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Items 913 to 924 of 13914 total
- ReferenceP. Kaminska et al. (Mar 2024) EMBO Reports 25 5
SorLA restricts TNFα release from microglia to shape a glioma-supportive brain microenvironment
SorLA, encoded by the gene SORL1 , is an intracellular sorting receptor of the VPS10P domain receptor gene family. Although SorLA is best recognized for its ability to shuttle target proteins between intracellular compartments in neurons, recent data suggest that also its microglial expression can be of high relevance for the pathogenesis of brain diseases, including glioblastoma (GBM). Here, we interrogated the impact of SorLA on the functional properties of glioma-associated microglia and macrophages (GAMs). In the GBM microenvironment, GAMs are re-programmed and lose the ability to elicit anti-tumor responses. Instead, they acquire a glioma-supporting phenotype, which is a key mechanism promoting glioma progression. Our re-analysis of published scRNA-seq data from GBM patients revealed that functional phenotypes of GAMs are linked to the level of SORL1 expression, which was further confirmed using in vitro models. Moreover, we demonstrate that SorLA restrains secretion of TNFα from microglia to restrict the inflammatory potential of these cells. Finally, we show that loss of SorLA exacerbates the pro-inflammatory response of microglia in the murine model of glioma and suppresses tumor growth.Catalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ 05310 STEMdiffâ„¢ Hematopoietic Kit Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 05310 Product Name: STEMdiffâ„¢ Hematopoietic Kit ReferenceS. Kaur et al. (Mar 2024) Frontiers in Cell and Developmental Biology 12 Suppl. ment_1Effects of a humanized CD47 antibody and recombinant SIRPα proteins on triple negative breast carcinoma stem cells
Signal regulatory protein-α (SIRPα, SHPS-1, CD172a) expressed on myeloid cells transmits inhibitory signals when it engages its counter-receptor CD47 on an adjacent cell. Elevated CD47 expression on some cancer cells thereby serves as an innate immune checkpoint that limits phagocytic clearance of tumor cells by macrophages and antigen presentation to T cells. Antibodies and recombinant SIRPα constructs that block the CD47-SIRPα interaction on macrophages exhibit anti-tumor activities in mouse models and are in ongoing clinical trials for treating several human cancers. Based on prior evidence that engaging SIRPα can also alter CD47 signaling in some nonmalignant cells, we compared direct effects of recombinant SIRPα-Fc and a humanized CD47 antibody that inhibits CD47-SIRPα interaction (CC-90002) on CD47 signaling in cancer stem cells derived from the MDA-MB- 231 triple-negative breast carcinoma cell line. Treatment with SIRPα-Fc significantly increased the formation of mammospheres by breast cancer stem cells as compared to CC-90002 treatment or controls. Furthermore, SIRPα-Fc treatment upregulated mRNA and protein expression of ALDH1 and altered the expression of genes involved in epithelial/mesenchymal transition pathways that are associated with a poor prognosis and enhanced metastatic activity. This indicates that SIRPα-Fc has CD47-mediated agonist activities in breast cancer stem cells affecting proliferation and metastasis pathways that differ from those of CC-90002. This SIRPα-induced CD47 signaling in breast carcinoma cells may limit the efficacy of SIRPα decoy therapeutics intended to stimulate innate antitumor immune responses.Catalog #: Product Name: 34411 ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 05620 MammoCultâ„¢ Human Medium Kit 05893 AggreWellâ„¢ EB Formation Medium 01700 ALDEFLUORâ„¢ Kit Catalog #: 34411 Product Name: ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 Catalog #: 05620 Product Name: MammoCultâ„¢ Human Medium Kit Catalog #: 05893 Product Name: AggreWellâ„¢ EB Formation Medium Catalog #: 01700 Product Name: ALDEFLUORâ„¢ Kit ReferenceM. Dobersberger et al. (Mar 2024) Cell Reports Methods 4 4An engineering strategy to target activated EGFR with CAR T cells
