Browse
Submit Data
Databases
API
Help

Dataset Information

21 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long non-coding RNA AK096174 promotes cell proliferation and invasion in gastric cancer by regulating WDR66 expression.

ABSTRACT: Gastric cancer (GC) is one of the major causes of cancer deaths worldwide; however, the mechanism of carcinogenesis is complex and poorly understood. Long non-coding RNA (lncRNA) has been reported to be involved in the development of multiple cancers. Here, we identified a novel lncRNA, AK096174, which was up-regulated and associated with tumorigenesis, tumor size, metastasis, and poor prognosis in GC. Our data showed that AK096174 was highly expressed in the GC tissues and cell lines (SGC-7901, AGS, BGC-823, MGC-803), and patients with higher AK096174 expression had a poorer prognosis and shorter overall survival (OS). AK096174 knockdown inhibited the proliferation, migration, and invasiveness in SGC-7901 and BGC-823 cells, whereas AK096174 overexpression had the promoting effects. Furthermore, mechanistic investigation showed that AK096174 positively correlated with the expression of WD repeat-containing protein 66 (WDR66) gene at the translational level. Knockdown of WRD66 attenuated the positive impact of AK096174 in GC cells. The findings of the present study establish a function for AK096174 in GC progression and suggest it may serve as a potential target for GC therapy in the future.

SUBMITTER: Zhang Y

PROVIDER: S-EPMC6050193 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

Long non-coding RNA BCAR4 promotes liver cancer progression by regulating proliferation, migration and invasion.

Project description:Liver cancer (LC) is one of the primary contributors of cancer-associated death worldwide. Long non-coding RNAs (lncRNAs) have been shown to participate in almost every aspect of cell biology and serve fundamental roles in carcinogenesis and cancer progression, including in LC. However, the clinical significance and functional role of the lncRNA breast cancer anti-estrogen resistance 4 (BCAR4) in LC have not yet been identified. The present study measured the expression levels of BCAR4 in LC cells and tissues, and discovered that BCAR4 was upregulated in LC tissues compared with adjacent normal tissues. Furthermore, high BCAR4 expression was associated with the presence of multiple tumors and advanced Tumor-Node-Metastasis stages (III/IV). Survival analysis found that high BCAR4 expression indicated poor overall survival (OS) and progression-free survival (PFS). By analyzing the risk factors of poor OS and PFS using univariate analysis and multivariate analysis, high BCAR4 expression was revealed to be an independent risk factor of poor prognosis. In addition, the role of BCAR4 was further investigated in vitro, which revealed overexpression of BCAR4 to markedly promote the proliferation, migration and invasion of LC cells. Conversely, the loss of BCAR4 expression repressed the proliferation, migration and invasion of LC cells. In conclusion, BCAR4 is overexpressed in LC and is associated with LC progression. Therefore, BCAR4 may be used as a potential prognostic marker in LC.

| S-EPMC7400972 | biostudies-literature

Long non-coding RNA SUMO1P3 promotes tumour progression by regulating cell proliferation and invasion in glioma.

Project description:Gliomas account for 50% of primary brain tumours in the central nervous system. Small ubiquitin-like modifier 1 pseudogene 3 (SUMO1P3), a newly identified long non-coding RNA (lncRNA), serves an oncogenic role in various types of cancer. The aim of the present study was to investigate the effect of SUMO1P3 on glioma progression. The results demonstrated that SUMO1P3 expression was upregulated in glioma tissues and cell lines. Furthermore, SUMO1P3 was associated with a poor overall survival of patients with glioma. The results of the in vitro cell proliferation and flow cytometry assays demonstrated that SUMO1P3-knockdown suppressed cell proliferation and cell cycle. The results of the wound healing and Transwell assays demonstrated that SUMO1P3-knockdown significantly repressed cell migration and invasion. In addition, SUMO1P3 promoted glioma by regulating the expression levels of β-catenin, cyclin-D1, N-cadherin and E-cadherin. Overall, the results of the present study suggested that SUMO1P3 may act as an oncogene by regulating cell proliferation, cell cycle, cell migration and invasion in glioma, and may represent a novel diagnostic biomarker and therapeutic target for glioma.

| S-EPMC8005699 | biostudies-literature

Long Non-Coding RNA NRON promotes Tumor Proliferation by regulating ALKBH5 and Nanog in Gastric Cancer.

Project description:Long non-coding RNAs (lncRNAs) act as tumor suppressors or oncogenes in tumor development and progression. In this study, we explored the expression and biological role of lncRNA NRON in gastric cancer (GC). We observed that lncNRON was upregulated in GC tissues and cell lines, and high lncNRON expression was associated with malignant features and poor prognosis in GC patients. LncNRON was found to promote the proliferation and tumorigenicity of GC cells. Mechanistically, lncNRON exerted its oncogenic functions by binding to the N6-methyladenosine eraser ALKHB5 and mediating Nanog mRNA decay. In conclusion, our results suggest that lncNRON serves as an oncogenic lncRNA in GC and thus may be a promising prognostic factor and potential therapeutic target for GC patients.

| S-EPMC8518016 | biostudies-literature

Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer.

