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Non-coding RNAs participate in the regulatory network of CLDN4 via ceRNA-mediated miRNA evasion (lncRNA)

ABSTRACT: Thousands of genes have been well demonstrated to play important roles in cancer progression. As genes do not function in isolation, they can be grouped into “networks” based on their interactions. In this study, we discover a network regulating Claudin-4 (CLDN4) in gastric cancer. We observe that CLDN4 is up-regulated in gastric cancer and is associated with poor prognosis. CLDN4 reinforce proliferation, invasion, and EMT in AGS, HGC-27, and SGC-7901 cells, which could be reversed by miR-596 and miR-3620-3p. Additionally, lncRNA-KRTAP5-AS1 and lncRNA-TUBB2A could act as competing endogenous RNAs to affect the function of CLDN4. Our results suggest that non-coding RNAs (ncRNAs) play important roles in the regulatory network of CLDN4. As such, ncRNAs should be considered as potential biomarkers and therapeutic targets against gastric cancer

ORGANISM(S): Homo sapiens

PROVIDER: GSE99416 | GEO | 2017/05/31

SECONDARY ACCESSION(S): PRJNA388527

REPOSITORIES: GEO

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Non-coding RNAs participate in the regulatory network of CLDN4 via ceRNA-mediated miRNA evasion (miRNA)

Project description:Thousands of genes have been well demonstrated to play important roles in cancer progression. As genes do not function in isolation, they can be grouped into “networks” based on their interactions. In this study, we discover a network regulating Claudin-4 (CLDN4) in gastric cancer. We observe that CLDN4 is up-regulated in gastric cancer and is associated with poor prognosis. CLDN4 reinforce proliferation, invasion, and EMT in AGS, HGC-27, and SGC-7901 cells, which could be reversed by miR-596 and miR-3620-3p. Additionally, lncRNA-KRTAP5-AS1 and lncRNA-TUBB2A could act as competing endogenous RNAs to affect the function of CLDN4. Our results suggest that non-coding RNAs (ncRNAs) play important roles in the regulatory network of CLDN4. As such, ncRNAs should be considered as potential biomarkers and therapeutic targets against gastric cancer

2017-05-31 | GSE99415 | GEO

HGC-RACK1

Project description:MicroRNA microarray profiling analysis was performed on human gastric cancer HGC cells after RACK1 silenced or not

2016-03-01 | E-MTAB-3484 | biostudies-arrayexpress

Long non-coding RNA ncRuPAR regulates gastric cancer cell proliferation and apoptosis via phosphoinositide 3-kinase/protein kinase B signaling

Project description:Objective: To determine the effect and mechanism of the long non-coding RNA (lncRNA) ncRuPAR (non-protein coding RNA, upstream of coagulation factor II thrombin receptor [F2R]/protease-activated receptor-1 [PAR-1]) in human gastric cancer. Methods: HGC-27-ncRuPAR overexpression and MGC-803-ncRuPAR-RNAi knockdown gastric cancer cell lines were established. We assessed the effect of ncRuPAR on cell proliferation, apoptosis, migration, and invasion using Cell Counting Kit 8, flow cytometry, scratch and transwell assays, respectively. Differentially expressed genes in HGC-27-ncRuPAR overexpression and HGC-27-empty vector cell lines were identified using Affymetrix GeneChip microarray analysis. Ingenuity Pathway Analysis (IPA) of the microarray results was subsequently conducted to identify ncRuPAR-enriched pathways, followed by validation using real time-quantitative PCR (RT-qPCR). As one of the top enriched pathways, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway was further examined by western blotting to determine its role in ncRuPAR-mediated regulation of gastric cancer pathogenesis. Results: ncRuPAR inhibited human gastric cancer cell proliferation and induced G1/S phase arrest and apoptosis, but did not affect migration or invasion in vitro. Overexpression of ncRuPAR in vitro was found to inhibit its known target PAR-1, as well as PI3K/Akt signaling. The downstream targets of PI3K/Akt, cyclin D1 was downregulated, but there was no change in expression level of B-cell lymphoma 2 (Bcl-2). Conclusions: We showed that lncRNA-ncRuPAR could inhibit tumor cell proliferation and promote apoptosis of human gastric cancer cells, potentially by inhibiting PAR-1, PI3K/Akt signaling, and cyclin D1. The results suggest a potential role for lncRNAs as key regulatory hubs in GC progression.

