Transcriptomic analysis of gastric cancer cells in response to stable over-expression of circular RNA derived from CTNNB1 gene (circ-CTNNB1)
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PROVIDER: PRJNA493202 | ENA |
REPOSITORIES: ENA
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Project description:Circular RNAs (circRNAs), a subclass of noncoding RNAs characterized by covalently closed continuous loops, play emerging roles in tumorigenesis and aggressiveness. However, the functions and underlying mechanisms of circRNAs in regulating the Wnt/β-catenin signaling and cancer progression still remain elusive. We identify one intronic circRNA derived from CTNNB1 (circ-CTNNB1) as a novel driver of cancer progression. To investigate the mechanisms underlying the oncogenic functions of circ-CTNNB1, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human gastric cancer AGS cells in response to stable over-expression of circ-CTNNB1. The results showed that stable over-expression of circ-CTNNB1 led to altered expression of 2230 human mRNAs, including 1244 up-regulated genes and 986 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to circ-CTNNB1 over-expression in human cancer cells, and these findings will help us understand the pathogenesis of cancer progression.
2019-09-30 | GSE120496 | GEO
Project description:Circular RNAs (circRNAs), a subclass of noncoding RNAs characterized by covalently closed continuous loops, play emerging roles in tumorigenesis and aggressiveness. However, the functions and underlying mechanisms of circRNAs in regulating neuroblastoma progression still remain elusive. We identify one circRNA derived from CUX1 (circ-CUX1) as a novel driver of neuroblastoma progression. To investigate the mechanisms underlying the oncogenic functions of circ-CUX1, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human neuroblastoma IMR32 cells in response to stable over-expression of circ-CUX1. The results showed that stable over-expression of circ-CUX1 led to altered expression of 1215 human mRNAs, including 781 up-regulated genes and 434 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to circ-CUX1 over-expression in human tumor cells, and these findings will help us understand the pathogenesis of tumor progression.
2019-11-07 | GSE136135 | GEO
Project description:Transcriptomic analysis of neuroblastoma cells in response to stable over-expression of circular RNA derived from CUX1 gene (circ-CUX1)
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Project description:Circular RNAs (circRNAs) represent a class of covalently closed RNAs, derived from a non-canonical splicing event, ubiquitously expressed among Eukaryotes and conserved among different species. We identified a circRNA (circ-ZNF609) involved in the regulation of human primary myoblast proliferation. Upon its depletion, the percentage of proliferating myoblasts was highly reduced. To deepen our knowledge about circ-ZNF609 role in cell cycle regulation, we studied its expression and function in Rhabdomyosarcoma (RMS), a pediatric skeletal muscle malignancy. We found that circ-ZNF609 is up-regulated in biopsies from both the two major RMS subtypes, the alveolar (ARMS) and the embryonal (ERMS), and we discovered that its knock-down blocks proliferation of an ERMS-derived cell line, while it has no effect on ARMS-derived cells. To understand the mechanism through which circ-ZNF609 affects cell proliferation we compared the different effects of circ-ZNF609 depletion in ERMS and ARMS and we identified genes and pathways on which the circRNA acts.
2018-12-14 | GSE117609 | GEO
Project description:Argonaute 2 (AGO2) is the core component of microRNA (miRNA)-induced silencing complex, and plays a compelling role in tumorigenesis and aggressiveness. Recent studies have implicated the emerging roles of circular RNAs (circRNAs) in cancer progression. However, the roles of circRNAs in regulating the functions of AGO2 in cancer still remain elusive. We indentify one intronic circRNA derived from AGO2 gene (circAGO2) as a novel regulator of AGO2-miRNA complexes and cancer progression. To investigate the mechanisms underlying the oncogenic functions of circAGO2, we employed the Illumina HiSeq X Ten as a discovery platform to analyze the transcriptome profiling changes of human gastric cancer MKN-45 cells in response to stable over-expression of circAGO2. The results showed that stable over-expression of circAGO2 led to altered expression of 624 human mRNAs, including 257 up-regulated genes and 367 down-regulated genes. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to circAGO2 over-expression in human cancer cells, and these findings will help us understand the pathogenesis of cancer progression.
2019-05-30 | GSE114055 | GEO
Project description:Circular RNAs (circRNA) are a novel class of widespread non-coding RNAs (ncRNAs) that regulate gene expression in mammals. Recent studies demonstrate that functional peptides can be encoded by short open reading frames (sORFs) in ncRNAs, including circRNAs. In this study, through deep RNA sequencing on human endometrial cancer (EC) samples and their paired adjacent normal tissues, we uncovered that the circRNA hsa-circ-0000437 is significantly reduced in EC compared to matched paracancerous tissue. The hsa-circ-0000437 contains a sORF encoding a functional peptide termed as CORO1C-47aa. Overexpression of CORO1C-47aa is capable of inhibiting angiogenesis at the initiation stage by suppressing endothelial cell proliferation, migration, and differentiation through competing with TACC3 to bind to ARNT and suppress VEGF. The anti-tumor effects of CORO1C-47aa on EC progression suggest that CORO1C-47aa has a potential value in anti-carcinoma therapies and deserves further investigation.