Project description:Abnormal expression of long non-coding RNA (lncRNAs) often contributes to unrestricted growth and invasion of cancer cells. LncRNA XIST expression is up-regulated in several cancers, however, its modulatory mechanism in gastric cancer (GC) has not been elucidated. In the present study, we found that XIST expression was significantly increased in GC tissues and cell lines. LncRNA XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to GC cell growth. LncRNA XIST also contributed to GC cell invasion both in vitro and in vivo. We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis. Our findings suggested that lncRNA XIST may be a candidate prognostic biomarker and a target for new therapies in GC patients.

| S-EPMC5354817 | biostudies-other

A novel long non-coding RNA SLNCR1 promotes proliferation, migration, and invasion of melanoma via transcriptionally regulating SOX5.

Project description:Steroid receptor RNA activator (SRA)-like non-coding RNA (SLNCR1) has been implicated in various tumorigenic processes, but the precise regulatory role in melanoma progression remains uncertain. We performed a comprehensive analysis to investigate the prognostic value of SLNCR1 expression in patients with melanoma by TCGA database and melanoma tissue samples via the Kaplan-Meier method. Subsequently, we conducted qRT-PCR and Fluorescence in Situ Hybridization (FISH) assays to identify SLNCR1 expression levels and localization in tissues and cells, respectively. Loss-of-function assays utilizing shRNAs vectors were used to investigate the potential impact of SLNCR1. Our data showed that SLNCR1 is significantly up-regulated in human malignant melanoma tissues and cell lines and functions as an oncogene. Silencing of SLNCR1 suppressed melanoma cell proliferation, migration, invasion, and inhibited tumorigenesis in a mouse xenograft model. Additionally, we employed bioinformatic predictive analysis, combined with dual-luciferase reporter analysis and functional rescue assays, to elucidate the mechanistic target of the SLNCR1/SOX5 axis in melanoma. Mechanistically, we discovered that SLNCR1 promotes EMT of human melanoma by targeting SOX5, as downregulation of SLNCR1 expression leads to a decrease in SOX5 protein levels and inhibits melanoma tumorigenesis. Our research offers promising insights for more precise diagnosis and treatment of human melanoma.

| S-EPMC10984963 | biostudies-literature

Long Non-coding RNA AK025387 Promotes Cell Migration and Invasion of Gastric Cancer.

Project description:Gastric cancer is one of the most common cancers in the world, and long non-coding RNAs (lncRNAs) play a crucial role in proliferation, metastasis, and invasion of gastric cancer. However, there are very few researches focusing on the effects of lncRNAs on metastatic gastric cancer. In this research, we identify one kind of lncRNA, called AK025387, which is highly expressed in metastatic gastric cancer samples compared with non-metastatic gastric cancer samples. The expression of AK025387 is significantly positively correlated with lymph node metastasis. The in situ hybridization demonstrates that AK025387 is located in both nucleus and cytoplasm, but mostly in cytoplasm. AK025387 promotes gastric cancer cells migratory and invasive ability, but it inhibits apoptosis in vitro. Furthermore, AK025387 regulates Raf-1, mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK), and extracellular signal-regulated kinase (ERK) and is involved in mitogen-activated protein kinase (MAPK) signaling pathway to perform its biological functions. We conclude that AK025387 is highly expressed in metastatic gastric cancer, and its biological functions suggest the potential of AK025387 to be a biomarker of metastatic gastric cancer.

| S-EPMC7251172 | biostudies-literature

Long non-coding RNA CCAT2 promotes prostate cancer cell proliferation and invasion by regulating the Wnt/?-catenin signaling pathway

Project description:Long non-coding RNA colon cancer associated transcript 2 (CCAT2) is dysregulated in a number of different types of human cancer, and affects cancer progression via the Wnt/?-catenin signaling pathway. However, the roles of CCAT2 and the Wnt/?-catenin signaling pathway in prostate cancer (PCa) are not completely understood. The present study aimed to investigate the potential mechanism of CCAT2 in PCa. In the present study, the reverse transcription-quantitative PCR (RT-qPCR) results indicated that CCAT2 expression was significantly upregulated in PCa tissues, and DU145 and PC3 cell lines compared with normal prostate tissues and the epithelial RWPE-1 cell line, respectively. Functional assays indicated that CCAT2 downregulation inhibited DU145 and PC3 cell proliferation, cell cycle, migration and invasion. In addition, the luciferase reporter assay, RT-qPCR and western blotting results indicated that CCAT2 regulated transcription factor 7 like 2 (TCF7L2) expression by binding to microRNA-217. Further western blotting and TOPFlash assays indicated that CCAT2-knockdown inhibited the Wnt/?-catenin signaling pathway in DU145 and PC3 cell lines by inhibiting the expression of TCF7L2. However, CCAT2-knockdown-mediated effects were reversed by the Wnt/?-catenin signaling pathway activator lithium chloride (LiCl). Further cell experiments suggested that LiCl treatment reversed CCAT2-knockdown-mediated inhibition of PCa cell proliferation, cell cycle, epithelial-mesenchymal transition, migration and invasion. Overall, the results indicated that CCAT2 regulated PCa via the Wnt/?-catenin signaling pathway; therefore, CCAT2 may exhibit key role during the progression of PCa and may serve as a therapeutic target for the disease.

| S-EPMC7439128 | biostudies-literature

Long non-coding RNA LINC01225 promotes proliferation, invasion and migration of gastric cancer via Wnt/β-catenin signalling pathway.

