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OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

ABSTRACT: Transcriptome analysis of the function of OLFM4 MV on gastric cancer HGC-27 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE240275 | GEO | 2024/09/18

REPOSITORIES: GEO

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OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

Project description:This SuperSeries is composed of the SubSeries listed below.

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OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

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OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

Project description:OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

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OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

Project description:OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

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RNA sequencing for RWPE1 cells, OLFM4-Active RWPE1 cells and OLFM4-KO RWPE1 cells

Project description:OLFM4 gene expressing in RWPE1 stem/progenitor-like cells. To study OLFM4 gene functions and molecular mechanisms, we generated OLFM4-avtive and OLFM4-knock out-GFP reporter RWPE1 cells with CRISP-Cas 9 system. The cell transcriptome was studied with RNA sequencing.

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OLFM4 expression in breast tumor samples

Project description:Here we describe the first study which used SWATH MS as a tool for robust identification and quantification of breast tissus proteins. By employing a spectral library containing 3200 proteins, we show that this strategy allows the quantification of OLFM4 in each sample together with a deep proteomic coverage which provide a more comprehensive idea of the OLFM4 function in the breast cancer.

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RNA sequencing analysis of gene expression profiles of OLFM4-RET fusion in HEK293 cells

Project description:The purpose of this assay is to determine the gene expression profiles induced by OLFM4-RET fusion, therefore further understanding the molecular mechanim of oncognesis by OLFM4-RET

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OLFM4 promotes the progression of intestinal metaplasia through MYH9/GSK3β/β-catenin pathway

Project description:Intestinal metaplasia (IM), precancerous lesions of gastric carcinoma (PLGC) induced by factors like nitrite, Helicobacter pylori, or bile acid, carries a high risk of progressing to gastric cancer. IM is categorized into complete intestinal metaplasia (CIM) and incomplete intestinal metaplasia (IIM). Patients with IIM are at a higher risk of developing gastric cancer, emphasizing its importance for early screening. Besides the diagnostic challenges, the mechanisms underlying its progression remain a mystery. OLFM4, a gene associated with stemness characteristics, has been linked to promoting gastric and colorectal cancers. Our investigation used pathological sections from two clinical centers, biopsies of IM tissues, PLGC cell models, animal models, and organoids to explore OLFM4's role in IIM. OLFM4 expression was observed highly in IIM, with superior diagnostic accuracy of IIM compared to CDX2 and MUC2 for the first time. OLFM4, along with MYH9, was highly expressed in IM organoids and PLGC animal models. OLFM4, in combination with MYH9, accelerated the ubiquitination of GSK3β and resulted in increased β-catenin levels through the Wnt signaling pathway, finally promoting the proliferation and invasion abilities of PLGC cells. In conclusion, OLFM4 serves as a novel biomarker for IIM and is utilized as an important auxiliary means to delimit the key population for early gastric cancer screening. This study provides new insights into the mechanisms of progression and a new target of therapy in intestinal metaplasia.

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