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Microarray analysis of gene expression profiles in response to tomato leaves extract treatment in MCF-7 breast cancer cells

ABSTRACT: Microarray analysis was performed to evaluate the global gene expression profiles of MCF-7 breast cancer cells treated with tomato leaves extract (TLE) in 1 hr and 48 hrs of treatment. Several of genes with p < 0.05 and fold-change cut-off <2.00 from human genome had significantly changed after the treatments. Its showed the greatest roles in cancer cells growth and were found either to be down-regulated or up-regulated in cells after the treatment.TLE gave significant expression effects towards several genes such as CRYAB, PIM1, BTG1, CYR61, HIF1A, CEBP-beta, TXNIP, THBS1, HMG1L1 and HIST2H3D genes. These results demonstrate the potent activity of TLE as an anti-cancer agent.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33443 | GEO | 2011/11/05

SECONDARY ACCESSION(S): PRJNA148699

REPOSITORIES: GEO

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Microarray analysis of gene expression profiles in response to tomato leaves extract treatment in MCF-7 breast cancer cells

Project description:Microarray analysis was performed to evaluate the global gene expression profiles of MCF-7 breast cancer cells treated with tomato leaves extract (TLE) in 1 hr and 48 hrs of treatment. Several of genes with p < 0.05 and fold-change cut-off <2.00 from human genome had significantly changed after the treatments. Its showed the greatest roles in cancer cells growth and were found either to be down-regulated or up-regulated in cells after the treatment.TLE gave significant expression effects towards several genes such as CRYAB, PIM1, BTG1, CYR61, HIF1A, CEBP-beta, TXNIP, THBS1, HMG1L1 and HIST2H3D genes. These results demonstrate the potent activity of TLE as an anti-cancer agent. We analyzed untreated (0 hr) and treated MCF-7 breast cancer cells (after 1 hr and 48hrs) using the Affymetrix Human Exon 1.0 ST platform. Chip array was scanned by Affymetrix Microarray Suite/GCOS. Experiment were performed in triplicates. Raw data was processed by GeneSpringGX v7.2 (Agilent Technology, USA).

2011-11-05 | E-GEOD-33443 | biostudies-arrayexpress

Loss of Pim1 Imposes a Hyperadhesive Phenotype on Endothelial Cells

Project description:Background: PIM1 is a constitutively active serine-threonine kinase regulating cell survival and proliferation. Increased PIM1 expression has been correlated with cancer metastasis by facilitating migration and anti-adhesion. Endothelial cells play a pivotal role in these processes by contributing a barrier to the blood stream. Here, we investigated whether PIM1 regulates mouse aortic endothelial cell (MAEC) monolayer integrity. Methods: Pim1-/-MAEC were isolated from Pim1 knockout mice and used in trypsinization-, wound closure assays, electrical cell-substrate sensing, immunostaining, cDNA transfection and as RNA source for microarray analysis. Results: Pim1-/-MAEC displayed decreased migration, slowed cell detachment and increased electrical resistance across the endothelial monolayer. Reintroduction of Pim1- cDNA into Pim1-/-MAEC significantly restored wildtype adhesive characteristics. Pim1-/--MAEC displayed enhanced focal adhesion and adherens junction structures containing vinculin and M-NM-2-catenin, respectively. Junctional molecules such as Cadherin 13 and matrix components such as Collagen 6a3 were highly upregulated in Pim1-/- cells. Intriguingly, extracellular matrix deposited by Pim1-/- cells alone was sufficient to induce the hyperadhesive phenotype in wildtype endothelial cells. Conclusion: Loss of Pim1 induces a strong adhesive phenotype by enhancing endothelial cell-cell and cell-matrix adhesion by the deposition of a specific extracellular matrix. Targeting PIM1 function therefore might be important to promote endothelial barrier integrity. Pim-1-/- mouse aortic endothelial cells were compared to wildtype cells

2012-10-29 | E-GEOD-32059 | biostudies-arrayexpress

Upregulation of CYR61 by TGF-β and YAP signaling exerts a counter-suppression of hepatocellular carcinoma

