Project description:To investigate the function of GFI1 in GC, we ectopically expressed GFI1 in HS746T cells and analysised the transciptional data from HS746T GFI1 over-expression cells and wild type cells by human microarray
Project description:The histone demethylase JMJD1A(Jumoji domain containing 1A) is overexpressed in multiple cancers and promotes cancer progression. However, the role and mechanism of JMJD1A in gastric cancer remains poorly understood.Here, we found that JMJD1A could suppress gastric cancer cell proliferation, migration, invasion and xenograft tumor growth. Using RNA sequencing, we identified RUNX3 as a novel target gene of JMJD1A.
Project description:This study propose HOXC10 overexpression by reduced DNA methylation promotes gastric cancer progression through regulation of CST1 and S100P.
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.
Project description:Gastric cancer is still one of the most common cancer types and third leading cause of cancer deaths worldwide. Recent studies have showed that the Hippo signaling pathway plays a critical role in progression of gastric cancer. It is of great importance to demonstrate the regulation of Hippo signaling pathway and the degradation of YAP protein in gastric cancer. In this study, we found that OTUB1 is a critical factor to facilitate gastric cancer cell stemness and progression, which deubiquitinated and stabilized YAP protein.
Project description:Gastric cancer remains one of the leading causes of cancer-related mortality worldwide, highlighting the urgent need for novel biomarkers and therapeutic targets. Ribosomal proteins have emerged as critical regulators of tumorigenesis beyond their canonical roles in protein synthesis. In this study, we investigated the expression, functional role, and underlying mechanism of RPL27 in gastric cancer. RPL27 was significantly upregulated in gastric cancer tissues compared with adjacent normal tissues, as demonstrated by Western blot and immunohistochemistry. High RPL27 expression correlated with poor overall survival and showed potential as a prognostic biomarker. Functional assays revealed that RPL27 knockdown significantly suppressed gastric cancer cell proliferation, migration, and invasion. Transcriptomic analysis identified FMC1 as a key RPL27-downstream molecule, to regulate mitochondrial function, including membrane potential, morphology, DNA copy number, and ATP5A expression. Rescue experiments demonstrated that knockdown of FMC1 or treatment with the OXPHOS inhibitor oligomycin A partially reversed the malignant phenotypes induced by RPL27 overexpression. Furthermore, RPL27 knockdown significantly inhibited tumor growth in a xenograft mouse model. Collectively, our findings establish RPL27 as a novel oncogenic driver in gastric cancer and reveal that RPL27 promotes tumor progression through FMC1-dependent oxidative phosphorylation, suggesting that the RPL27-FMC1-mitochondrial function axis may represent a promising vulnerability for further investigation in gastric cancer.