2022-08-19 | GSE211598 | GEO

Differential gene expression between BGC-823/NC and BGC-823/MTA2, SGC-7901/NC and SGC-7901/shMTA2 cells

Project description:Metastasis associated 1 family, member 2 (MTA2) gene is classified to metastasis associated gene family. We have previously reported that MTA2 gene was overexpressed in gastric cancer tissues, correlating with tumor invasion, lymph node metastasis, and advanced TNM stage. MTA2 knockdown significantly inhibited gastric cancer cell invasion and metastasis. Yet, its molecular mechanisms are still unclear. The aim of this study is to investigate the molecular mechanisms of MTA2 in regulating malignant behaviors of gastric cancer. This experiment captures the expression data between BGC-823/NC and BGC-823/MTA2, SGC-7901/NC and SGC-7901/shMTA2 cells using Whole human genome microarray 4×44K (Design ID: 014850, Agilent technologies).

2015-04-08 | E-MTAB-3469 | biostudies-arrayexpress

RNA-sequencing of SGC-7901 cells with and without PUM1 knockdown

Project description:In order to explore the effect of RNA-binding protein PUM1 on proliferation, metastasis and metabolism of gastric cancer, we established PUM1 stable knockdown SGC-7901 cell lines. We then performed gene expression profiling analysis using data obtained from RNA-seq of PUM1-knockdown and negative control SGC-7901 cells.

2022-09-10 | GSE212848 | GEO

Expression profiling on HPSE deleted SGC-7901 gastric cancer cells

Project description:HPSE plays important roles in gastric cancer cell proliferation, apoptosis and metastasis.The aim of this study is to explore molecular mechanism underling roles of HPSE in gastric cancer cell proliferation, survival, migration and metastasis. SGC-7901 gastric cancer cells were transfected with HPSE siRNA (10nM) or scramble control siRNA, RNA were extracted 24hours after transfectioin and hybridized to Affymetrix microarrays. 3 biological repeats were used for each condition.

2013-12-02 | E-GEOD-34080 | biostudies-arrayexpress

The microarrays from human gastric cancer SGC-7901 cells

Project description:NUAK1 was highly expressed in tumors, and promoted their invasion and metastasis.. The study is to explore the downstream of NUAK1 in human gastric cancer SGC-7901 cells

2021-01-01 | GSE123924 | GEO

HBXIP-mediated cell cycle, apoptosis and autophagy participate in the inhibitory effect of Germacrone on gastric cancer cells

Project description:As a monocyclic sesquiterpene, Germacrone has remarkable anti-tumor effect in a variety of cancers such as hepatocellular carcinoma, gastric cancer, and breast cancer. However, the mechanism of Germacrone on gastric cancer was still unclear. In our study, Germacrone inhibited gastric cancer cells proliferation in a dose-dependent manner. As shown, Germacrone induced G0 / G1 phase arrest and apoptosis in gastric cancer. Germacrone increased the expression of LC3ii/LC3i, p62. Then combined with CQ, the expression of LC3ii/LC3i, p62 continued to increase. As a result, Germacrone partially blocked the autophagy process. Through proteomic technology, a total of 596 proteins were screened and the top hits were Hepatitis B X-interacting protein (HBXIP). Overexpression of HBXIP delayed the cycle arrest, induction of apoptosis, and autophagy inhibition induced by Germacrone. Germacrone inhibits proliferation in gastric cancer cells by inhibiting HBXIP, and this process is related to G0 / G1 phase arrest, induction apoptosis, and autophagy inhibition.

2020-10-14 | PXD021980 | iProX

Alteration of biological behavior caused by IRX1 overexpression in gastric cancer

Project description:To explore the functon of IRX1 in gastric cancer, we employed whole genome microarray expression profiling as a discovery platform to identify gene expression changes in three samples. We constructed the eukaryotic expression vector pEGFP-IRX1. The pEGFP-IRX1 expression vector was transfected into SGC-7901 gastric cancer cells by Lipofectamine 2000. The IRX1 protein was mainly observed in nuclei. Naive SGC7901 and empty vector pEGFP-N1 transfected cells were used as controls. Gene expression profiles were compared between parental gastric cancer cell line SGC7901 and cells transfected with pEGFP-IRX1 and pEGFP-N1.

2010-08-18 | E-GEOD-17399 | biostudies-arrayexpress

MiRNA Expression Profiling in Cisplatin Resistance Human Gastric Cancer Cell Lines and Their Parental Cell Lines

Project description:Cisplatin is the first-line agent utilized for the clinical treatment of a wide variety of solid tumors including gastric cancer. However, the intrinsic or acquired cisplatin resistance is often occurred in patients with gastric cancer and resulted in failure of cisplatin therapy. In order to investigate if miRNA involves in cisplatin resistance of human gastric cancer, we first screened and compared the expression of miRNAs between cisplatin resistant gastric cancer cell lines SGC-7901/DDP and BGC-823/DDP and their sensitive parental cells by miRNAs microarray.

2016-09-05 | GSE86195 | GEO

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