Project description:TGF-β and Hippo signaling are two critical pathways engaged in cancer progression by regulating both oncogenes and tumor suppressors, yet how the two pathways coordinately exert their functions in the development of hepatocellular carcinoma (HCC) remains elusive. In this study, we firstly conducted an integrated analysis of public liver cancer databases and our experimental TGF-β target genes, identifying CYR61 as a pivotal gene relating to HCC development. Evidence revealed that CYR61 is a direct target gene of TGF-β in liver cancer cells. In addition, TGF-β-stimulated Smad2/3 and the Hippo pathway downstream effectors YAP and TEAD4 can form a protein complex on the promoter of CYR61, thereby activating the promoter activity and stimulating CYR61 gene transcription in a collaborative manner. Functionally, depletion of CYR61 enhanced TGF-β- or YAP activation-mediated growth and migration of liver cancer cells. Consistently, ectopic expression of CYR61 was capable of impeding TGF-β- or YAP-induced malignant transformation of HCC cells in vitro, and attenuating HCC xenograft growth in nude mice. Finally, Downregulation of CYR61 expression in HCC tissues than that in normal liver tissues is well associated with a bad clinical outcome in patients. Together, these results add new evidence for the interplay between TGF-β and Hippo signaling and unveil an important tumor suppressor function of CYR61 in liver cancer.

2023-08-19 | GSE240760 | GEO

Loss of Pim1 Imposes a Hyperadhesive Phenotype on Endothelial Cells

Project description:Background: PIM1 is a constitutively active serine-threonine kinase regulating cell survival and proliferation. Increased PIM1 expression has been correlated with cancer metastasis by facilitating migration and anti-adhesion. Endothelial cells play a pivotal role in these processes by contributing a barrier to the blood stream. Here, we investigated whether PIM1 regulates mouse aortic endothelial cell (MAEC) monolayer integrity. Methods: Pim1-/-MAEC were isolated from Pim1 knockout mice and used in trypsinization-, wound closure assays, electrical cell-substrate sensing, immunostaining, cDNA transfection and as RNA source for microarray analysis. Results: Pim1-/-MAEC displayed decreased migration, slowed cell detachment and increased electrical resistance across the endothelial monolayer. Reintroduction of Pim1- cDNA into Pim1-/-MAEC significantly restored wildtype adhesive characteristics. Pim1-/--MAEC displayed enhanced focal adhesion and adherens junction structures containing vinculin and β-catenin, respectively. Junctional molecules such as Cadherin 13 and matrix components such as Collagen 6a3 were highly upregulated in Pim1-/- cells. Intriguingly, extracellular matrix deposited by Pim1-/- cells alone was sufficient to induce the hyperadhesive phenotype in wildtype endothelial cells. Conclusion: Loss of Pim1 induces a strong adhesive phenotype by enhancing endothelial cell-cell and cell-matrix adhesion by the deposition of a specific extracellular matrix. Targeting PIM1 function therefore might be important to promote endothelial barrier integrity.

2012-10-29 | GSE32059 | GEO

Gene expression in Trp53 and Rb1 double knockout mouse prostate epithelial cancer cells expressing PIM1

Project description:To identify the downstream molecules that mediate PIM1 induced aggressive prostate cancer cells, p53 and Rb-deficient mouse prostate epithelial cells were transduced with PIM1 lentivirus and performed a gene expression profile microarray.

2018-08-21 | GSE118786 | GEO

Downregulation of CYR61 promotes hepatocellular carcinoma progression by ameliorating the protumor functions of TGF-β/YAP and impeding the activation of stromal hepatic stellate cells

