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Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE147985 | GEO | 2020/08/05

REPOSITORIES: GEO

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Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway [microarray]

Project description:To determine the circRNA expression profile in BCa and matched non-tumor tissues, we uesed circRNA microArray analysis form Arraystar to examine the expression of circRNAs in BCa and matched non-tumor tissues.

2020-08-05 | GSE147984 | GEO

Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway [RNA-seq]

Project description:Purpose:The purpose of this study is to investigate the potential mechanisms that triggering the onset of bladder cancer and to screen differential expressed genes. Methods: We screened differentially expressed genes with the data obtained from RNA-seq on Bladder carcinoma samples and matched normal samples. Functional annotation analysis and protein-protein interaction (PPI) network were performed to investigate the potential key pathways and genes that play significant roles in BCa. Furthermore, the ceRNA network was established and the Gene Set Enrichment Analysis (GSEA) was executed to dig key circRNAs. Results: Following the identification of differentially expressed genes, functional annotation analysis was conducted, suggesting that differentially expressed mRNAs (DEMs) were mainly involved in cell cycle related pathways. The top 11 genes with the highest degree were extracted from PPI network. The predicted regulatory relationships among the differentially expressed genes were found and the ceRNA network was established. Finally, GSEA was conducted on the circRNAs and the key biological pathways were identified. Conclusion: Our study is the pioneering research to analyze the pathogenesis of BCa with integrated informatics and we have identified several hub genes, which reveals that the generation of BCa is closely related to cell cycle.

2020-08-05 | GSE147983 | GEO

Novel circRNA_0071196/miRNA?19b?3p/CIT axis is associated with proliferation and migration of bladder cancer.

Project description:Circular RNAs (circRNAs) are non?coding RNAs that are connected at the 3' and 5' ends by an exon or intron. Studies increasingly show that circRNAs play an important role in tumorigenesis by acting as a 'sponge' for microRNAs (miRNAs), which abrogates the latter's effect on their target mRNAs. To identify a possible circRNA/miRNA/mRNA network in bladder cancer (BCa), we analyzed the circRNA and mRNA expression profiles of BCa and adjacent normal bladder tissues. A total of 127 circRNAs and 1,612 mRNAs were differentially expressed in the tumor tissues, and were primarily associated with cancer?related pathways. A competing endogenous RNAs (ceRNA) network was then constructed which predicted a regulatory axis of circRNA_0071196, miRNA?19b?3p and its target gene citron Rho?interacting serine/threonine kinase (CIT). Luciferase reporter assay validated the relationship between circRNA_0071196 and miRNA?19b?3p and of the latter with CIT. Furthermore, CIT was overexpressed in the BCa tissues, and was found to be correlated with metastasis and tumor histological grade. Knockdown of CIT in the human bladder cancer cell line 5367 significantly inhibited the proliferation, migration and colony formation capacity of the cells, and also upregulated the mediators of the p53 and RhoA?ROCK signaling cascades that regulate cell cycle and migration. Taken together, our findings indicate that circRNA?0071196 upregulates CIT levels in BCa by sponging off miRNA?19b?3p, and the circRNA_0071196/miRNA?19b?3p/CIT axis is a potential therapeutic target in BCa.

| S-EPMC7384843 | biostudies-literature

Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway

Project description:Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway

| PRJNA622741 | ENA

Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway [microarray]

Project description:Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway [microarray]

| PRJNA622743 | ENA

Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway [RNA-seq]

Project description:Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway [RNA-seq]

| PRJNA622744 | ENA

CHD4 mediates proliferation and migration of non-small cell lung cancer via the RhoA/ROCK pathway by regulating PHF5A.

Project description:BackgroundChromodomain helicase DNA-binding protein 4 (CHD4) has been shown to contribute to DNA repair and cell cycle promotion; however, its roles in cancer initiation and progression remain largely unknown. This study aimed to demonstrate the role of CHD4 in the development of non-small cell lung cancer (NSCLC) and determine the potential mechanisms of action.MethodsBy using immunohistochemistry, the expression levels were evaluated in both cancer and non-cancerous tissues. Subsequently, CHD4 knockdown and overexpression strategies were employed to investigate the effects of CHD4 on cell proliferation, migration, along with the growth and formation of tumors in a xenografts mouse model. The protein expression levels of CHD4, PHF5A and ROCK/RhoA markers were determined by Western blot analysis.ResultsCompared with non-cancerous tissues, CHD4 was overexpressed in cancer tissues and CHD4 expression levels were closely related to clinical parameters of NSCLC patients. In H292 and PC-9 cell lines, CHD4 overexpression could promote the proliferative and migratory potential of NSCLC cells. Furthermore, down-regulation of CHD4 could reduce the proliferative and migratory ability in A549 and H1299 cell lines. Meanwhile, knockdown of CHD4 could decrease the tumorigenicity in nude mice. Finally, we demonstrated that one of the mechanisms underlying the promotive effect of CHD4 on NSCLC proliferation and migration may be through its interaction with PHD finger protein 5A (PHF5A) and subsequent activation of the RhoA/ROCK signaling pathway.ConclusionsCHD4, which is highly expressed in cancer tissue, could be an independent prognostic factor for NSCLC patients. CHD4 plays an important role in regulating the proliferative and migratory abilities of NSCLC via likely the RhoA/ROCK pathway by regulating PHF5A.

