Effect of knocking down PIEZO1 in gastric cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE228690 | GEO | 2023/12/08
REPOSITORIES: GEO
Similar Datasets
Project description:In gastric cancer (GC), PIEZO1 was suggested to promote cell migration by interacting with Trefoil factor family 1 (TFF1) and serve as a therapeutic target against invasion and metastasis. In addition, PIEZO1 demonstrates abundant expression in most GC cell lines and primary samples and highly-expressed PIEZO1 is associated with poor disease-specific survival. As Yoda1 is known to be an agonist of PIEZO1, we try to explore the PIEZO1 function in GC by Yoda1 treatment.
2023-12-08 | GSE228691 | GEO
Project description:HOX proteins play fundamental roles during ontogenesis by interacting with other non-HOX gene-encoded partners and performing transcriptional functions, while aberrant activation of HOX members drives tumorigenesis. In this study, gastric cancer (GC) expression microarray data indicates that HOXB9 is a prominent upregulated HOX member in GC samples and is significantly associated with clinical outcomes and advanced TNM stages. However, the functional role of HOXB9 in GC remains contradictory in previous reports, and the regulatory mechanisms are elusive. By in silico and experimental analyses, we found HOXB9 was upregulated by a vital cell cycle-related transcription factor E2F1. Depleting HOXB9 causes G1 phase cell cycle arrest by downregulating CDK6 and a subset of cell cycle-related genes. Meanwhile, HOXB9 contributes to cell division and maintains the cytoskeleton in GC cells. PBX2 is a potential transcription factor for CDK6. We verified that HOXB9 interacts with PBX2 to form a heterodimer and upregulates CDK6. Knocking down CDK6 can phenocopy the tumor-suppressive effects of HOXB9 depletion. Inhibiting HOXB9 can enhance the anti-tumor effect of CDK6 inhibitors on GC growth. In conclusion, we elucidate the oncogenic role of HOXB9 and reveal CDK6 as its potent downstream modulator in GC.
2023-01-31 | GSE223763 | GEO
Project description:Purpose: Knocking down NCOA4 disrupted Thyroid hormone receptor beta agonist,GC-1, mediated terminal human erythroblast differentiation. Therefore, we conducted RNA-seq to profile the transcriptome changes in NCOA4 knocked down human erythroblasts.. Methods: Human CD34+ cells were transduced by lentiviruses encoding shRNAs targeting either LacZ (control) or NCOA4 atday 1 of culture. At day 14, cells were switched to terminal differentiation medium. Results: Using an optimized data analysis workflow, we have identified an ensemble of genes whose expression are discrupted by NCOA4 knockdown. Conclusions: There is a significant correlation between the degree of GC-1-mediated gene activation and the degree of NCOA4 knockdown-mediated gene repression.
2017-09-06 | GSE102582 | GEO
Project description:Piezo1 is a mechanosensitive ion channel that has gained recognition for its role in regulating diverse physiological processes. However, the influence of Piezo1 in inflammatory disease, including infection and tumor-immunity, is not well-studied. We postulated that Piezo1 links physical forces to immune regulation in myeloid cells. We discovered signal transduction via Piezo1 in myeloid cells and established this channel as the primary sensor of mechanical stress in these cells. Global inhibition of Piezo1 was protective against both cancer and septic shock and resulted in a diminution in suppressive myeloid cells. Moreover, deletion of Piezo1 in myeloid cells protected against cancer and increased survival in poly-microbial sepsis. Mechanistically, we show that mechanical stimulation promotes Piezo1-dependent myeloid cell expansion by suppressing Rb. We further show Piezo1-mediated silencing of Rb is regulated via upregulation of HDAC2. Collectively, our work uncovers Piezo1 as a targetable immune checkpoint that drives immune-suppressive myelopoiesis in cancer and infectious disease.
2020-08-21 | GSE155340 | GEO
Project description:The expression level of mRNA after knocking-down lncRNA-MEG3 showed a great significance. We performed microarray and transcriptome profiling in C2C12 cells after transfection lncRNA-MEG3 48 hours later to detail the expression of mRNA after knocking-down lncRNA-MEG3.
