RNA-seq profiling of breast cancer cell-line samples with LRIG1 and EGFR L747A manipulation
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE336902 | GEO | 2026/07/13
REPOSITORIES: GEO
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Project description:RNA-seq profiling of breast cancer cell-line samples with LRIG1 and EGFR L747A manipulation
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Project description:As LRIG1 known to be a negative regulator of EGFR, we postulate that restored LRIG1 expression will change the transcription profile through the regulation of EGFR as well as its downstream signal cascades. Thus, we conducted a time-course microarray study to examine the effect of restored LRIG1 expression in NPC line, TW01-LG1/a, which the LRIG1 expression is under the control of a promoter with Doxycycline response element.
2013-05-02 | GSE37349 | GEO
Project description:As LRIG1 known to be a negative regulator of EGFR, we postulate that restored LRIG1 expression will change the transcription profile through the regulation of EGFR as well as its downstream signal cascades. Thus, we conducted a time-course microarray study to examine the effect of restored LRIG1 expression in NPC line, TW01-LG1/a, which the LRIG1 expression is under the control of a promoter with Doxycycline response element. We established stable transfectants of the LRIG1 gene in the TW01 cells which the expression of LRIG1 protein was barely detectable. To control the expression of LRIG1, the coding sequences were placed under the control of a promoter with doxycycline (Dox)-response element using the Tetoff system. Thus the LRIG1 expression could be turn on by removing Dox from the culture medium. Cellular total RNA were harvested along a time course of 12, 24, 36, and 48 hr following LRIG1 turn on expression, and then subjected to exon array analysis (Affymatrix Human Gene 1.0 ST), using the LRIG1 non-expressing sample (with Dox) as control for all comparison. For each time-point, a biological replicate was included.
2013-05-02 | E-GEOD-37349 | biostudies-arrayexpress
Project description:Adult Neural Stem Cells (aNSCs) in the ventricular-subventricular zone (V-SVZ) are largely quiescent. Here, we characterize the mechanism underlying the functional role of a cell-signalling inhibitory protein, LRIG1, in the control of aNSCs proliferation. Using constitutive Lrig1 knockout models, we show that Lrig1 ablation results in increased aNSCs proliferation with no change in neuronal progeny and that this hyperproliferation likely does not result from activation of the epidermal growth factor receptor (EGFR). Loss of LRIG1, however, does lead to impaired activation of canonical transforming growth factor beta (TGFβ) and bone morphogenic protein (BMP) signalling pathways. Biochemically, we show in vitro that LRIG1 is able to bind TGFβ/BMP receptors and the TGFβ1 ligand. Finally, we show that the consequences of these interactions are to facilitate SMAD phosphorylation and pathway activation. Collectively, these data suggest that, unlike in embryonic neural stem cells where EGFR is the primary mechanism of action, LRIG1 and TGFβ pathways positively work together to fulfill their inhibitory roles in aNSCs.
2024-07-08 | GSE263575 | GEO
Project description:Adult neural stem cells (NSCs) must tightly regulate quiescence and proliferation. Single cell analysis has suggested a continuum of cell states as NSCs exit quiescence. Here we capture and characterize in vitro primed quiescent NSCs and identify LRIG1 as an important regulator. We show that BMP-4 signaling induces a dormant non-cycling quiescent state (d-qNSCs), whereas combined BMP-4/FGF-2 signalling induces a distinct primed quiescent state poised for cell cycle re-entry. Primed quiescent NSCs (p-qNSCs) are defined by high levels of LRIG1 and CD9, as well as an interferon response signature, and can efficiently engraft into the adult subventricular zone (SVZ) niche. Genetic disruption of Lrig1 in vivo within the SVZ NSCs leads an enhanced proliferation. Mechanistically, LRIG1 primes quiescent NSCs for cell cycle re-entry and EGFR responsiveness by enabling EGFR protein levels to increase but limiting signaling activation. LRIG1 is therefore an important functional regulator of NSC exit from quiescence.
2021-03-18 | GSE168189 | GEO
Project description:Regulatory T cell (Treg) is the immune-suppressive T cell subset and the crucial component for preventing autoimmunity. The molecules defining the suppressive population of T cells phenotypically and functionally remain to be discovered. In this study, we report that Lrig1 is highly expressed in suppressive CD4+ T cell populations. We performed RNA-seq analysis of CD4+Lrig1+ and CD4+Lrig1- T cells from mouse splenocytes to analyze the genes involeved in the suppressive function of T cells.
2023-07-16 | GSE236988 | GEO
Project description:Cancer immunotherapies boost antitumor immunity and improve the survival of cancer patients. V-domain Immunoglobulin Suppressor of T cell Activation (VISTA) is an immune 20 checkpoint target but presents elusive signaling mechanisms. We report a novel VISTA binding partner, Leucine-Rich Repeats and Immunoglobulin Like Domains 1 (LRIG1), which acts as an inhibitory receptor by engaging VISTA and suppressing T cell receptor signaling pathways. Mice with T cell-specific LRIG1 deletion developed superior antitumor T cell responses. Mechanistically, LRIG1-deficient tumor-specific CD8+ cytotoxic T cells (CTLs) exhibited longer 25 persistence due to improved expansion and survival and greater effector function. Sustained tumor control was also associated with a reduction of quiescent CTLs (TCF1+ CD62Lhi PD-1low) and a reciprocal increase in progenitor and memory-like CTLs (TCF1+ PD-1+). In human melanoma, an elevated LRIG1 expression on tumor-infiltrating CD8+ CTLs correlated with resistance to immunotherapies. Taken together, these results delineate the role of LRIG1 as an inhibitory 30 immune checkpoint receptor and propose a rationale for targeting the VISTA/LRIG1 axis for cancer immunotherapy.
2024-10-17 | PXD050084 | Pride
Project description:Expression profiling array of Lrig1 expressing and non-expressing cells isolated by flow cytometry from the intestinal epithelium of Lrig1:eGFPiresCreERT2 (Lrig1 KI) animals.
2013-08-15 | E-MTAB-1602 | biostudies-arrayexpress
Project description:Identifying progenitor cells in laryngeal and vocal fold (VF) mucosa is essential for advancing stem cell-based tissue engineering and therapies for treatment of VF diseases. In this study, we used the Lrig1 gene as a marker for tissue-resident stem cells within murine laryngeal and VF mucosa. We show that Lrig1⁺ cells exhibited hallmark features of quiescent stem cells: slow-cycling, persistence and differentiation potential. Transcriptionally, they suppress transcription of cell type–specific genes and proliferation, while activating a global transcriptional program related to RNA metabolism, epigenetic regulation and protein ubiquitination – supporting quiescence and readiness for activation. Lrig1+ cells were enriched in basal, parabasal, and immature secretory populations and were spatially shielded from direct stress exposure to prevent their premature or chronic mobilization. Notably, we detected analogous Lrig1-expressing cells in human laryngeal and VF tissues, emphasizing the translational relevance of our findings. To investigate how Lrig1⁺ cell quiescence is regulated, we conditionally deleted Notch1, leading to epithelial hyperplasia, expansion of secretory cell populations, and mucus hyperproduction. In summary, Lrig1 marks a conserved, quiescent stem cell population in the larynx and VFs, with quiescence maintained through Notch1 signaling.
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Project description:RNA-seq analysis of Lrig1+ and Lrig1- CD4+ T cells in mouse spleen
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