| S-EPMC7106713 | biostudies-literature

Annexin V-induced rat Leydig cell proliferation involves Ect2 via RhoA/ROCK signaling pathway.

Project description:This study investigated the effect of annexin V on the proliferation of primary rat Leydig cells and the potential mechanism. Our results showed that annexin V promoted rat Leydig cell proliferation and cell cycle progression in a dose- and time-dependent manner. Increased level of annexin V also enhanced Ect2 protein expression. However, siRNA knockdown of Ect2 attenuated annexin V-induced proliferation of rat Leydig cells. Taken together, these data suggest that increased level of annexin V induced rat Leydig cell proliferation and cell cycle progression via Ect2. Since RhoA activity was increased following Ect2 activation, we further investigated whether Ect2 was involved in annexin V-induced proliferation via the RhoA/ROCK pathway, and the results showed that annexin V increased RhoA activity too, and this effect was abolished by the knockdown of Ect2. Moreover, inhibition of the RhoA/ROCK pathway by a ROCK inhibitor, Y27632, also attenuated annexin V-induced proliferation and cell cycle progression. We thus conclude that Ect2 is involved in annexin V-induced rat Leydig cell proliferation through the RhoA/ROCK pathway.

| S-EPMC5380157 | biostudies-literature

NRF2 promotes breast cancer cell proliferation and metastasis by increasing RhoA/ROCK pathway signal transduction.

Project description:Nuclear factor erythroid 2-related factor (NRF2) is an important transcription factor in oxidative stress regulation. Overexpression of NRF2 is associated with human breast carcinogenesis, and increased NRF2 mRNA levels predict poor patient outcome for breast cancer. However, the mechanisms linking gain of NRF2 expression and poor prognosis in breast cancer are still unclear. Here, we provide evidence that NRF2 deletion inhibits proliferation and metastasis of breast cancer cells by down-regulating RhoA. Restoration of RhoA in MCF7 and MDA-MB-231 cells induced NRF2 knockdown-suppressed cell growth and metastasis in vitro, and NRF2 silencing suppressed stress fiber and focal adhesion formation leading to decreased cell migration and invasion. Mechanistic studies showed that NRF2 binds to the promoter region of estrogen-related receptor ? (ERR1) and may function as a silencer. This may enhance RhoA protein stability and lead to RhoA overexpression in breast cancer cell. Our findings indicate that NRF2 silencing-mediated reduction of RhoA expression contributes, at least in part, to the poor outcome of breast cancer patients with high NRF2 expression.

| S-EPMC5342001 | biostudies-literature

Gastrin stimulates pancreatic cancer cell directional migration by activating the G?12/13-RhoA-ROCK signaling pathway.

Project description:The mechanism by which gastrin promotes pancreatic cancer cell metastasis is unclear. The process of directing polarized cancer cells toward the extracellular matrix is principally required for invasion and distant metastasis; however, whether gastrin can induce this process and its underlying mechanism remain to be elucidated. In this study, we found that gastrin-induced phosphorylation of paxillin at tyrosine 31/118 and RhoA activation as well as promoted the metastasis of PANC-1 cancer cells. Depletion of G?12 and G?13 inhibited the phosphorylation of paxillin and downstream activation of GTP-RhoA, blocked the formation and aggregation of focal adhesions and facilitated polarization of actin filaments induced by gastrin. Suppression of RhoA and ROCK also exhibited identical results. Selective inhibition of the CCKBR-G?12/13-RhoA-ROCK signaling pathway blocked the reoriented localization of the Golgi apparatus at the leading edge of migrated cancer cells. YM022 and Y-27632 significantly suppressed hepatic metastasis of orthotic pancreatic tumors induced by gastrin in vivo. Collectively, we demonstrate that gastrin promotes Golgi reorientation and directional polarization of pancreatic cancer cells by activation of paxillin via the CCKBR-G?12/13-RhoA-ROCK signal pathway.

| S-EPMC5938061 | biostudies-literature

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