Chimeric antigen receptor (CAR) TÂ cells have shown remarkable response rates in hematological malignancies. In contrast, CAR TÂ cell treatment of solid tumors is associated with several challenges, in particular the expression of most tumor-associated antigens at lower levels in vital organs, resulting in on-target/off-tumor toxicities. Thus, innovative approaches to improve the tumor specificity of CAR TÂ cells are urgently needed. Based on the observation that many human solid tumors activate epidermal growth factor receptor (EGFR) on their surface through secretion of EGFR ligands, we developed an engineering strategy for CAR-binding domains specifically directed against the ligand-activated conformation of EGFR. We show, in several experimental systems, that the generated binding domains indeed enable CAR TÂ cells to distinguish between active and inactive EGFR. We anticipate that this engineering concept will be an important step forward to improve the tumor specificity of CAR TÂ cells directed against EGFR-positive solid cancers.Catalog #: Product Name: 15021 RosetteSepâ„¢ Human T Cell Enrichment Cocktail Catalog #: 15021 Product Name: RosetteSepâ„¢ Human T Cell Enrichment Cocktail ReferenceM. Ghashghaei et al. (Mar 2024) Nature Communications 15Translation efficiency driven by CNOT3 subunit of the CCR4-NOT complex promotes leukemogenesis
Protein synthesis is frequently deregulated during tumorigenesis. However, the precise contexts of selective translational control and the regulators of such mechanisms in cancer is poorly understood. Here, we uncovered CNOT3, a subunit of the CCR4-NOT complex, as an essential modulator of translation in myeloid leukemia. Elevated CNOT3 expression correlates with unfavorable outcomes in patients with acute myeloid leukemia (AML). CNOT3 depletion induces differentiation and apoptosis and delayed leukemogenesis. Transcriptomic and proteomic profiling uncovers c-MYC as a critical downstream target which is translationally regulated by CNOT3. Global analysis of mRNA features demonstrates that CNOT3 selectively influences expression of target genes in a codon usage dependent manner. Furthermore, CNOT3 associates with the protein network largely consisting of ribosomal proteins and translation elongation factors in leukemia cells. Overall, our work elicits the direct requirement for translation efficiency in tumorigenesis and propose targeting the post-transcriptional circuitry via CNOT3 as a therapeutic vulnerability in AML. Subject terms: Acute myeloid leukaemia, Translation, RNA decayCatalog #: Product Name: 04100 MethoCult™ H4100 Catalog #: 04100 Product Name: MethoCult™ H4100 ReferenceM. S. Haney et al. (Mar 2024) Nature 628 8006APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia
Several genetic risk factors for Alzheimer’s disease implicate genes involved in lipid metabolism and many of these lipid genes are highly expressed in glial cells 1 . However, the relationship between lipid metabolism in glia and Alzheimer’s disease pathology remains poorly understood. Through single-nucleus RNA sequencing of brain tissue in Alzheimer’s disease, we have identified a microglial state defined by the expression of the lipid droplet-associated enzyme ACSL1 with ACSL1-positive microglia being most abundant in patients with Alzheimer’s disease having the APOE4/4 genotype. In human induced pluripotent stem cell-derived microglia, fibrillar Aβ induces ACSL1 expression, triglyceride synthesis and lipid droplet accumulation in an APOE-dependent manner. Additionally, conditioned media from lipid droplet-containing microglia lead to Tau phosphorylation and neurotoxicity in an APOE-dependent manner. Our findings suggest a link between genetic risk factors for Alzheimer’s disease with microglial lipid droplet accumulation and neurotoxic microglia-derived factors, potentially providing therapeutic strategies for Alzheimer’s disease. Subject terms: Alzheimer's disease, Microglia, NeuroimmunologyCatalog #: Product Name: 05832 STEMdiff™ Neural Rosette Selection Reagent 05833 STEMdiff™ Neural Progenitor Medium 05310 STEMdiff™ Hematopoietic Kit Catalog #: 05832 Product Name: STEMdiff™ Neural Rosette Selection Reagent Catalog #: 05833 Product Name: STEMdiff™ Neural Progenitor Medium Catalog #: 05310 Product Name: STEMdiff™ Hematopoietic Kit ReferenceM. Du et al. (Mar 2024) Journal of Experimental & Clinical Cancer Research : CR 43C/EBPα-p30 confers AML cell susceptibility to the terminal unfolded protein response and resistance to Venetoclax by activating DDIT3 transcription
