Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA341865 | ENA |
REPOSITORIES: ENA
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Project description:Increasing evidence points to an important functional or regulatory role of long noncoding RNA in cellular processes as well as some cancer diseases result from the aberrant lncRNA expression. LncRNA could participate in the cancer progross and develop a significant role through the interaction with proteins. In the present study, we report a lncRNA termed uc.345 that is up-regulated in tumor tissues, compared to the corresponding noncancerous tissues. We found that a higher uc.345 expression lever was significantly more frequent in tissues with increased depth of invasion and advanced TNM tumor node metastasis T stage. Moreover, uc.345 serves as an independent risk factor for pancreatic cancer patients’ overall survival (OS). Through soft agar assay and tumor xenograft model, our results indicate that uc.345 could stimulate tumor growth in vitro and in vivo. We also found the uc.345 could upregulate the hnRNPL protein level, furthermore, we demonstrate that the inhibition of (hnRNPL) by its association with uc.345 contributes to depress tumorgenesis in vitro. Collectively, these results demonstrate that uc.345 functions as an oncogenic lncRNA that promotes tumor progression and serves as a poor predictor for pancreatic cancer patients' overall survival.
2016-09-06 | GSE86436 | GEO
Project description:Ovarian cancer has the highest mortality rate among gynecologic tumors worldwide, with unclear underlying mechanisms of pathogenesis. RNA-binding proteins (RBPs) primarily direct post-transcriptional regulation through modulating RNA metabolism. Recent evidence demonstrates that RBPs are also implicated in transcriptional control. However, the role and mechanism of RBP-mediated transcriptional regulation in tumorigenesis remain largely unexplored. Here, we show that the RBP heterogeneous ribonucleoprotein L (hnRNPL) interacts with chromatin and regulates gene transcription by forming phase-separated condensates in ovarian cancer. hnRNPL phase separation activates PIK3CB transcription and glycolysis, thus promoting ovarian cancer progression. Notably, we observe that the PIK3CB promoter is transcribed to produce a non-coding RNA which interacts with hnRNPL and promotes hnRNPL condensation. Furthermore, hnRNPL is significantly amplified in ovarian cancer, and its high expression predicts poor prognosis for ovarian cancer patients. By using cell-derived xenograft and patient-derived organoid models, we show that hnRNPL knockdown suppresses ovarian tumorigenesis. Together, our study reveals that phase separation of the chromatin-associated RBP hnRNPL promotes PIK3CB transcription and glycolysis to facilitate tumorigenesis in ovarian cancer. The formed hnRNPL-PIK3CB-AKT axis depending on phase separation can serve as a potential therapeutic target for ovarian cancer.
2025-02-14 | GSE289102 | GEO
Project description:Ovarian cancer has the highest mortality rate among gynecologic tumors worldwide, with unclear underlying mechanisms of pathogenesis. RNA-binding proteins (RBPs) primarily direct post-transcriptional regulation through modulating RNA metabolism. Recent evidence demonstrates that RBPs are also implicated in transcriptional control. However, the role and mechanism of RBP-mediated transcriptional regulation in tumorigenesis remain largely unexplored. Here, we show that the RBP heterogeneous ribonucleoprotein L (hnRNPL) interacts with chromatin and regulates gene transcription by forming phase-separated condensates in ovarian cancer. hnRNPL phase separation activates PIK3CB transcription and glycolysis, thus promoting ovarian cancer progression. Notably, we observe that the PIK3CB promoter is transcribed to produce a non-coding RNA which interacts with hnRNPL and promotes hnRNPL condensation. Furthermore, hnRNPL is significantly amplified in ovarian cancer, and its high expression predicts poor prognosis for ovarian cancer patients. By using cell-derived xenograft and patient-derived organoid models, we show that hnRNPL knockdown suppresses ovarian tumorigenesis. Together, our study reveals that phase separation of the chromatin-associated RBP hnRNPL promotes PIK3CB transcription and glycolysis to facilitate tumorigenesis in ovarian cancer. The formed hnRNPL-PIK3CB-AKT axis depending on phase separation can serve as a potential therapeutic target for ovarian cancer.
2025-02-13 | GSE289074 | GEO
Project description:Ovarian cancer has the highest mortality rate among gynecologic tumors worldwide, with unclear underlying mechanisms of pathogenesis. RNA-binding proteins (RBPs) primarily direct post-transcriptional regulation through modulating RNA metabolism. Recent evidence demonstrates that RBPs are also implicated in transcriptional control. However, the role and mechanism of RBP-mediated transcriptional regulation in tumorigenesis remain largely unexplored. Here, we show that the RBP heterogeneous ribonucleoprotein L (hnRNPL) interacts with chromatin and regulates gene transcription by forming phase-separated condensates in ovarian cancer. hnRNPL phase separation activates PIK3CB transcription and glycolysis, thus promoting ovarian cancer progression. Notably, we observe that the PIK3CB promoter is transcribed to produce a non-coding RNA which interacts with hnRNPL and promotes hnRNPL condensation. Furthermore, hnRNPL is significantly amplified in ovarian cancer, and its high expression predicts poor prognosis for ovarian cancer patients. By using cell-derived xenograft and patient-derived organoid models, we show that hnRNPL knockdown suppresses ovarian tumorigenesis. Together, our study reveals that phase separation of the chromatin-associated RBP hnRNPL promotes PIK3CB transcription and glycolysis to facilitate tumorigenesis in ovarian cancer. The formed hnRNPL-PIK3CB-AKT axis depending on phase separation can serve as a potential therapeutic target for ovarian cancer.