Project description:Hepatic stellate cells (HSCs) in the tumor microenvironment play a pivotal role in the development of hepatocellular carcinoma (HCC), which is the major form of primary liver cancers and one of the most lethal cancer types worldwide. TGF-β and Hippo signaling are two critical pathways regulating HSC activation and HCC development through their downstream transcriptional regulators, i.e., Smad proteins and YAP/TEADs, respectively. However, how the two pathways coordinately exert their functions in HCC remains elusive. In this study, we performed integrated analyses of public liver cancer databases and clinical cancer tissues, leading to identification of CYR61 as one of the key candidate genes that may regulate liver cancer progression. TGF-β-activated Smad2/3 and YAP/TEAD4 can form a protein complex to induce CYR61 expression in both cancer cells and stellate cells. As a secreted matricellular protein, CYR61 exerts its tumor suppressor functions via acting on cancer cells directly or regulating the stromal stellate cells. On one hand, CYR61 ameliorates TGF-β- or YAP-mediated liver cancer cell proliferation, colony formation and invasion in vitro, and also tumor growth in nude mice. On the other, CYR61 also impedes cancer cell- or TGF-β-induced stellate cell activation, thereby mitigating the tumor-promoting functions of HSCs as assessed both in vitro and in vivo. In support of its tumor suppressor function, the expression of CYR61 is reduced in HCC tissues and cell lines when compared with their normal counterparts, which is associated with a shorter survival period in cancer patients. Together, these results add new evidence for the interplay between TGF-β and Hippo signaling in regulating gene transcription, and unveil a pivotal role of CYR61 in suppressing liver cancer progression by controlling the activation of hepatic stellate cells in the tumor microenvironment.

2023-01-11 | GSE222402 | GEO

Tetracycline-Inducible Cyr61 effect on LN229 glioma cells

Project description:Glioblastoma multiforme is the most common and aggressive form of brain cancer. The use of oncolytic HSV-1 (oHSV) to selectively target brain cancer cells leading to their lytic destruction has shown to be very promising in a preclinical setting, but is lacking efficacy in clinical trials. Cyr61, a secreted extracellular matrix protein which functions to promote angiogenesis, migration, proliferation and tumorigenesis, was found to be upregulated rapidly following oHSV infection. Here we show, using microarray analysis, that Cyr61 expression leads to the induction of several genes with type 1 interferon function. We show that Cyr61 mediated type 1 IFN induction is through its interaction with integrin alpha6beta1 on the cell surface and results in oHSV inhibition, reducing the efficacy of this therapy. We used microarray to detail the global program of gene expression underlying Cyr61 mediated oncolytic HSV-1 inhibition and identified distinct classes of up-regulated genes during this process. Tetracycline-Inducible glioma cells expressing Cyr61 protein in the presence of doxycycline were treated with or without doxycycline for 24 hours. RNA was extracted and hybridized on Affymetrix microarray. Two groups: Â± dox to induce cyr61, performed in triplicate.

2012-04-03 | E-GEOD-29384 | biostudies-arrayexpress

Integrative analysis of transcriptomics and clinical data uncovers the tumorsuppressive activity of MITF in prostate cancer

Project description:The dysregulation of gene expression is an enabling hallmark of cancer. Computational analysis of transcriptomics data from human cancer specimens, complemented with exhaustive clinical annotation, provides an opportunity to identify core regulators of the tumorigenic process. Here we exploit well-annotated clinical datasets of prostate cancer for the discovery of transcriptional regulators relevant to prostate cancer. Following this rationale, we identify Microphthalmia-associated transcription factor (MITF) as a prostate tumor suppressor among a subset of transcription factors. Importantly, we further interrogate transcriptomics and clinical data to refine MITF perturbation-based empirical assays and unveil Crystallin Alpha B (CRYAB) as an unprecedented direct target of the transcription factor that is, at least in part, responsible for its tumor-suppressive activity in prostate cancer. This evidence was supported by the enhanced prognostic potential of a signature based on the concomitant alteration of MITF and CRYAB in prostate cancer patients. In sum, our study provides proof-of-concept evidence of the potential of the bioinformatics screen of publicly available cancer patient databases as discovery platforms, and demonstrates that the MITF-CRYAB axis controls prostate cancer biology.

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Loss of BTG1 function promotes ETV6-RUNX1-mediated leukemic transformation by upregulation of BCL6

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BTG1 modulates ATF4 function in response to cellular stress: implications for tumor cell survival

Project description:Analysis of the effect of glutamine starvation in mouse embryonic fibroblasts (MEFs) with and without Btg1 at gene expression level. The hypothesis tested in the present study was that loss of Btg1 affect the expression of stress-response genes. Results provide important information of the differentially expressed genes regulated by Btg1 upon glutamine deprivation, explaining the survival advantage of tumor cells harboring Btg1 loss under cellular stress condition.

2014-11-26 | GSE63642 | GEO

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