Similar Datasets
Project description:During aging, the accumulation of senescent cells has a pivotal role in age-related dysfunctions. At geriatric age, the emergence of muscle stem cells (MuSCs) exhibiting senescence markers identified in vitro studies have been reported. However, whether they are in cellular senescence and thus have lost their function is unclear, due to the lack of specific marker for senescent cells. Here, by tracing genetically labeled MuSCs throughout life, we found an unknown MuSC population termed GERI-MuSCs that lost conventional MuSC markers at geriatric age. Although they have several known senescence features, they retain considerable functionalities of in vitro proliferation and in vivo myogenesis, suggesting they are not in cellular senescence. These results highlight the potential discrepancies between aging process in vivo and cellular senescence characterized in vitro. Importantly, we found new markers, CD63 and CD200, inclusive of GERI-MuSCs, which provide a crucial tool for a deeper investigation on in vivo senescence.
2024-12-31 | GSE254476 | GEO
Project description:During aging, the accumulation of senescent cells has a pivotal role in age-related dysfunctions. At geriatric age, the emergence of muscle stem cells (MuSCs) exhibiting senescence markers identified in vitro studies have been reported. However, whether they are in cellular senescence and thus have lost their function is unclear, due to the lack of specific marker for senescent cells. Here, by tracing genetically labeled MuSCs throughout life, we found an unknown MuSC population termed GERI-MuSCs that lost conventional MuSC markers at geriatric age. Although they have several known senescence features, they retain considerable functionalities of in vitro proliferation and in vivo myogenesis, suggesting they are not in cellular senescence. These results highlight the potential discrepancies between aging process in vivo and cellular senescence characterized in vitro. Importantly, we found new markers, CD63 and CD200, inclusive of GERI-MuSCs, which provide a crucial tool for a deeper investigation on in vivo senescence.
2024-12-31 | GSE254475 | GEO
Project description:Non-senescent, conventional marker-negative geriatric muscle stem cells identified by new CD63/CD200 markers
| PRJNA1070635 | ENA
Project description:Non-senescent, conventional marker-negative geriatric muscle stem cells identified by new CD63/CD200 markers [scRNA-seq]
| PRJNA1070639 | ENA
Project description:Non-senescent, conventional marker-negative geriatric muscle stem cells identified by new CD63/CD200 markers [RNA-seq]
| PRJNA1070632 | ENA
Project description:Elucidating the genes regulated during cell-cell communication remains fascinating considering the importance of cell recognition and downstream signaling through development and in many diseases. In the peripheral nervous system, the interaction between Schwann cells (SCs) and axons is crucial as it allows their survival and induces SCs to differentiate and engage a process of myelination. To get further insight the molecular mechanisms resulting from this cell interaction, comparative gene analysis between SCs and SCs co-cultured with DRG neurons were performed and led us to identify a set of 32 genes regulated in SCs in the early stage of neuron-SC contact. Expression of several candidates were analyzed by QPCR during development and we demonstrate using a blocking antibody approach in an in vitro myelination assay that one candidate was not only upregulated in response to axonal contact but also controls peripheral myelination.
