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Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression

ABSTRACT: We sought to elucidate the molecular mechanisms whereby LIN28B functions by comparing the gene expression profile of cells constitutively expressing LIN28B to empty vector controls. Accordingly, we performed microarray analysis on total RNA isolated from empty vector LoVo and LIN28B-expressing LoVo colon cancer cell lines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26334 | GEO | 2010/12/29

SECONDARY ACCESSION(S): PRJNA142243

REPOSITORIES: GEO

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Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression

Project description:We sought to elucidate the molecular mechanisms whereby LIN28B functions by comparing the gene expression profile of cells constitutively expressing LIN28B to empty vector controls. Accordingly, we performed microarray analysis on total RNA isolated from empty vector LoVo and LIN28B-expressing LoVo colon cancer cell lines. Constitutive LIN28B expression was achieved in the LoVo (ATCC #CCL-229) colon cancer cell line via retroviral transduction of MSCV-PIG-LIN28B. Contol = empty vector MSCV-PIG.

2010-12-29 | E-GEOD-26334 | biostudies-arrayexpress

Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression

Project description:We sought to elucidate functions of LIN28B and potential mechanisms whereby it may promote metastasis by comparing the gene expression profile of LIN28B metastases to primary tumors. Accordingly, we performed microarray analysis on total RNA isolated from empty vector tumors, LIN28B-LoVo tumors, and LIN28B-LoVo metastases Constitutive LIN28B expression was achieved in the LoVo (ATCC #CCL-229) colon cancer cell line via retroviral transduction of MSCV-PIG-LIN28B. xenografts were produced via injection of 1x106 cells subcutaneously into the rear flanks of nude mice. Microarrays were conducted on primary tumors from empty vector and LIN28B-expressing cells, as well as metastases derived from primary tumors constitutively expressing LIN28B. (Note: metastases did not occur with empty vector tumors)

2010-12-29 | E-GEOD-26335 | biostudies-arrayexpress

Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression

2010-12-29 | GSE26335 | GEO

LIN28B and colon cancer

Project description:This SuperSeries is composed of the following subset Series: GSE26334: Expression data from LoVo colon cancer lines +/- constitutive LIN28B expression GSE26335: Expression data from xenograft tumors derived from LoVo colon cancer lines +/- constitutive LIN28B expression Refer to individual Series

2010-12-29 | E-GEOD-26336 | biostudies-arrayexpress

Expression data from human colorectal cancer cell line LoVo

Project description:PEAK1 overexpression vector and negative control vector were transiently transfected into LoVo cells, respectively, and named LoVo-PEAK1 and LoVo-control groups. LoVo cells of different groups were determined to investigate the different expressions of mRNA using a global gene microarray.

2018-01-10 | GSE108947 | GEO

Lin28b promotes fetal B lymphopoiesis through the transcription factor Arid3a [Lin28b & Let7 transduction]

Project description:Mouse B cell precursors from fetal liver and adult bone marrow generate distinctive B cell progeny when transplanted into immunodeficient recipients, supporting a two-pathway model for B lymphopoiesis, fetal “B-1” and adult “B-2”. Recently Lin28b was shown to be important for the switch between fetal and adult pathways; however, neither the mechanism of Lin28b action nor the importance of BCR signaling in this process was addressed. Here we report important advances in our understanding of the regulation of B 1/B-2 development. First, modulation of Let-7 in fetal Pro-B cells is sufficient to alter fetal B-1 development to produce B cells resembling the progeny of adult B-2 development. Second, intact BCR signaling is required for generation of B1a B cells from Lin28b-transduced bone marrow progenitors, supporting a requirement for ligand-dependent selection, as is the case for normal B1a B cells. Third, the VH repertore of Lin28b-induced bone marrow B1a B cells differs from that of normal B1a. Finally we identify the Arid3a transcription factor as a key target of Let-7, whose ectopic expression is sufficient to induce B-1 development in adult Pro-B cells and whose knockdown blocks B-1 development in fetal Pro-B cells. 2 individual sorts of bone marrow Pro-B cells 4 days after Lin28b retroviral transduction (and 2 sorts of empty vector control) and 2 individual sorts of fetal liver Pro-B cells 4 days after Let-7b retroviral transduction (and 2 sorts of empty vector controls).

