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Expression data of cDNA from the ACHN control and Kindlin-2-depleting cells

ABSTRACT: Kindlin-2, an integrin-interacting FERM-domain-containing protein, has been known to play critical roles for tumor progression. However, the role of Kindlin-2 in renal cell carcinoma (RCC) progression has not been reported. We aim to investigate the role of Kindlin-2 in the progression of RCC and the underlying mechanisms. To uncover the related pathway in which Kindlin-2 is involved to promote clear cell renal cell carcinoma progression, ACHN control and Kindlin-2-depleting cells were analyzed by Affymetrix GeneChip human Gene 1.0 ST Arrays.

ORGANISM(S): Homo sapiens

PROVIDER: GSE76020 | GEO | 2015/12/16

SECONDARY ACCESSION(S): PRJNA306017

REPOSITORIES: GEO

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Expression data of cDNA from the ACHN control and Kindlin-2-depleting cells

Project description:Kindlin-2, an integrin-interacting FERM-domain-containing protein, has been known to play critical roles for tumor progression. However, the role of Kindlin-2 in renal cell carcinoma (RCC) progression has not been reported. We aim to investigate the role of Kindlin-2 in the progression of RCC and the underlying mechanisms. To uncover the related pathway in which Kindlin-2 is involved to promote clear cell renal cell carcinoma progression, ACHN control and Kindlin-2-depleting cells were analyzed by Affymetrix GeneChip human Gene 1.0 ST Arrays. ACHN cells were transfected with control short hairpin RNA (shRNA) or Kindlin-2 shRNA. ACHN control and Kindlin-2-depleting cells cDNAs were hybridized to Affymetrix GeneChip Human Gene 1.0 ST arrays. Data were analyzed by Expression Console 1.4.1.

2015-12-16 | E-GEOD-76020 | biostudies-arrayexpress

Phosphoproteomics of Human ACHN cells by estrogen

Project description:To find out the potential targets in response to estrogen treatment on ACHN cell, a human renal cell carcinoma (RCC) cell line. Since estrogen can repress ACHN growth in a partly estrogen receptor-dependent manner, it is possible that phosphorylation state in ACHN cells is regulated.

2016-04-26 | PXD001962 | Pride

Transcriptome sequencing (RNA-Seq) of ACHN cells upon treatment of the 25nM,50nM Piericidin A or DMSO(0.1%) for exploring the mechanism of Piericidin A against the renal cell carcinoma

Project description:Piericidin A (PA), the most common member of the family of piericidins, is fermented from Streptomyces#sp.HBERC#58855. We have found that PA had significant cytostatic activity against the ACHN cells, which can be used as a potential drug against renal cell carcinoma (RCC). Therefore, we used the second-generation transcriptome sequencing (RNA-seq) to determine the expression changes of various genes in ACHN cells treated with PA (25nM,50nM) or DMSO (0.1%), so that we can investigate the molecular mechanism of PA against the RCC.

2021-06-19 | GSE116158 | GEO

DNase-seq from ACHN (ENCSR257BGZ)

Project description:DNase-seq on cell line ACHN (epithelial cell from 22 year old male human kidney, renal cell adenocarcinoma) For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2016-12-07 | GSE90316 | GEO

Mechanism of Kindlin-2 regulating invasion and metastasis of human Hepatocellular carcinoma

Project description:To explore the mechanism of Kindlin-2 regulating invasion and metastasis of human Hepatocellular carcinoma, we performed gene expression microarray analysis on Kindlin-2 knockdown LM3 cells and the control cells to compare the gene expression levels between the two groups.

