KLF7 regluate migration and cancer stemness in OSCC [RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1202564 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:KLF7 regluate migration and cancer stemness in OSCC [ChIP-seq]
| PRJNA1202562 | ENA
Project description:In this study, we aim to analyze the role and mechanism of transcription factor KLF7 in oral cancer. We used CHIP-seq to analyze the binding sites of KLF7 on the genome of oral cancer cell line CAL27 Meanwhile, we also analyzed the changes in gene expression after CAL27 overexpression of KLF7 using transcriptome sequencing
2025-02-01 | GSE285331 | GEO
Project description:In this study, we aim to analyze the role and mechanism of transcription factor KLF7 in oral cancer. We used CHIP-seq to analyze the binding sites of KLF7 on the genome of oral cancer cell line CAL27 Meanwhile, we also analyzed the changes in gene expression after CAL27 overexpression of KLF7 using transcriptome sequencing
2025-02-01 | GSE285330 | GEO
Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. KLF7 overexpression in HSPCs expression array: Lin- c-Kit+ Sca-1+ cells transduced with a KLF7 expressing or control (empty vector) lentivirus. Expression profiles of KLF7 overexpressing vs controls HSPCs. Cells were harvested 72 hrs post-transduction to compare expression profiles of control vs KLF7 overexpressing HSPCs
2012-08-24 | E-GEOD-40327 | biostudies-arrayexpress
Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. KLF7 KO vs WT HSPC expression array: KLS (lineage- c-Kit+ Sca-1+) cells were sorted from the bone marrow of Klf7-/- chimeras at 12 weeks post-transplant. Fetal liver cells were used to establish chimeric mice (C57Bl/6 background) containing a mixture of Klf7+/+ and Klf7-/- bone marrow cells.
2012-08-24 | E-GEOD-40323 | biostudies-arrayexpress
Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. KLF7 overexpression in HSPCs expression array: Lin- c-Kit+ Sca-1+ cells transduced with a KLF7 expressing or control (empty vector) lentivirus. Expression profiles of KLF7 overexpressing vs controls HSPCs.
2012-08-24 | GSE40327 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with a dismal prognosis. Currently, there is no effective therapy to treat PDAC, and thus detailed molecular and functional evaluation of PDAC is needed to identify and develop better therapeutic strategies. Here we show that the transcription factor Kruppel-like factor 7 (KLF7) is overexpressed in PDAC and that inhibition of KLF7 blocks PDAC tumor growth and metastasis in cell culture and in mice. KLF7 expression in PDAC can be upregulated due to activation of a MAP kinase pathway or inactivation of the tumor suppressor p53, two alterations that occur in a large majority of PDACs. ShRNA-mediated knockdown of KLF7 inhibits the expression of interferon-stimulated genes (ISGs), which are necessary for KLF7-mediated PDAC tumor growth and metastasis. KLF7 knockdown also results in the downregulation of Discs Large MAGUK Scaffold Protein 3 (DLG3), resulting in Golgi complex fragmentation, and reduced protein glycosylation leading to reduced secretion of cancer-promoting growth factors such as chemokines. Genetic or pharmacological activation of Golgi complex fragmentation blocks PDAC growth and metastasis similar to KLF7 inhibition. Our results demonstrate a therapeutically amenable, KLF7-driven pathway that promotes PDAC growth and metastasis by activating ISGs and maintaining Golgi complex integrity.
2020-04-16 | GSE107184 | GEO
Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. KLF7 KO vs WT HSPC expression array: KLS (lineage- c-Kit+ Sca-1+) cells were sorted from the bone marrow of Klf7-/- chimeras at 12 weeks post-transplant.
2012-08-24 | GSE40323 | GEO
Project description:KLF7, a member of the KLF family, is an evolutionarily conserved zinc finger-containing transcription factor. Previous studies demonstrated that KLF7 possesses diverse regulatory functions related to embryogenesis, cell growth, proliferation, and differentiation. Our results reveal that there was an increased abundance of KLF7 in OSM-treated HaCaT cells. Mechanistically, our results showed that OSM induces epidermal keratinocyte differentiation through phosphorylation of STAT5, which binds to the promoter and activates KLF7 transcription.
2022-06-01 | GSE154053 | GEO
Project description:Breast cancer metastasis is driven by profound remodeling of the intracellular cytoskeleton enabling efficient cell migration. Anillin is a unique cytoskeletal scaffolding protein that regulates actin filaments, microtubules, septin polymers and Rho GTPases. Anillin is markedly overexpressed in breast cancer and other solid cancer, however its functions in cancer cells remain poorly understood. This study aims at investigating the roles of anillin in regulating breast cancer cell migration, invasion and metastasis. CRISPR/Cas9 technology was used to deplete anillin in highly metastatic MDA-MB-231and BT549 cells and to overexpress it in poorly invasive MCF10AneoT cells. These loss-of-function and gain-of-function studies demonstrated that anillin is necessary and sufficient to accelerate migration, invasion and anchorage-independent growth of breast cancer cells in vitro. Furthermore, loss of anillin markedly attenuated both primary tumor growth and metastasis of breast cancer in vivo. In breast cancer cells, anillin was localized in the nucleus, however anillin knockout affected the cytoplasmic/cortical events such as the organization of actin cytoskeleton and cell-matrix adhesions. This was accompanied by a global transcriptional reprogramming of anillin-depleted breast cancer cells that resulted in suppression of their stemness and induction of the mesenchymal to epithelial trans-differentiation. Such trans-differentiation was manifested by upregulation of basal keratins along with increased expression of E-cadherin and P-cadherin. Knockdown of E-cadherin reversed attenuated migration and invasion of anillin-deficient cells. Our study provides the first evidence that anillin plays causal roles in breast cancer development and metastasis in vitro and in vivo and unravels novel functions of anillin in regulating breast cancer stemness and differentiation.
2020-01-01 | GSE131120 | GEO