Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1994160.fastq.gz | Fastqsanger.gz | |||
| ERR1994170.fastq.gz | Fastqsanger.gz | |||
| ERR1994161.fastq.gz | Fastqsanger.gz | |||
| ERR1994171.fastq.gz | Fastqsanger.gz | |||
| ERR1994162.fastq.gz | Fastqsanger.gz |
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Project description:Gallbladder cancer (GBC) comprises the most common biliary tract cancer (BTC). However, GBC is a rare disease often manifesting as aggressive malignancy due to its late diagnosis and resistance to chemotherapy. The identification of molecular drivers of GBC and identification of targeted therapies is still urgently needed. This study combined proteomic analysis of GBC patient samples, functional and molecular characterization of potential oncogenes, and identification of potential therapy strategy for GBC. We identified Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 (CEACAM6) as one of the strongest and most significant upregulated proteins in GBC samples. Functional analysis and in vivo mouse models revealed that CEACAM6 supported the initial steps of cancer metastasis by decreasing cell adhesion while promoting migration and invasion of GBC cells. BirA-BioID followed by mass-spectrometry revealed Integrin Beta-1 (ITGB1) and Protein Kinase C Delta (PRKCD) as direct molecular and functional partners of CEACAM6 in supporting GBC cell migration through regulation of ERK and AKT downstream target genes MMP13, MMP14, and OCLN. Conversely, CEACAM6 knockdown abolished GBC aggressiveness, and treatment using AKT inhibitor Capivasertib and ERK inhibitor Ulixertinib counter-acted the CEACAM6-induced migration.These findings demonstrate that CEACAM6 is crucial for gallbladder oncogenesis through ERK and AKT signaling, providing insights into the design of therapeutic strategies for GBC.
2024-10-30 | GSE243305 | GEO
Project description:Purpose: The uncommonness of gallbladder cancer in the developed world has contributed to the generally poor understanding of the disease. The development of new and effective treatment has been and continues to be a major public health imperative. Methods: We report mutational and copy number analysis of 44 predominantly early-staged gallbladder tumors and 5-gallbladder cancer cell lines by a combination of directed and whole exome sequencing at an average coverage of 100X and above. Using gallbladder cancer cell lines and xenograft mouse models we performed phospho-proteome array profiling, followed by an in-depth functional characterization. Results: We describe recurrent activating ERBB2 somatic mutation in 6 of 44 gallbladder primary tumors with an overall mutation frequency of 13%, along with KRAS activating mutations in 3 of 44 samples. Consistent with whole exome findings, a phospho-proteomic array profile of 49-tyrosine kinase revealed constitutive phosphorylation of ERBB2 and EGFR that were found to heterodimerize. We demonstrate that treatment with ERBB2-specific, EGFR-specific shRNA or with covalent EGFR family inhibitor BIBW-2992 inhibits transformation, survival, migration, invasion, and tumor forming characteristics of gallbladder cancer cells harboring wild type or KRAS (G13D) but not KRAS (G12V) mutation. Furthermore, we show in vivo reduction in tumor size is paralleled by a reduction in the amounts of phospho-ERK in KRAS (G13D) but not in KRAS (G12V) xenografts, validating the in vitro findings Conclusion: Findings from this study implicate ERBB2 as an important therapeutic target in early stage gallbladder cancer. We also present the first evidence that the presence of KRAS (G12V), but not KRAS (G13D) mutation, may preclude gallbladder cancer patients to respond to anti-EGFR treatment, similar to the clinical algorithm commonly practiced to opt for anti-EGFR treatment in colorectal cancer.
2018-12-29 | E-MTAB-6619 | biostudies-arrayexpress
Project description:To further understand the molecular mechanisms in the development of gallbladder cancer, we employed this microarray to identify lncRNAs associated with gallbladder cancer.
2016-01-08 | GSE76633 | GEO
Project description:Gemcitabine resistance in gallbladder cancer poses a significant challenge to patient prognosis. This study identified RUVBL2 as a critical factor contributing to gemcitabine resistance in gallbladder cancer. Further analysis, combining ChIP-seq and gene enrichment studies, revealed that RUVBL2 regulates the mitophagy pathway. This regulation helps maintain intracellular redox homeostasis in gallbladder cancer cells following gemcitabine treatment.
2026-01-30 | GSE317548 | GEO
Project description:Sox17 expression is important for development of gallbladder and bile duct systems in embryo, and it is reported that gallbladder hypoplasia in Sox17 hetero genic embryo. Additionally it was reported that hepatitis was occurred in Sox17 hetero genic newborn by gallbladder hypoplasia. So, we examined Sox17 gene cascade and the role for the formation of gallbladder and bile duct systems by microarray analysis on Sox17 hetero genic gallbladder in day 15 of pregnancy when Sox17 express and gallbladder epithelium alternated morphology. We detected that expression of Sonic hedgehog (shh) signal genes decreased in sox17+/- gallbladder and cysticduct as compared with the wildtype gallbladders.These arry analysis in gallbladder and cysticduct reveal expression of shh in developmental gallbladder is downstream in sox17+/- and gene expression in sox17+/- gallbladder was similar in cysticduct .
2017-05-30 | GSE74576 | GEO
Project description:MicroRNAs (miRNAs) play a critical role in the progression of cancer. However, little is known on the miRNAs expression profiles of gallbladder cancer.We performed this microarray to identify miRNAs associated with gallbladder cancer.
2016-11-18 | GSE90001 | GEO
Project description:To further understand the molecular mechanisms in the development of gallbladder cancer, we employed this microarray to identify lncRNAs associated with gallbladder cancer. 9 pairs of gallbladder cancer tissues and paired normal gallbladder tissues were collected after colecystectomy.
2016-01-08 | E-GEOD-76633 | biostudies-arrayexpress
Project description:We determined the global microRNA expression profiles of primary human gallbladder cells and genetically reprogrammed human gallbladder cells and compared with pancreatic beta cells to ascertain the degree of cellular transdifferentatiation of insulin-producing human gallbladder cells to become beta-like cells. First, we cultured patient-derived gallbladder cells and then we transduced these with beta cell transcription factors to reprogram gallbladder cells to become beta-like cells. We used a pan-islet surface monoclonal antibody to enrich for insulin-producing reprogrammed human gallbladder cells using FACS.
2017-08-02 | E-MTAB-5554 | biostudies-arrayexpress