Novel circRNA_103758-miRNA-19b-3p-CIT axis is associated with proliferation and migration of bladder cancer via RhoA-ROCK signaling pathway
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE147985 | GEO | 2020/08/05
REPOSITORIES: GEO
Similar Datasets
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
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
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
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
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
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
Project description:Oral squamous cell carcinoma (OSCC) is one of the most common digestive tumors, which has high mortality rate. Long non-coding RNAs (lncRNA) and MicroRNAs (miRNAs) are associated with the cell cycle and differentiation during the occurrence and development of malignant tumors. This research aimed to investigate the effects of lncRNA SNHG20 on the progress of oral squamous cell carcinoma (OSCC) cells. Ninety pairs of tumor tissues and paracancerous tissues were collected from patients with OSCC and the CAL27 and SCC25 OSCC cells were selected for the following experiments. RT-qPCR was used for detecting the expression of SNHG20, miR-19b-3p, and RAB14. Western blotting was used to detect the protein levels of RAB14. MTT assay was employed to assess cell proliferation. Transwell assay was used to determine the cell migration and invasion abilities. Furthermore, luciferase reporter and RNA pull-down assays were used to verify the binding of SNHG20/RAB14 to miR-19b-3p. Then, the function of the SNHG20/miR-19b-3p/RAB14 axis in OSCC was explored. The results indicated that lncRNA SNHG20 was upregulated in the tissues. Furthermore, bioinformatic analysis showed that both SNHG20 and RAB14 could bind to miR-19b-3p. RAB14 was upregulated, and miR-19b-3p was downregulated in the tissues. The knockdown of SNHG20 inhibited cell proliferation, migration, and invasion. Contrarily, the knockdown of miR-19b-3p reversed the effects of si-SNHG20 on cell proliferation, migration, and invasion, and the overexpression of RAB14 reversed the effects of miR-19b-3p mimic on the cell biological functions. LncRNA SNHG20 affects cell proliferation, migration, and invasion via the miR-19b-3p/RAB14 axis in OSCC.
| S-EPMC8806619 | biostudies-literature
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
Project description:We have discovered a previously uncharacterized tumor suppressor function of Numb in the homeostasis of the normal bladder mucosa. Targeted ablation of Numb in the basal layer of the urothelium drives spontaneous bladder tumorigenesis, driving progression from preneoplastic to preinvasive and overtly invasive tumors, and accelerates tumorigenesis in the presence of oncogenic insults. Using 3D-Matrigel organoid cultures to recapitulate bladder tumorigenesis in vitro, we found that Numb deficiency enhances the proliferative and invasive potential of both mouse and human bladder cancer cells. Integrative transcriptomic and functional analyses revealed that downregulation of the canonical Hippo pathway, resulting in enhanced YAP transcriptional activity, underlies the biological aggressiveness of Numb-deficient bladder cancer. These molecular events are dependent on the activation of RhoA/ROCK signaling subsequent to Numb loss. Thus, a dysfunctional Numb–RhoA/ROCK–Hippo/YAP regulatory network is at play in aggressive Numb-deficient bladder cancers, opening avenues for the development of targeted therapies. Furthermore, retrospective cohort studies revealed that a Numb-deficient status correlates with worse overall survival in post-cystectomy muscle-invasive bladder cancer (MIBC) patients and increased risk of progression to MIBC in non-muscle-invasive bladder cancer (NMIBC) patients. The Numb-deficient status was associated with a 27-gene prognostic signature that has the potential to identify high-risk NMIBC patients who are eligible for targeted RhoA/ROCK/YAP therapies.
2024-10-11 | GSE256272 | GEO
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