2017-04-19 | GSE97951 | GEO

Loss of Kindlin-1 drives a more aggressive phenotype in cutaneous squamous cell carcinoma

Project description:Kindler syndrome (KS) is a rare genodermatosis resulting from loss-of-function mutations in FERMT1, the gene that encodes Kindlin-1. KS patients have a high propensity to develop aggressive and metastatic cutaneous squamous cell carcinoma (SCC). In this study, we show that loss of Kindlin-1 in a mouse model of cutaneous SCC leads to increased migration, invasion and degradation of collagen. Loss of Kindlin-1 increased tumor growth in vivo and in 3D spheroids, which was associated with the development of a hypoxic tumor environment and increased glycolysis. One of the most highly upregulated genes in Kindlin-1-depleted tumors was Mmp13, and the increased expression of MMP13 was responsible for driving the increased migration and invasion of the Kindlin-1-depleted SCC cells. These results provide evidence that Kindlin-1 loss in SCC can promote migration and invasion through the upregulation of MMP13, and offer novel insights into how Kindlin-1 loss leads to the development of a hypoxic environment that is permissive for tumor growth.

2023-07-14 | GSE236883 | GEO

dePillis2013 - Mathematical modeling of regulatory T cell effects on renal cell carcinoma treatment

Project description:Mathematical modeling of regulatory T cell effects on renal cell carcinoma treatment Lisette dePillis 1, , Trevor Caldwell 2, , Elizabeth Sarapata 2, and Heather Williams 2, 1. Department of Mathematics, Harvey Mudd College, Claremont, CA 91711 2. Harvey Mudd College, Claremont, CA 91711, United States, United States, United States Abstract We present a mathematical model to study the effects of the regulatory T cells (Treg) on Renal Cell Carcinoma (RCC) treatment with sunitinib. The drug sunitinib inhibits the natural self-regulation of the immune system, allowing the effector components of the immune system to function for longer periods of time. This mathematical model builds upon our non-linear ODE model by de Pillis et al. (2009) [13] to incorporate sunitinib treatment, regulatory T cell dynamics, and RCC-specific parameters. The model also elucidates the roles of certain RCC-specific parameters in determining key differences between in silico patients whose immune profiles allowed them to respond well to sunitinib treatment, and those whose profiles did not. Simulations from our model are able to produce results that reflect clinical outcomes to sunitinib treatment such as: (1) sunitinib treatments following standard protocols led to improved tumor control (over no treatment) in about 40% of patients; (2) sunitinib treatments at double the standard dose led to a greater response rate in about 15% the patient population; (3) simulations of patient response indicated improved responses to sunitinib treatment when the patient's immune strength scaling and the immune system strength coefficients parameters were low, allowing for a slightly stronger natural immune response. Keywords: Renal cell carcinoma, mathematical modeling., sunitinib, immune system, regulatory T cells.

2024-09-02 | BIOMD0000000908 | BioModels

Study the role of miRNAs in metastasis progression of RCC cell lines

Project description:This study investigates for the miRNAs that drive or regulates Renal Cell Carcinoma (RCC) metastatic progression using two different RCC cell lines, the metastatic (LM2 and LM1) and non-metastatic (SN12C).

2010-08-19 | GSE23690 | GEO

ELOVL5 promotes cell proliferation and invasion in renal cell carcinoma

Project description:Fatty acid is a main component of lipid. The differences of chain-length and pattern of saturation / desaturation in fatty acid are essential for diversity of biological lipid functions. Elongation of very-long-chain fatty acids (ELOVL) plays a critical role in regulating the elongation of fatty acid and ELOVL 1 to 7 are reported in the present. In several cancers but renal cell carcinoma (RCC), the relationship between ELOVLs and cancer progression has been reported. In TCGA cohort, ELOVL5 expression is associated with advanced TNM stage and poor prognosis. We performed CRISPR-Cas9 targeted knockout of ELOVL5 in 2 different RCC cell lines, ACHN and 786-O, respectively. ELOVL5 knockout significantly suppressed cellular invasion, migration and proliferation in vitro and in vivo. In ingenuity Pathway Analysis, Akt signaling activation was decreased in ELOVL5-KO cells. In western blotting analysis, the phosphorylation level of Akt was inhibited in ELOVL5-KO cells. Resultantly, it was suggested that ELOVL5 is involved in the phosphorylation level of Akt and affects cancer progression in RCC.

2022-08-17 | GSE192403 | GEO

Hi-C from ACHN (ENCSR343VKT)

Project description:HiC experiment done on ACHN For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2017-10-23 | GSE105556 | GEO

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