Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1155917 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30542763_1.fastq.gz | Fastqsanger.gz | |||
| SRR30542763_2.fastq.gz | Fastqsanger.gz | |||
| SRR30542764_1.fastq.gz | Fastqsanger.gz | |||
| SRR30542764_2.fastq.gz | Fastqsanger.gz | |||
| SRR30542765_1.fastq.gz | Fastqsanger.gz |
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Project description:Specificity protein 1 (SP1) is an essential transcription factor regulating multiple cancer-related genes. Since aberrant expression of SP1 was known to be related to cancer development and progression, we focused on SP1 expression in gastric carcinoma and its correlation with disease outcomes. We discovered a different relationship between SP1 expression and patient survival in intestinal- and diffuse-type gastric cancer. In diffuse-type gastric cancer, patient survival decreased as SP1 expression increased (P < 0.05) in accordance with previously published papers, whereas the lack of SP1 expression in intestinal-type gastric cancer was correlated significantly with poor survival (P < 0.05). When SP1 downregulation was forced in high SP1 expressor intestinal-type gastric cell line MKN28 with siRNA, both migration and invasion were increased but cell proliferation was decreased. In accordance with these results, microarray data in siRNA-transfected MKN28 showed that genes inhibiting migration were downregulated and the expression of genes negatively facilitating proliferation was increased. Both migration and invasion, however, in low SP1 expressor intestinal-type gastric cell line AGS were decreased by forced SP1 expression. In contrast to intestinal-type, in diffuse-type gastric cell line SNU484, high SP1 expressor, both migration and invasion were decreased by siRNA. Contrary to previous studies, which did not reflect differences between the 2 histological types, our results showed that low expression of SP1 is involved in cancer progression and metastasis, and has a different effect on intestinal-type compared to diffuse-type gastric adenocarcinoma. 2 samples for MKN28 cells: si-SP1 against si-control and dyeswap of it upon 72 hour
2012-01-01 | E-GEOD-34792 | biostudies-arrayexpress
Project description:Background: The lack of obvious symptoms of early gastric cancer (GC) as well as the absence of sensitive and specific biomarkers results in poor clinical outcomes. Tubulin is currently emerging as important regulators of the microtubule cytoskeleton and thus have a strong potential to be implicated in a number of disorders, however, its mechanism of action in gastric cancer is still unclear. Tubulin alpha-1C(TUBA1C) is a subtype of α-tubulin, high TUBA1C expression has been shown to be closely related to a poor prognosis in in various cancers,this study, for the first time, revealed the mechanism of TUBA1C promotes malignant progression of gastric cancer in vitro and in vivo. Methods: The expression of lncRNA EGFR-AS1 was detected in human GC cell lines by qRT–PCR. Mass spectrometry experiments following RNA pulldown assays found that EGFR-AS1 directly binds to TUBA1C, the CCK8, EdU, transwell, wound-healing, cell cycle assays and animal experiments were conducted to investigate the function of TUBA1C in GC. Combined with bioinformatics analyses, reveal interaction between Ki-67, E2F1, PCNA and TUBA1C by western blot. Rescue experiments furtherly demonstrated the relationship of EGFR-AS1and TUBA1C. Results: TUBA1C was proved to be a direct target of EGFR-AS1, TUBA1C promotes gastric cancer proliferation, migration and invasion by accelerating the progression of the cell cycle from the G1 phase to the S phase and activating the expression of oncogenes: Ki-67,E2F1 and PCNA. Conclusions: TUBA1C is a new potential target of LncRNA EGFR-AS1 promotes gastric cancer progression and could be a novel biomarker and therapeutic target for GC.
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Project description:Rho-GTPases are small GTP-binding proteins that contribute to the epithelial-to-mesenchymal transition by regulating several cellular processes including organization of the actin cytoskeleton, cell motility, transcription, and cell proliferation. Overexpression of RhoC-GTPases (RhoC) in breast cancer has been implicated in poor disease prognosis due to increased cancer cells invasion, migration, and motility, which warranted its consideration as a therapeutic target for inhibiting breast cancer metastasis. Using silencing RNA (siRNA) molecules to knockdown RhoC expression is a promising approach to inhibit breast cancer metastases.
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Project description:Specificity protein 1 (SP1) is an essential transcription factor regulating multiple cancer-related genes. Since aberrant expression of SP1 was known to be related to cancer development and progression, we focused on SP1 expression in gastric carcinoma and its correlation with disease outcomes. We discovered a different relationship between SP1 expression and patient survival in intestinal- and diffuse-type gastric cancer. In diffuse-type gastric cancer, patient survival decreased as SP1 expression increased (P < 0.05) in accordance with previously published papers, whereas the lack of SP1 expression in intestinal-type gastric cancer was correlated significantly with poor survival (P < 0.05). When SP1 downregulation was forced in high SP1 expressor intestinal-type gastric cell line MKN28 with siRNA, both migration and invasion were increased but cell proliferation was decreased. In accordance with these results, microarray data in siRNA-transfected MKN28 showed that genes inhibiting migration were downregulated and the expression of genes negatively facilitating proliferation was increased. Both migration and invasion, however, in low SP1 expressor intestinal-type gastric cell line AGS were decreased by forced SP1 expression. In contrast to intestinal-type, in diffuse-type gastric cell line SNU484, high SP1 expressor, both migration and invasion were decreased by siRNA. Contrary to previous studies, which did not reflect differences between the 2 histological types, our results showed that low expression of SP1 is involved in cancer progression and metastasis, and has a different effect on intestinal-type compared to diffuse-type gastric adenocarcinoma.
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Project description:In recent years, gastric cancer (GC) has garnered significant attention due to its poor response to treatment, unfavorable prognosis, and the lack of reliable biomarkers for predicting disease progression and therapeutic outcomes. α-Ketoglutarate (α-KG), a critical metabolite involved in cellular energy metabolism and epigenetic regulation during tumor development, has emerged as a potential prognostic biomarker for GC. To explore this potential, we utilized publicly available datasets from the TCGA and GEO databases to analyze α-KG-related genes and establish the α-KG Index (AKGI). By evaluating the predictive performance of the AKGI model, we confirmed its robust capability to predict survival outcomes in gastric cancer patients.By analyzing signaling pathways and biological functions correlated with AKGI, we elucidated the regulatory mechanisms and biological roles of α-KG in gastric cancer. These insights were validated through cellular experiments, where α-KG treatment was shown to significantly inhibit gastric cancer cell proliferation, migration, and invasion.Taken together, our data demonstrate AKGI offers a valuable framework for advancing our understanding of the role and mechanisms of α-KG in gastric cancer.
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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.
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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.
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