2025-02-13 | GSE289075 | GEO
Project description:Bladder cancer stem cells (CSCs) contribute to tumorigenesis, recurrence and chemoresistance of bladder cancer. However, the molecular mechanisms underlying their self-renewal are poorly unknown. Long noncoding RNAs (lncRNAs) act as crucial regulators in a lot of human cancers, yet their potential roles and molecular mechanisms in bladder CSCs are poorly understood. The goal of this study is to identify the differentially expressed lncRNAs in bladder CSCs (UM-UC-3 4th spheres), its two differentiation sublines and bladder non-CSCs (UM-UC-3). Our study reveals that deregulation of lncRNAs is involved in the bladder CSCs.
2019-09-22 | GSE107857 | GEO
Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal.
2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
| 2330122 | ecrin-mdr-crc
Project description:Pancreatic cancer is the most highly lethal disease with an increasing incidence. Accumulating evidence shows that as an initiating event of pancreatic tumorigenesis, mutant KRAS requires additional factors to promote pancreatic cancer progression. Peroxisome proliferator-activated receptor-delta/beta (PPAR-d) is a ligand-activating transcription factor that modulates many critical cellular functions and is upregulated in human pancreatic cancer tissues. To study PPAR-d's effects on mutant KRAS-initiated pancreatic tumorigenesis, we have generated a novel transgenic mouse model with simultaneously targeted PPAR-d overexpression and KrasG12D mutation (KRASmu) in pancreatic epithelial cells (called KC/Pd mice). Our preliminary data showed that PPAR-d ligand GW501516 strongly promoted pancreatic tumorigenesis in KRASmu mice (KC), and PPAR-d upregulation dramatically enhanced these effects in KC/Pd mice. However, molecular mechanisms by which PPAR-d and its synthetic ligand GW501516 promote KRASmu-initiated pancreatic tumorigenesis remains largely unknown. We have therefore performed genome-wide mRNA seq profiling analysis for pancreatic tissues from KC [WT] and KC/Pd (PD) mice fed GW501516 diet to discover the critical genes/pathways directly regulated by PPAR-d overactivation that accelerate pancreatic cancer progression. Pancreatic tissues of GW-treated KC/Pd (PD-GW) and KC (WT-GW) mice had distinctive differential expression patterns with 1498 differentially expressed genes (DEGs) according to a cut-off of p(Adj)<.05, including 709 upregulated DEGs and 789 downregulated DEGs. Furthermore, Gene set enrichment analyses of these 1498 DEGs using the ?Hallmark gene sets? category showed that the top enriched pathways included IL6-JAK-STAT3, inflammatory response, and KRAS signaling. Thus, the RNA-seq profiling analyses provide us important clues for molecular mechanisms by which PPAR-d overactivation promotes pancreatic cancer progression.
2022-03-02 | GSE176135 | GEO
Project description:Long noncoding RNA LNMAT1 promotes lymphatic metastasis in bladder cancer
| PRJNA417154 | ENA
Project description:To further explore the differential expression profile of super-enhancer long noncoding RNA (LncRNA) in human bladder cancer, we have employed super-enhancer lncRNA microarray expression profiling as a discovery platform to identify potential differential expression profile of super-enhancer lncRNA between human bladder cancer cell (UM-UC-3 cell) and urothelial immortalized cell (SV-HUC-1 cell). Results showed that a large number of differentially expressed super-enhancer lncRNA were found between UM-UC-3 cell and SV-HUC-1 cell. In this study, We verified 5 up-regulated differentially expressed super-enhancer lncRNAs using qPCR, of which the highest fold change is LINC00162. Then we further explored the biological function and mechanism of LINC00162 in bladder cancer in this study.
2020-12-22 | GSE159682 | GEO
Project description:Ultraconserved regions (UCRs) are segments of the human genome located in both intragenic and intergenic regions that are highly conserved in orthologous regions of the human, rat, and mouse genomes. Their transcriptional products, called T-UCRs, compose a new category of long noncoding RNA (lncRNAs). Most importantly, recent data suggests that T-UCRs are altered at the transcriptional level in human tumorigenesis and the aberrant T-UCRs expression profiles can be used to differentiate human cancer types. MicroRNAs and other types of non-codingRNAs have been shown to greatly contribute at biological function of cancer and are increasingly being used to help prognosticate patients with bladder cancer, this is not yet the case for T-UCRs. The presence and the roles for T-UCRs across different species is largely unknown rendering their investigation particularly important in our understanding the biology of cancer. Using genome-wide profiling, we identified 293 T-UCRs that were dysregulated in bladder tumor (n = 24) but not normal bladder tissues (n = 17) samples. The greatest change in expression was for the ultraconserved element 8 (uc.8+), whose expression significantly increased (6.7 fold; P = 0.001) in bladder cancer tissues. Dysregulated expression was validated for several T-UCRs in 60 patients and 16 healthy donors. We found that T-UCR 8+ acts as a natural decoy RNA for miR-596 in patients and bladder cancer cells. As a result, expression of matrix metallopeptidase 9, a direct target of this microRNA, was upregulated, thereby promoting cancer cell growth, migration, and invasion. We also observed that mir-596 mediated a network of interactions among uc.8+, uc.339+, uc.195+, and uc.388+, which appeared to be dysregulated in bladder tumors. Transcribed ultraconserved ncRNAs provide an evolutionarily-conserved regulatory layer that modulates miRNA levels, and opens up the possibility for the development of useful markers for diagnosis and prognosis, as well as for the development of new RNA-based cancer therapies.
2016-03-23 | GSE68594 | GEO