qPCR technologe.The proliferation and colony formation ability of colon cancer cells were significantly reduced after RAC1 knockdown. More 1200 known genes were found to be involved in the RAC1 functions related tumorigenesis by genechip analysis, these genes related to cell proliferation/apoptosis and cell cycle process. qRT-PCR results showed an expression pattern consistent with that of the genechip analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE78093 | GEO | 2016/02/20

SECONDARY ACCESSION(S): PRJNA312594

REPOSITORIES: GEO

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Silcening RAC1 expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

Project description:In this study,RAC1 expression was silenced by RNA interference in colon cancer cell lines, and investigate the correlation between RAC1 expression and colon cancer proliferation,and differential expressed genes were analized by gene assay and qPCR technologe.The proliferation and colony formation ability of colon cancer cells were significantly reduced after RAC1 knockdown. More 1200 known genes were found to be involved in the RAC1 functions related tumorigenesis by genechip analysis, these genes related to cell proliferation/apoptosis and cell cycle process. qRT-PCR results showed an expression pattern consistent with that of the genechip analysis. Lentivirus-mediated RNA interference was used to knockdown RAC1 expression in colon cancer cell lines. And cell proliferation assays . GeneChip analysis were carried out for mRNA expression profiling, followed, the expressed levels of mRNA and protein were measured by Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot, respectively.

2016-02-20 | E-GEOD-78093 | biostudies-arrayexpress

Silcening YWHAE gene expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

2016-02-20 | GSE78094 | GEO

Silcening YWHAE gene expression suppresses the proliferation of colon cancer cells by inducing gene differentially expressed.

Project description:In this study,YWHAE expression was silenced by RNA interference in colon cancer cell lines, and investigate the correlation between YWHAE expression and colon cancer proliferation,and differential expressed genes were analized by gene assay and qPCR technologe.The proliferation and colony formation ability of colon cancer cells were significantly reduced after YWHAE knockdown. More 1200 known genes were found to be involved in the YWHAE functions related tumorigenesis by genechip analysis, these genes related to cell proliferation/apoptosis and cell cycle process. qRT-PCR results showed an expression pattern consistent with that of the genechip analysis. Lentivirus-mediated RNA interference was used to knockdown YWHAE expression in colon cancer cell lines. And cell proliferation assays . GeneChip analysis were carried out for mRNA expression profiling, followed, the expressed levels of mRNA and protein were measured by Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot , respectively.

2016-02-20 | E-GEOD-78094 | biostudies-arrayexpress

Rac1-mediated DNA damage and inflammation promote Nf2 tumorigenesis but also limit cell cycle progression by inducing p53 checkpoint and cellular senescence

Project description:Neurofibromatosis type 2 (NF2) is caused by mutations of the tumor suppressor MERLIN/NF2. Prior studies established Yap as the driver of proliferation and tumorigenesis upon Nf2 inactivation in a well defined, genetically engineered murine liver model. Here, we report that in this model system Nf2 tumorigenesis also involves DNA damage and inflammation via Rac1-mediated production of ROS. Ablation of Rac1 blocks Nf2 tumorigenesis in spite of hyperactivation of the cyclinD1-pRb-E2F1 pathway and profound increase in liver size associated with the loss of Rac1-dependent p53 checkpoint and senescence programs. Surprisingly, Erk, Akt and Stat3 signaling does not correlate with proliferation or tumorigenesis despite being activated in Nf2 deficient livers, indicating a lesser role of these pathways for Nf2 tumorigenesis. Because a senescence gene signature is associated with benign NF2 tumors but not with malignant NF2 mutant mesotheliomas, we conclude that senescence may underlie the benign nature of NF2.

2016-12-01 | GSE70742 | GEO

Tiam1 methylation by NSD2 promotes Rac1 signaling activation and cancer metastasis

Project description:Metastasis is the key cause of failure of cancer therapy or mortality, but targeting metastatic seeding and colonization remains an unresolved challenge. Here, we report a novel molecular event in cancer metastasis mediated by NSD2/Rac1 signaling and provide a detailed mechanistic investigation of cancer metastasis. We found that NSD2, a histone methyltransferase responsible for di-methylating histone 3 at lysine 36, was overexpressed in metastatic tumors, and overexpressed NSD2 enhanced tumor metastasis both in vitro and in vivo. We further investigated that NSD2 promoted tumor metastasis by activating the Rac1 signaling pathway. Mechanistically, NSD2 methylated Tiam1, a guanine nucleotide exchange factor that facilitates GDP-Rac1 to GTP-Rac1 transition at K724. We demonstrated that Tiam1 K724 methylation plays a crucial role in Tiam1 activation and GDP-Rac1 to GTP-Rac1 transition. Specifically, we identified that Tiam1 K724 methylation could be a predictive factor in cancer prognosis, and we demonstrated that pharmacological blocking of Tiam1 K724 methylation by employing a transmembrane peptide inhibited tumor metastasis both in vitro and in vivo. Thus, NSD2-methylated Tiam1 promoted Rac1 signaling activation and cancer metastasis, which might provide novel insights into tumor metastasis inhibition.

