Expression profiling of AKTP primary tumors cells with high or low expression of Emp1
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ABSTRACT:
PROVIDER: PRJNA785641 | ENA |
REPOSITORIES: ENA
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Project description:Hematopoietic stem cells (HSCs) play a crucial role in lifelong hematopoiesis by generating all blood lineages. The long-term maintenance of HSCs relies on the regulation of endoplasmic reticulum (ER) stress at a low level. However, the precise control of ER stress in HSCs remains largely unknown. In this study, we demonstrate that suppression of ER stress enhances the in vitro maintenance and in vivo repopulation capacity of HSCs, while also protecting HSCs against radiation-induced injury. Integrated multi-omics analysis has revealed that epithelial membrane protein 1 (Emp1) functions as an ER stress sensor in HSCs. Loss of Emp1 leads to increased protein aggregates and elevated ER stress, ultimately resulting in impaired HSC maintenance and self-renewal. Mechanistically, EMP1 is located within the ER and interacts with ceramide synthase 2 (CERS2) to limit the production of dihydroceramides (dhCers), which are a class of sphingolipids. DhCers accumulate in Emp1-deficient HSCs and directly induce protein aggregation. Inhibition of CERS2 significantly restores the maintenance of Emp1-deficient HSCs. Furthermore, Emp1 deficiency renders HSCs more susceptible to radiation, while overexpression of Emp1 or inhibition of CERS2 protects HSCs against radiation-induced injury. These findings highlight the critical role played by the EMP1-CERS2-dhCers axis in constraining ER stress and preserving HSC potential, uncovering a new link between sphingolipid metabolism and HSC homeostasis, and have clinical implications.
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Project description:Hematopoietic stem cells (HSCs) play a crucial role in lifelong hematopoiesis by generating all blood lineages. The long-term maintenance of HSCs relies on the regulation of endoplasmic reticulum (ER) stress at a low level. However, the precise control of ER stress in HSCs remains largely unknown. In this study, we demonstrate that suppression of ER stress enhances the in vitro maintenance and in vivo repopulation capacity of HSCs, while also protecting HSCs against radiation-induced injury. Integrated multi-omics analysis has revealed that epithelial membrane protein 1 (Emp1) functions as an ER stress sensor in HSCs. Loss of Emp1 leads to increased protein aggregates and elevated ER stress, ultimately resulting in impaired HSC maintenance and self-renewal. Mechanistically, EMP1 is located within the ER and interacts with ceramide synthase 2 (CERS2) to limit the production of dihydroceramides (dhCers), which are a class of sphingolipids. DhCers accumulate in Emp1-deficient HSCs and directly induce protein aggregation. Inhibition of CERS2 significantly restores the maintenance of Emp1-deficient HSCs. Furthermore, Emp1 deficiency renders HSCs more susceptible to radiation, while overexpression of Emp1 or inhibition of CERS2 protects HSCs against radiation-induced injury. These findings highlight the critical role played by the EMP1-CERS2-dhCers axis in constraining ER stress and preserving HSC potential, uncovering a new link between sphingolipid metabolism and HSC homeostasis, and have clinical implications.
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Project description:Hematopoietic stem cells (HSCs) play a crucial role in lifelong hematopoiesis by generating all blood lineages. The long-term maintenance of HSCs relies on the regulation of endoplasmic reticulum (ER) stress at a low level. However, the precise control of ER stress in HSCs remains largely unknown. In this study, we demonstrate that suppression of ER stress enhances the in vitro maintenance and in vivo repopulation capacity of HSCs, while also protecting HSCs against radiation-induced injury. Integrated multi-omics analysis has revealed that epithelial membrane protein 1 (Emp1) functions as an ER stress sensor in HSCs. Loss of Emp1 leads to increased protein aggregates and elevated ER stress, ultimately resulting in impaired HSC maintenance and self-renewal. Mechanistically, EMP1 is located within the ER and interacts with ceramide synthase 2 (CERS2) to limit the production of dihydroceramides (dhCers), which are a class of sphingolipids. DhCers accumulate in Emp1-deficient HSCs and directly induce protein aggregation. Inhibition of CERS2 significantly restores the maintenance of Emp1-deficient HSCs. Furthermore, Emp1 deficiency renders HSCs more susceptible to radiation, while overexpression of Emp1 or inhibition of CERS2 protects HSCs against radiation-induced injury. These findings highlight the critical role played by the EMP1-CERS2-dhCers axis in constraining ER stress and preserving HSC potential, uncovering a new link between sphingolipid metabolism and HSC homeostasis, and have clinical implications.