2022-02-17 | PXD026046 | Pride
Project description:Stable activation of the WNT signaling effector beta-catenin (CTNNB1(ex3) in ovarian granulosa cells results in the formation of premalignant lesions that develop into granulosa cell tumors (GCTs) spontaneously later in life. Loss of the tumor suppressor gene Pten accelerates GCT formation in the CTNNB1 strain. Conversely, expression of oncogenic KRASG12D causes the dramatic arrest of proliferation, differentiation and apoptosis in granulosa cells, and consequently, small abnormal follicle-like structures devoid of oocytes accumulate in the ovary. Because of the potent anti-proliferative effects of KRASG12D in granulosa cells, we sought to determine if KRASG12D would block precancerous lesion and tumor formation in follicles of the CTNNB1 mutant mice. Unexpectedly, transgenic Ctnnb1;Kras mutant mice developed early-onset GCTs leading to premature death in a manner similar to theCtnnb1;Pten mutant mice. Moreover, the GCTs in the Ctnnb1;Kras mutant mice exhibited increased GC proliferation, decreased apoptosis and impaired differentiation. Microarray and RT-PCR analyses revealed that ovaries from mice expressing dominant-stable CTNNB1 with either Pten loss or KRAS activation were unpredictably similar. Specifically, gene regulatory processes induced by CTNNB1 were mostly enhanced by either KRAS activation or Pten loss in remarkably similar patterns and degree. Furthermore, the concomitant activation of CTNNB1 and KRAS in Sertoli cells resulted in the development of granulosa cell tumors of the testis. RT-PCR studies showed a partial overlap in gene regulatory processes associated with tumor development in the ovary and testis. Together, these results suggest that KRAS activation and Pten loss induce GCT development from premalignant lesions via highly similar molecular mechanisms. four samples: average of two wild type samples (previously submitted as GSM403220 and GSM403221), beta-Catenin constitutively active mutant, beta-Catenin;Pten double mutant, and beta-Catenin;Kras(G12D) double mutant
2011-09-19 | E-GEOD-27656 | biostudies-arrayexpress
Project description:Stable activation of the WNT signaling effector beta-catenin (CTNNB1(ex3) in ovarian granulosa cells results in the formation of premalignant lesions that develop into granulosa cell tumors (GCTs) spontaneously later in life. Loss of the tumor suppressor gene Pten accelerates GCT formation in the CTNNB1 strain. Conversely, expression of oncogenic KRASG12D causes the dramatic arrest of proliferation, differentiation and apoptosis in granulosa cells, and consequently, small abnormal follicle-like structures devoid of oocytes accumulate in the ovary. Because of the potent anti-proliferative effects of KRASG12D in granulosa cells, we sought to determine if KRASG12D would block precancerous lesion and tumor formation in follicles of the CTNNB1 mutant mice. Unexpectedly, transgenic Ctnnb1;Kras mutant mice developed early-onset GCTs leading to premature death in a manner similar to theCtnnb1;Pten mutant mice. Moreover, the GCTs in the Ctnnb1;Kras mutant mice exhibited increased GC proliferation, decreased apoptosis and impaired differentiation. Microarray and RT-PCR analyses revealed that ovaries from mice expressing dominant-stable CTNNB1 with either Pten loss or KRAS activation were unpredictably similar. Specifically, gene regulatory processes induced by CTNNB1 were mostly enhanced by either KRAS activation or Pten loss in remarkably similar patterns and degree. Furthermore, the concomitant activation of CTNNB1 and KRAS in Sertoli cells resulted in the development of granulosa cell tumors of the testis. RT-PCR studies showed a partial overlap in gene regulatory processes associated with tumor development in the ovary and testis. Together, these results suggest that KRAS activation and Pten loss induce GCT development from premalignant lesions via highly similar molecular mechanisms.
2011-09-20 | GSE27656 | GEO
Project description:Beta-catenin (CTNNB1) is a major component of Wnt signaling pathway and a crucial player in gastric cancer. To delineate the complex transcription program governed by CTNNB1 in gastric cancer cells, CTNNB1 was silenced in AGS, a commonly used Wnt signaling activated gastric cancer cell line and the resultant changes in genome-wide mRNA expression pattern was profiled using Affymetrix Human Gene 1.0 ST Array.
2015-12-01 | GSE61687 | GEO
Project description:The recent advances in anti-cancer treatments have led to a steady increase in the number of cancer survivors, paradoxically also enhancing the number of HF patients who suffer from the undesired cardiotoxic side effects of these anti-tumor treatments. Therapeutic options to reduce or reverse chemotherapy-induced HF are not available. Circular RNAs exhibit high druggability due to the high stability of their special closed loop structure. Circ-INSR overexpression prevents doxorubicin-induced cardiac dysfunction in preclinical murine and human models. Circ-INSR mimics produced in vitro also reduced cardiomyocyte death under doxorubicin stress, highlighting the potential of Circ-INSR-based RNA therapy for future clinical applications.
2022-10-01 | GSE199081 | GEO