Similar Datasets
Project description:Mouse Mist1 and Lrig1 apc tumors
| PRJNA804102 | ENA
Project description:To comprehensively assess the immune milieu of WT and SCID mT3-2D tumors, we employed NanoString nCounter immune profiling. The two groups of samples exhibited distinct immune profiles and indicated greater upregulation of immune-related genes in mT3-2D WT tumors than in SCID tumors.
2021-02-26 | GSE165165 | GEO
Project description:Lrig1 is an intestinal stem cell marker important for epithelial homeostasis. However, the position of the Lrig1(+) population in the intestinal crypt has been debated, largely due to discrepant staining patterns using two Lrig1 antibodies. Here, we set out to decipher the differences between these Lrig1 antibodies to clarify their use for Lrig1-related studies. We confirmed that the commercially available Lrig1-R&D antibody stained the bottom third of the colonic crypt, whereas an independently generated Lrig1-VU antibody recognized a subset of anti-Lrig1-R&D(+) cells. Biochemically, we found that anti-Lrig1-VU recognized a non-glycosylated form of Lrig1; in contrast, anti-Lrig1-R&D recognized both glycosylated and non-glycosylated forms of Lrig1. In addition, we generated a reporter mouse (Lrig1-Apple) as an independent readout of Lrig1 transcriptional activity. Flow cytometry of isolated colonic epithelial cells from Lrig1-Apple mice demonstrated anti-Lrig1-R&D recognized mostly RFP-hi cells, while anti-Lrig1-VU recognized cells that were largely RFP-mid. Of note, by qRT-PCR, Lgr5 was expressed in the RFP-hi population, but not in the RFP-mid population. We conclude that anti-Lrig1-R&D appears to recognize all Lrig1(+) cells, while anti-Lrig1-VU recognizes a subpopulation of Lrig1(+) cells.
| S-EPMC4320017 | biostudies-literature
Project description:Background & aimsEarly embryogenesis involves cell fate decisions that define the body axes and establish pools of progenitor cells. Development does not stop once lineages are specified; cells continue to undergo specific maturation events, and changes in gene expression patterns lead to their unique physiological functions. Secretory pancreatic acinar cells mature postnatally to synthesize large amounts of protein, polarize, and communicate with other cells. The transcription factor MIST1 is expressed by only secretory cells and regulates maturation events. MIST1-deficient acinar cells in mice do not establish apical-basal polarity, properly position zymogen granules, or communicate with adjacent cells, disrupting pancreatic function. We investigated whether MIST1 directly induces and maintains the mature phenotype of acinar cells.MethodsWe analyzed the effects of Cre-mediated expression of Mist1 in adult Mist1-deficient (Mist1(KO)) mice. Pancreatic tissues were collected and analyzed by light and electron microscopy, immunohistochemistry, real-time polymerase chain reaction analysis, and chromatin immunoprecipitation. Primary acini were isolated from mice and analyzed in amylase secretion assays.ResultsInduced expression of Mist1 in adult Mist1(KO) mice restored wild-type gene expression patterns in acinar cells. The acinar cells changed phenotypes, establishing apical-basal polarity, increasing the size of zymogen granules, reorganizing the cytoskeletal network, communicating intercellularly (by synthesizing gap junctions), and undergoing exocytosis.ConclusionsThe exocrine pancreas of adult mice can be remodeled by re-expression of the transcription factor MIST1. MIST1 regulates acinar cell maturation and might be used to repair damaged pancreata in patients with pancreatic disorders.
| S-EPMC3664941 | biostudies-literature
Project description:Based on RNA-seq technology, we studies gene expression profiles in tumor lysis isolated from mouse tumors before and after rMVA treatment. We identified differential gene expressions comparing treated tumors with non-treated tumors. The difference of tumor gene expression between WT and STING KO mice were also identified.