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2014-02-01 | E-GEOD-53618 | biostudies-arrayexpress
Project description:To illustrate EMP1-interacting proteins, we performed co-immunoprecipitation (co-IP) followed by mass spectrometry using HSPCs (Lin-c-Kit+) to characterize protein interactomes of EMP1. Murine HSPCs (Lin-c-Kit+) were infected with retrovirus to force EMP1 overexpression (with HA tag). Then IgG or HA antibodies were used to conducted co-immunoprecipitation (co-IP), followed by and mass spectrometry analysis.
2025-03-13 | PXD055884 | Pride
Project description:High grade serous ovarian cancers (HGSC) are deadly malignancies that relapse despite carboplatin chemotherapy. Many commercially ovarian cancer cell lines are not good models for HGSC. Here we demonstrate that 3 low passage cell lines derived from HGSC have similar transcriptomes to their parental bulk tumors. These cell lines recapitulated tumor characteristics of the primary cancer and had responded to therapy in the same manner as primary HGSC cells, demonstrating they are accurate models for HGSCs. mRNA profiles of low passage high grade serous tumor cell lines and their parental tumors, generated by next generation sequencing, were compared.
2015-08-01 | E-GEOD-70073 | biostudies-arrayexpress
Project description:PurposePhyllodes tumors (PTs) are biphasic tumors accounting for 0.3-1.5% of all breast tumors. Epithelial membrane proteins (EMPs) have been reported in various malignant tumors but their expression in PTs is unclear. In this study, we aimed to evaluate the expression of EMP1, EMP2, and EMP3 in breast phyllodes tumors (PTs), and to investigate their clinical implications.MethodsIn total, 185 PTs were used for constructing a tissue microarray. Immunohistochemical staining for EMP1, EMP2, and EMP3 was performed, and the results were analyzed along with the clinicopathologic parameters.ResultsIn total, 185 PTs were included in this study, and comprised 138 benign, 32 borderline, and 15 malignant PTs. In malignant PTs, the epithelial component showed decreased expression of EMP1 (P = 0.027), EMP2 (P = 0.004), and EMP3 (P = 0.032), compared to the benign and borderline PTs. Conversely, stromal component of borderline and malignant PTs showed higher expression of EMP1 (P = 0.027), EMP2 (P = 0.004), and EMP3 (P = 0.032) compared to benign PTs. Expression of EMP1 and EMP3 correlated positively with stromal cellularity and cellular atypia (P < 0.001). In the univariate analysis, stromal EMP3 was associated with shorter disease-free survival (P < 0.001), and shorter overall survival (P = 0.034).ConclusionThe expression of EMP1, EMP2, and EMP3 is decreased in the epithelial component and is increased in the stromal component of PT with higher histologic grade. Thus, stromal EMP3 expression may serve as an independent prognostic factor in PT.
| S-EPMC7454950 | biostudies-literature
Project description:High grade serous ovarian cancers (HGSC) are deadly malignancies that relapse despite carboplatin chemotherapy. Many commercially ovarian cancer cell lines are not good models for HGSC. Here we demonstrate that 3 low passage cell lines derived from HGSC have similar transcriptomes to their parental bulk tumors. These cell lines recapitulated tumor characteristics of the primary cancer and had responded to therapy in the same manner as primary HGSC cells, demonstrating they are accurate models for HGSCs.
2015-08-01 | GSE70073 | GEO