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STIL/AURKA axis promotes cell proliferation by influencing primary cilia formation in bladder cancer

ABSTRACT: Our research showed that primary cilia was reduced in human bladder cancer (BLCA) cells, and PC deficiency promote cell proliferation. However, the concrete mechanisms remain unknown. SCL/TAL1 interrupting locus (STIL), a PC-related protein, was screened in our previous study and could influence the cell cycle by regulating PC in tumor cells. To elucidate the function of STIL for PC to explore the underlying mechanism of PC in BLCA, we establisded siNC and siSTIL EJ cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE211563 | GEO | 2023/03/31

REPOSITORIES: GEO

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Loss of colonic primary cilia promotes inflammation and carcinogenesis

Project description:Primary cilia (PC) are important signaling hubs in cells and we explored their role in colorectal cancer (CRC) and colitis. In the colon we found PC to be mostly present on different subtypes of fibroblasts and exposure of mice to either chemically induced colitis-associated colon carcinogenesis (CAC) or dextran sodium sulfate (DSS)-induced acute colitis decreased PC numbers. We employed conditional knock-out strains for the PC essential genes, Kif3A and Ift88, to generate mice with reduced numbers of PC on colonic fibroblasts. These mice showed an increased susceptibility in the CAC model as well as in DSS-induced colitis. Secretome and immunohistochemical analyses of DSS-treated mice displayed an elevated production of the pro-inflammatory cytokine IL-6 in PC-deficient colons. An inflammatory environment diminished PC presence in primary fibroblast cultures. This was triggered by IL-6 as identified by RNAseq analysis together with blocking experiments, suggesting an activation loop between IL-6 production and PC loss. Notably, an analysis of PC presence on biopsies of patients with ulcerative colitis as well as CRC patients revealed decreased numbers of PC on colonic fibroblasts in pathological versus surrounding normal tissue. Taken together, we provide evidence that a decrease in colonic PC numbers promotes colitis and CRC.

2022-11-29 | PXD033440 | Pride

Loss of colonic primary cilia promotes inflammation and carcinogenesis.

Project description:Primary cilia (PC) are important signaling hubs and their deregulation is associated with various diseases. The 2P-CF cultures plus starvation mimic the in vivo proportion of PC on colonic fibroblasts (CF) in an intact colon and thus allow to explore the biology of PC. We generated conditioned starvation medium from colons of DSS treated (termed inflammatory conditioned medium, i.e. inf-CM) and untreated control animals (termed co-CM) and cultured 2P-CF in those media for 24 hours. 30-40% of 2P-CF starved in control medium displayed PC, whereas PC number on 2P-CF starved in inf-CM was consistently lower. We performed RNAseq analysis of 2P-CF starved in inf-CM or in co-CM to gain insight in the molecular traits of those cell cultures.

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Project description:Purpose: To investigate the tumor-promoting role of STIL in bladder cancer. Method: We established the STIL knockout cell line in which the target gene was knocked out by sgRNA. RNA was extracted from cells using trizol reagent(Invitrogen) Result: Through RNA-sequencing analysis of wild-type and STIL-deficient UMUC3 cell lines, the downstream signaling pathways that STIL may be involved in were determined. We found that the PI3K/AKT/mTOR signaling pathway and c-myc were significantly inactivated when STIL was knocked out in bladder cancer. Our RNA-sequencing analysis results showed that the downstream molecules of c-myc (MCM4, HSPD1, EIF2S2, DDX21, DDX18, CBX3, ABCE1) were significantly down-regulated in bladder cancer cells after knockout. Conclusion: STIL enhances the PI3K/AKT/mTOR pathway, which consequently upgraded the expression of c-myc, ultimately promoting the occurrence and progression of bladder cancer C. STIL may suggest potential utility for bladder cancer therapy.

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Primary cilia and SHH signaling impairments in human and mouse models of Parkinson’s disease

Project description:Parkinson’s disease (PD) as a progressive neurodegenerative disorder arises from multiple genetic and environmental factors. However, underlying pathological mechanisms remain poorly understood. Using multiplexed single-cell transcriptomics, we analyze human neural precursor cells (hNPCs) from sporadic PD (sPD) patients. Alterations in gene expression appear in pathways related to primary cilia (PC). Accordingly, in these hiPSC-derived hNPCs and neurons, we observe a shortening of PC. Additionally, we detect a shortening of PC in PINK1-deficient human cellular and mouse models of familial PD. Furthermore, in sPD models, the shortening of PC is accompanied by an increased SHH signal transduction. Inhibition of this pathway rescues the alterations in PC morphology and mitochondrial dysfunction. Thus, increased SHH activity due to ciliary dysfunction is needed for the development of pathoetiological phenotypes observed in sPD, like mitochondrial dysfunction. In sum, altered PC function is part of early PD pathoetiology and inhibiting the overactive SHH signaling is a potential neuroprotective therapy.

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Therapeutically actionable signaling node to rescue AURKA driven loss of primary cilia in VHL-deficient cells.

Project description: Not available

| S-EPMC8128866 | biostudies-literature

MYBL2 promotes proliferation and metastasis of bladder cancer through transactivation of CDCA3

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2022-05-02 | GSE201875 | GEO

MYBL2 promotes proliferation and metastasis of bladder cancer through transactivation of CDCA3

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Melatonin inhibited tumorigenesis of bladder cancer via suppressing PPARγ/ENO1 mediated glycolysis

Project description:Bladder cancer (BLCA) is one of the most malignant human cancers in the world. The increasingly prominent phenomenon of chemoresistance has become an essential obstacle to clinical treatment for BLCA, and there is an urgent need to explore novel drugs to improve the current clinical status. Melatonin is a well-known natural hormone that showed a potential anti-cancer effect in multiple human cancers. In our study, we comprehensively explored the inhibitory effect of melatonin on BLCA and found that it could suppress the glycolysis process in BLCA cells. Moreover, we discovered that the ninth step enzyme ENO1 of glycolysis was the downstream effector of melatonin and could be a predictive biomarker of BLCA patients.

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Gene expression data by the leaves of Eriobotrya japonica (Ej) on the LPS-stimulated human gingival fibroblast

Project description:The leaf of Eriobotrya japonica (Ej) has been used for a long time as an oriental medicine to treat pulmonary inflammatory diseases. This study investigated the gene expression changes by lipopolysaccharide (LPS) stimulation in the cultured human gingival fibroblast and the gene expression changes by the leaves of Ej when challenged with LPS using a microarray chip. Human gingival fibroblast were divided into three experimental groups; â C: Control, â¡ LPS: LPS-treatment only, â¢ LPS-Ej: LPS- and Ej-treatments. Total RNA was isolated from each experimental fibroblast (3 experimental group Ã 1 sample of each experimental group = total 3 samples).

2010-10-23 | E-GEOD-24832 | biostudies-arrayexpress

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