2020-12-24 | GSE155070 | GEO
Project description:The mechanisms by which physical forces regulate cells to determine complexities of vascular structure and function are enigmatic. Here we show the role the ion channel subunit Piezo1 (FAM38A). Disruption of mouse Piezo1 gene disturbed vascular development and was embryonic lethal within days of the heart beating to cause blood flow. Importance of Piezo channels as sensors of blood flow was indicated by Piezo1 dependence of shear stress-evoked ionic current and calcium influx in endothelial cells and the ability of exogenous Piezo1 to confer shear stress sensitivity on cells that otherwise lacked. Downstream of this calcium influx was proteoase activity and spatial organization of endothelial cells to the polarity of the applied force. Without Piezo1, normal endothelial cell organization was lacking. The data suggest Piezo1 channels as pivotal integrators of vascular architacture with physiological mechanical force.
2014-08-08 | PXD001099 | Pride
Project description:Piezo1 is a stretch-gated ion channel required for mechanosensation in many organ systems. Recent provocative findings describe a new role for Piezo1 in the gut, suggesting that it is a sensor of microbial single-stranded RNA (ssRNA) rather than mechanical force. If true, this would redefine the scope of Piezo biology. Here, we sought to replicate the central finding that fecal ssRNA is a natural agonist of Piezo1. While we observed that fecal extracts and ssRNA stimulate calcium influx in certain cell lines, this response was independent of Piezo1. Additionally, sterilized dietary extracts devoid of gut biome RNA showed similar cell line-specific stimulatory activity to fecal extracts. Together, our data highlight potential confounds inherent to gut-derived extracts, exclude Piezo1 as a receptor for ssRNA in the gut, and support a dedicated role for Piezo channels in mechanosensing.
2022-11-16 | GSE213903 | GEO
Project description:Tendon tissue growth is promoted by mechanical stimulation, but the mechanism is not well understood. Piezo1, a mechanical stress-responsive channel receptor, is expressed in tendon cells, and the fact that tendon tissue growth was accelerated in Piezo1 gain of function mice suggests that Piezo1 plays an important role in tendon tissue growth. RNA-seq of tendon tissues from these mice showed increased expression of tendon-related genes and decreased expression of muscle-related genes, suggesting that Piezo1 may play a role in maintaining and enhancing the properties of tendon cells.
2021-09-20 | GSE169261 | GEO
Project description:Muscle satellite cells (MuSCs), skeletal muscle-resident stem cells, are crucial for regeneration of myofibers. Mechanical cues are thought to be important for activation and proliferation of muscle satellite cells, but the molecular entity that senses biophysical forces in MuSCs remains to be elucidated. In this study, we identified PIEZO1, a mechanosensitive ion channel that is activated by membrane tension, as a critical determinant for myofiber regeneration. We investigated gene profiles of Piezo1-deficient MuSCs to understand the role of PIEZO1 during myogenesis. Our results suggest that PIEZO1 governs the cytoskeletal reorganization to regulate cellular events in MuSCs (i.e., activation, cell-division, and proliferation) during skeletal muscle regeneration.
2022-11-18 | GSE217417 | GEO
Project description:Mechanosensitive ion channels sense force and pressure in immune cells to drive the inflammatory response in highly mechanical organs. Here we report that Piezo1 channels repress group 2 innate lymphoid cells (ILC2s)-driven type 2 inflammation in the lungs. Piezo1 is induced on lung ILC2s upon activation, as genetic ablation of Piezo1 in ILC2s increases their function and exacerbates the development of airway hyperreactivity (AHR). Conversely, Piezo1 agonist Yoda1 reduces ILC2-driven lung inflammation. Mechanistically, Yoda1 inhibits ILC2 cytokine secretion and proliferation in a KLF2-dependent manner, as we further found that Piezo1 engagement reduces ILC2 oxidative metabolism. Consequently, in vivo Yoda1 treatment notably reduces the development of AHR in experimental models of ILC2-driven allergic asthma. Human circulating ILC2s express and induce Piezo1 upon activation, as Yoda1 treatment of humanized mice reduces human ILC2-driven AHR. Our studies define Piezo1 as a critical regulator of ILC2s and we propose the potential of Piezo1 activation as a novel therapeutic approach for the treatment of ILC2-driven allergic asthma.
2024-02-20 | GSE255882 | GEO