2023-07-23 | GSE237714 | GEO

Tiam1 methylation by NSD2 promotes Rac1 signaling activation and cancer metastasis II

2023-07-29 | GSE237996 | GEO

Transcriptome of K14 V12 Rac1 mice

Project description:Wholeskin from transgenic mice overexpressing epidermal specific (K14) activated mutant (V12) Rac1 analyzed with Illumina MouseRef8 v2 Gene Expression arrays Three V12 Rac1 7 day old pups compared to three 7 day old litter-mate controls

2016-06-13 | E-GEOD-71683 | biostudies-arrayexpress

Effect of Rac1 haploinsufficiency on the gene expression profile of mouse endothelial cells

Project description:The therapeutic potential of neurotrophic factors has been hampered by their inability to achieve adequate tissue penetration. Brain blood vessels, however, could be an alternative target for neuro-salvage therapies by virtue of their close proximity to neurons. Here we show that hemizygous deletion of Rac1 in mouse endothelial cells (ECs) attenuates brain injury and edema following focal cerebral ischemia. To explore the mechanisms whereby decrease of Rac1 in ECs provide neuroprotection, ECs were derived from Rac1+/+ and Rac1+/- mice. Microarray analysis was performed to determine the differential gene expression between Rac1+/+ and Rac1+/- ECs. Rac1+/+ and Rac1+/- ECs were cultured to subconfluence. Total RNA was extracted and reverse transcribed. Rac1+/+ (n = 2) and Rac1+/- (n = 2) EC cDNAs were labeled with Cy3 and Cy5, respectively, and equimolar mixtures of labeled Rac1+/+ and Rac1+/- probes were hybridized to 2 slides (sample #21648, #21649). Additionally, Rac1+/+ (n = 2) and Rac1+/- (n=2) EC cDNAs labeled with Cy5 and Cy3 (dye-swapping) were hybridized to 2 slides (sample #21650, #21651). Comparison of signal intensities between Rac1+/+ (channel 2) and Rac1+/- (channel 1) was conducted on each slide (sample), and the ratio of intensities from 4 slides were statistically assessed for each gene feature to investigate differential gene expression.

2009-03-15 | E-GEOD-15003 | biostudies-arrayexpress

Interacting partners of Rac1 (P29S/Q61L) compared to constitutively active Rac1 (Q61L)

Project description:Interactors of double mutant Rac1 (P29S/Q61L) compared to constitutively active Rac1 (Q61L).

2019-11-12 | PXD013941 | Pride

Unique vulnerability of RAC1-mutant melanoma to combined inhibition of CDK9 and immune checkpoints

Project description:RAC1P29S is the third most prevalent hotspot mutation in sun-exposed melanoma. RAC1 alterations in cancer are correlated with poor prognosis, resistance to standard chemotherapy, and insensitivity to targeted inhibitors. Although RAC1P29S mutations in melanoma and RAC1 alterations in several other cancers are increasingly evident, the RAC1-driven biological mechanisms contributing to tumorigenesis remain unclear. Lack of rigorous signaling analysis has prevented identification of alternative therapeutic targets for RAC1P29S-harboring melanomas. To investigate the RAC1P29S-driven effect on downstream molecular signaling pathways, we generated an inducible RAC1P29S expression melanocytic cell line and performed RNA-sequencing (RNA-seq) coupled with multiplexed kinase inhibitor beads and mass spectrometry (MIBs/MS) to establish enriched pathways from the genomic to proteomic level. Our proteogenomic analysis identified CDK9 as a potential new and specific target in RAC1P29S-mutant melanoma cells.In vitro, CDK9 inhibition impeded the proliferation of in RAC1P29S-mutant melanoma cells and increased surface expression of PD-L1 and MHC Class I proteins.In vivo, combining CDK9 inhibition with anti-PD-1 immune checkpoint blockade significantly inhibited tumor growthonly in melanomas that expressed the RAC1P29Smutation. Collectively, these results establish CDK9 as a novel target in RAC1-driven melanoma that can further sensitize the tumor to anti-PD-1 immunotherapy.

2024-06-12 | GSE248218 | GEO

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