2022-11-10 | GSE188496 | GEO
Project description:Comparative transcriptomic analysis of TAMs isolated from APC-WT and APC-KO MC38 orthotopic tumors express higher levels of multiple classical M2-like markers (CD163, CCL22, YM1) compared to APC-WT tumors after re-normalized the read counts of multiple M2 macrophage markers with housekeeping gene read counts (GAPDH and ACTB).
2022-07-13 | GSE200909 | GEO
Project description:We report the changes in gene expression in mouse prostate comparing normal wild type prostate to tumors generated by Cre mediated deletion of Pten or Apc, either with or without deletion of Tgfbr2. Pten single mutant tumors were isolated at either 8 weeks or 22 weeks of age, with high grade prostate intraepithelial neoplasia (HGPIN) as the main phenotype. Pten;Tgfbr2 double mutants were isolated at 8 weeks (primarily HGPIN), or at 11-14 weeks with extensive locally invasive cancer. Apc single mutants were isolated at 36 weeks old with adenosquamous HGPIN, or at 21-24 weeks of age for the Apc:Tgfbr2 double mutants, which had adenosquamous carcinoma. Ages for the two double mutant groups were based on initial signs of excess tumor burden. Wild type control prostates were isolated at around 20 weeks of age.
2018-05-14 | GSE108017 | GEO
Project description:Despite their divergent developmental ancestry, plasma cells and gastric zymogenic (chief) cells share a common function: high-capacity secretion of protein. Here we show that both cell lineages share increased expression of a cassette of 269 genes, most of which regulate endoplasmic reticulum (ER) and Golgi function, and they both induce expression of the transcription factors X-box binding protein 1 (Xbp1) and Mist1 during terminal differentiation. XBP1 is known to augment plasma cell function by establishing rough ER, and MIST1 regulates secretory vesicle trafficking in zymogenic cells. We examined morphology and function of plasma cells in wild-type and Mist1(-/-) mice and found subtle differences in ER structure but no overall defect in plasma cell function, suggesting that Mist1 may function redundantly in plasma cells. We next reasoned that MIST1 might be useful as a novel and reliable marker of plasma cells. We found that MIST1 specifically labeled normal plasma cells in mouse and human tissues, and, moreover, its expression was also characteristic of plasma cell differentiation in a cohort of 12 human plasma cell neoplasms. Overall, our results show that MIST1 is enriched upon plasma cell differentiation as a part of a genetic program facilitating secretory cell function and also that MIST1 is a novel marker of normal and neoplastic plasma cells in mouse and human tissues.
| S-EPMC3055710 | biostudies-literature
Project description: Not available
| S-EPMC8413138 | biostudies-literature
Project description:BACKGROUND:The loss of a single copy of adenomatous polyposis coli (Apc) in leucine-rich repeats and immunoglobulin-like domains 1 (Lrig1)-expressing colonic progenitor cells induces rapid growth of adenomas in mice with high penetrance and multiplicity. The tumors lack functional APC, and a genetic loss of heterozygosity of Apc was previously observed. METHODS:To identify genomic features of early tumorigenesis, and to profile intertumoral genetic heterogeneity, tumor exome DNA (n = 9 tumors) and mRNA (n = 5 tumors) sequences were compared with matched nontumoral colon tissue. Putative somatic mutations were called after stringent variant filtering. Somatic signatures of mutational processes were determined and splicing patterns were observed. RESULTS:The adenomas were found to be genetically heterogeneous and unexpectedly hypermutated, displaying a strong bias toward G:C > A:T mutations. A genetic loss of heterozygosity of Apc was not observed, however, an epigenetic loss of heterozygosity was apparent in the tumor transcriptomes. Complex splicing patterns characterized by a loss of intron retention were observed uniformly across tumors. CONCLUSION:This study demonstrates that early tumors originating from intestinal stem cells with reduced Lrig1 and Apc expression are highly mutated and genetically heterogeneous, with an inflammation-associated mutational signature and complex splicing patterns that are uniform across tumors.
| S-EPMC7023705 | biostudies-literature