2015-03-01 | E-GEOD-65534 | biostudies-arrayexpress

microRNA array of LoVo cells and LoVo-Small Extracellular Vesicles

Project description:LoVo cells were cultured in sEV-depleted (160,000xg, 16h) complete medium and the supernatant were collected after 72h. sEVs were purified and centrifuged at 100,000xg for 2.5h using a Beckman SW41Ti rotor to know the miRNA in LoVo cells and LoVo-Small Extracellular Vesicles

2019-07-01 | GSE117866 | GEO

LIN28B promotes cell invasion and colorectal cancer metastasis via CLDN1 and NOTCH3

Project description:The RNA-binding protein LIN28B is overexpressed in over 30% of patients with colorectal cancer (CRC) and is associated with poor prognosis. In the present study, we unravel a novel mechanism by which LIN28B regulates colonic epithelial cell-cell junctions and CRC metastasis. Using human CRC cells (DLD-1, Caco-2 and LoVo) with either knockdown or overexpression of LIN28B, we identified Claudin 1 (CLDN1) tight junction protein as a direct downstream target and effector of LIN28B. RNA immunoprecipitation revealed that LIN28B directly binds to and post-transcriptionally regulates CLDN1 mRNA. Furthermore, using in vitro assays and a novel murine model of metastatic CRC, we show that LIN28B-mediated CLDN1 expression enhances collective invasion, cell migration, and metastatic liver tumor formation. Bulk RNA-sequencing of the metastatic liver tumors identified NOTCH3 as a downstream effector of the LIN28B-CLDN1 axis. Additionally, genetic and pharmacologic manipulation of NOTCH3 signaling revealed that NOTCH3 was necessary for invasion and metastatic liver tumor formation. In summary, our results suggest that LIN28B promotes invasion and liver metastasis of CRC by post-transcriptionally regulating CLDN1 and activating NOTCH3 signaling. This discovery offers a promising new therapeutic option for metastatic CRC to the liver, an area where therapeutic advancements have been relatively scarce.

2023-09-14 | GSE234513 | GEO

Gene expression profiling in LoVo-P compared with LoVo-C cells

Project description:The differential expression of mRNA in LoVo-P cells compared with LoVo-C cells was successfully detected using the Arraystar Human LncRNA/mRNAArray V4.0, that used for the global profiling of 20730 human mRNA and 40173 long non-coding RNA (LncRNA) transcripts.

2017-09-20 | GSE103989 | GEO

LIN28B is overexpressed in specific subtypes of pediatric leukemia and regulates lncRNA H19 [Oci-AML3]

Project description:The stem cell gene LIN28B was recently shown to be overexpressed in a foetal-like subgroup of juvenile myelomonocytic leukaemia. Given the involvement of LIN28B in a variety of solid paediatric cancers, we conducted a meta-analysis of LIN28B levels using publicly available gene expression data of 1361 paediatric leukaemia samples. Interestingly, this analysis revealed LIN28B overexpression in 102 childhood leukaemia patients (7.5%), suggesting oncogenic activity for LIN28B in the context of paediatric haematological diseases. As the mode of action of LIN28B during normal and malignant haematopoiesis remains largely unexplored, we subsequently analysed the transcriptional consequences of LIN28B modulation on normal and malignant haematopoietic cells and identified the long non-coding RNA (lncRNA) H19 as the first LIN28B-regulated lncRNA. Oci-AML3 cells were retrovirally transduced with MSCV-PIG-LIN28B and MSCV-PIG-empty vectors (gifts from Johua Mendel lab), selected with puromycin and hybridized on Agilent microarray.

2016-04-07 | E-GEOD-79979 | biostudies-arrayexpress

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