2011-01-15 | GSE17366 | GEO
Project description:Elucidating the genes regulated during cell-cell communication remains fascinating considering the importance of cell recognition and downstream signaling through development and in many diseases. In the peripheral nervous system, the interaction between Schwann cells (SCs) and axons is crucial as it allows their survival and induces SCs to differentiate and engage a process of myelination. To get further insight the molecular mechanisms resulting from this cell interaction, comparative gene analysis between SCs and SCs co-cultured with DRG neurons were performed and led us to identify a set of 32 genes regulated in SCs in the early stage of neuron-SC contact. Expression of several candidates were analyzed by QPCR during development and we demonstrate using a blocking antibody approach in an in vitro myelination assay that one candidate was not only upregulated in response to axonal contact but also controls peripheral myelination. Three biological replicates each in dye swap for 22k slides and two biological replicates each in dye swap for NeuroDev2
2011-01-15 | E-GEOD-17366 | biostudies-arrayexpress
Project description:A better means to accurately identify malignant thyroid nodules and to distinguish them from benign tumors is needed. We previously identified markers for detecting thyroid malignancy, with sensitivity estimated at or close to 100%. One lingering problem with these markers was that false positives occurred with Hürthle cell adenomas (HCA) which lowered test specificity.To locate accurate diagnostic markers, we profiled in depth the transcripts of a HCA and a Hürthle cell carcinoma (HCC). From 1146 differentially expressed genes, 18 transcripts specifically expressed in HCA were tested by quantitative PCR in a wide range of thyroid tumors (n = 76). Sensibility and specificity were calculated using receiver operating characteristic (ROC). Selected markers were further validated in an independent set of thyroid tumors (n = 82) by immunohistochemistry. To define the panel that would yield best diagnostic accuracy, these markers were tested in combination with our previous identified markers.Seventeen of the 18 genes showed statistical significance based on a mean relative level of expression (P < 0.05). KLK1 (sensitivity = 0.97) and PVALB (sensitivity = 0.94) were the best candidate markers. The combination of PVALB and C1orf24 increased specificity to >97% and maintained sensitivity for detection of carcinoma.We identified tumor markers that can be used in combination for a more accurate preoperative diagnosis of thyroid nodules and for postoperative diagnosis of thyroid carcinoma in tumor sections. This improved test would help physicians rapidly focus treatment on true malignancies and avoid unnecessary treatment of benign tumors, simultaneously improving medical care and reducing costs.
| S-EPMC3038489 | biostudies-literature
Project description:BackgroundRecently, fusion variants of the breast cancer anti-oestrogen-resistance 4 (BCAR4) gene were recurrently discovered in lung adenocarcinoma from the genome-wide studies. However, the functional characterisation of BCAR4 fusion has not been investigated.MethodsBased on the analysis of RNA-sequencing data, we identified a fusion transcript of CD63-BCAR4 in a Korean patient with lung adenocarcinoma who did not harbour any known activating mutations in EGFR and KRAS genes. To investigate the oncogenic effect of CD63-BCAR4, in vitro and in vivo animal experiments were performed.ResultsIn vitro experiments showed strongly enhanced cell migration and proliferation by the exogenous expression of CD63-BCAR4 protein in bronchial epithelial cells. Cell migration was notably reduced after knockdown of BCAR4 fusion by small-interfering RNA. The tumorigenic and metastatic capability of the CD63-BCAR4 fusion was confirmed by using the mouse xenograft model. Fusion-overexpressed cells result in metastasis to the liver and lung as well as the primary tumours after subcutaneous injection into mice. Cyclin D1, MMP1, Slug and mesenchymal markers were significantly increased after CD63-BCAR4 overexpression in the in vitro and in vivo experiments.ConclusionsTaken together, our results suggest a newly identified fusion gene, CD63-BCAR4 as a potential novel oncogene in lung adenocarcinoma.
| S-EPMC7782829 | biostudies-literature
Project description:Pancreatic cancer is one of the deadliest cancers owing to its late diagnosis and of the strong resistance to available treatments. Despite a better understanding of the disease in the last two decades, no significant improvement in patient care has been made. Senescent cells are characterized by a stable proliferation arrest and some resistance to cell death. Increasing evidence suggests that multiple lines of antitumor therapy can induce a senescent-like phenotype in cancer cells, which may participate in treatment resistance. In this study, we describe that gemcitabine, a clinically-used drug against pancreatic cancer, induces a senescent-like phenotype in highly chemoresistant pancreatic cancer cells in vitro and in xenografted tumors in vivo. The use of ABT-263, a well-described senolytic compound targeting Bcl2 anti-apoptotic proteins, killed pancreatic gemcitabine-treated senescent-like cancer cells in vitro. In vivo, the combination of gemcitabine and ABT-263 decreased tumor growth, whereas their individual administration had no effect. Together these data highlight the possibility of improving the efficacy of conventional chemotherapies against pancreatic cancer by eliminating senescent-like cancer cells through senolytic intervention. Further studies testing different senolytics or their combination with available treatments will be necessary to optimize preclinical data in mouse models before transferring these findings to clinical trials.
| S-EPMC9899302 | biostudies-literature