Project description:Emerging evidence has classified the aberrant expression of long non-coding RNAs (lncRNAs) as a basic signature of various malignancies including gastric cancer (GC). LINC01225 has been shown to act as a hepatocellular carcinoma-related gene, with its expression pattern and biological function not clarified in GC. Here, we verified that LINC01225 was up-regulated in tumour tissues and plasma of GC. Analysis with clinicopathological information suggested that up-regulation of LINC01225 was associated with advanced disease and poorer overall survival. Receiver operating characteristic (ROC) analysis showed that plasma LINC01225 had a moderate accuracy for diagnosis of GC. In addition, knockdown of LINC01225 led to retardation of cell proliferation, invasion and migration, and overexpression of LINC01225 showed the opposite effects. Mechanistic investigations showed that LINC01225 silencing inhibited epithelial-mesenchymal transition (EMT) process and attenuated Wnt/β-catenin signalling of GC. Furthermore, ectopic expression of Wnt1 or suppression of GSK-3β abolished the si-LINC01225-mediated suppression against EMT, thereby promoting cell proliferation, invasion and migration of GC. In conclusion, LINC01225 promotes the progression of GC through Wnt/β-catenin signalling pathway, and it may serve as a potential target or strategy for diagnosis or treatment of GC.

| S-EPMC6815774 | biostudies-literature

Long non-coding RNA UCA1 enhances cervical cancer cell proliferation and invasion by regulating microRNA-299-3p expression.

Project description:The long non-coding RNA, urothelial cancer-associated 1 (UCA1) is an important regulator in several tumors. However, to the best of our knowledge, the clinical roles of UCA1 in cervical cancer remain unclear. Thus, the present study aimed to investigate the function and mechanism of UCA1 in cervical cancer. Reverse transcription-quantitative PCR analysis was performed to detect UCA1 and microRNA (miR)-299-3p expression in cervical cancer tissues and cell lines. The Cell Counting Kit-8 and Transwell assays were performed to assess cell proliferation and invasion, respectively. Furthermore, the dual-luciferase reporter assay was performed to confirm the association between UCA1 and miR-299-3p. Rescue experiments were performed to determine the mechanism of the UCA1/miR-299-3p axis. The results demonstrated that UCA1 expression was upregulated in cervical cancer tissues and cell lines. Furthermore, overexpression of UCA1 enhanced the proliferation and invasion of cervical cancer cells, the effects of which were reversed following UCA1 knockdown. Notably, UCA1 interacted with miR-299-3p and negatively regulated miR-299-3p expression. In addition, miR-299-3p expression was downregulated in cervical cancer tissues and cell lines. Overexpression of miR-299-3p suppressed the proliferation and invasion of cervical cancer cells, reversing the effects of UCA1 knockdown on cervical cancer cell proliferation. Taken together, the results of the present study suggest that UCA1 promotes cell proliferation and invasion by regulating miR-299-3p expression in cervical cancer.

| S-EPMC8442166 | biostudies-literature

Long non-coding RNA CCAT1 promotes cervical cancer cell proliferation and invasion by regulating the miR-181a-5p/MMP14 axis.

Project description:Cervical cancer is a serious threat to women's health and is the third most common malignancy in women worldwide. Recent studies indicate that the long non-coding RNA CCAT1 plays a role in the malignant behavior of many tumors. However, the role of CCAT1 in cervical cancer is still unknown. Our aim is to evaluate the expression and investigate the regulatory role and potential mechanism of CCAT1 in cervical cancer. CCAT1 expression was measured by qRT-PCR. In addition, CCK-8 assays, colony formation assays, qRT-PCR assays, Transwell assays and xenograft experiments were performed to determine the role of CCAT1 in the proliferation and invasion in cervical cancer cells. The expression of CCAT1 in the cervical cancer tissues was higher than in the adjacent normal tissues. Overexpressing CCAT1 promoted cervical cancer cell proliferation, colony formation, and invasion in vitro. Elevated CCAT1 suppressed miR-181a expression, which was accompanied by an increased expression of MMP14 and HB-EGF. In contrast, knocking down CCAT1 resulted in increased expression of miR-181a, along with decreased expression of MMP14 and HB-EGF. Thus, CCAT1 is a key oncogenic lncRNA associated with cervical cancer and plays a role in promoting cervical cancer cell proliferation and invasion by regulating the miR-181a-5p/MMP14 axis.

| S-EPMC6592243 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data