Acute myeloid leukemia (AML) with biallelic ( CEBPA bi ) as well as single mutations located in the bZIP region is associated with a favorable prognosis, but the underlying mechanisms are still unclear. Here, we propose that two isoforms of C/EBPα regulate DNA damage-inducible transcript 3 (DDIT3) transcription in AML cells corporately, leading to altered susceptibility to endoplasmic reticulum (ER) stress and related drugs. Human AML cell lines and murine myeloid precursor cell line 32Dcl3 cells were infected with recombinant lentiviruses to knock down CEBPA expression or over-express the two isoforms of C/EBPα. Quantitative real-time PCR and western immunoblotting were employed to determine gene expression levels. Cell apoptosis rates were assessed by flow cytometry. CFU assays were utilized to evaluate the differentiation potential of 32Dcl3 cells. Luciferase reporter analysis, ChIP-seq and ChIP-qPCR were used to validate the transcriptional regulatory ability and affinity of each C/EBPα isoform to specific sites at DDIT3 promoter. Finally, an AML xenograft model was generated to evaluate the in vivo therapeutic effect of agents. We found a negative correlation between CEBPA expression and DDIT3 levels in AML cells. After knockdown of CEBPA , DDIT3 expression was upregulated, resulting in increased apoptotic rate of AML cells induced by ER stress. Cebpa knockdown in mouse 32Dcl3 cells also led to impaired cell viability due to upregulation of Ddit3, thereby preventing leukemogenesis since their differentiation was blocked. Then we discovered that the two isoforms of C/EBPα regulate DDIT3 transcription in the opposite way. C/EBPα-p30 upregulated DDIT3 transcription when C/EBPα-p42 downregulated it instead. Both isoforms directly bound to the promoter region of DDIT3. However, C/EBPα-p30 has a unique binding site with stronger affinity than C/EBPα-p42. These findings indicated that balance of two isoforms of C/EBPα maintains protein homeostasis and surveil leukemia, and at least partially explained why AML cells with disrupted C/EBPα-p42 and/or overexpressed C/EBPα-p30 exhibit better response to chemotherapy stress. Additionally, we found that a low C/EBPα p42/p30 ratio induces resistance in AML cells to the BCL2 inhibitor venetoclax since BCL2 is a major target of DDIT3. This resistance can be overcome by combining ER stress inducers, such as tunicamycin and sorafenib in vitro and in vivo. Our results indicate that AML patients with a low C/EBPα p42/p30 ratio (e.g., CEBPA bi ) may not benefit from monotherapy with BCL2 inhibitors. However, this issue can be resolved by combining ER stress inducers. The online version contains supplementary material available at 10.1186/s13046-024-02975-3.Catalog #: Product Name: 03434 MethoCult™ GF M3434 Catalog #: 03434 Product Name: MethoCult™ GF M3434 ReferenceV. J. Forster et al. (Mar 2024) NPJ Precision Oncology 8Biallelic EPCAM deletions induce tissue-specific DNA repair deficiency and cancer predisposition
We report a case of Mismatch Repair Deficiency (MMRD) caused by germline homozygous EPCAM deletion leading to tissue-specific loss of MSH2. Through the use of patient-derived cells and organoid technologies, we performed stepwise in vitro differentiation of colonic and brain organoids from reprogrammed EPCAM del iPSC derived from patient fibroblasts. Differentiation of iPSC to epithelial-colonic organoids exhibited continuous increased EPCAM expression and hypermethylation of the MSH2 promoter. This was associated with loss of MSH2 expression, increased mutational burden, MMRD signatures and MS-indel accumulation, the hallmarks of MMRD. In contrast, maturation into brain organoids and examination of blood and fibroblasts failed to show similar processes, preserving MMR proficiency. The combined use of iPSC, organoid technologies and functional genomics analyses highlights the potential of cutting-edge cellular and molecular analysis techniques to define processes controlling tumorigenesis and uncovers a new paradigm of tissue-specific MMRD, which affects the clinical management of these patients. Subject terms: Paediatric cancer, Cancer geneticsCatalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ 05140 STEMdiffâ„¢ Intestinal Organoid Kit 08570 STEMdiffâ„¢ Cerebral Organoid Kit Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 05140 Product Name: STEMdiffâ„¢ Intestinal Organoid Kit Catalog #: 08570 Product Name: STEMdiffâ„¢ Cerebral Organoid Kit ReferenceY. Nakazawa et al. (Mar 2024) Nature Communications 15Delivery of a BET protein degrader via a CEACAM6-targeted antibody–drug conjugate inhibits tumour growth in pancreatic cancer models
Pancreatic ductal adenocarcinoma (PDAC) has the worst prognosis of all cancers. To improve PDAC therapy, we establish screening systems based on organoid and co-culture technologies and find a payload of antibody–drug conjugate (ADC), a bromodomain and extra-terminal (BET) protein degrader named EBET. We select CEACAM6/CD66c as an ADC target and developed an antibody, #84.7, with minimal reactivity to CEACAM6-expressing normal cells. EBET-conjugated #84.7 (84-EBET) has lethal effects on various PDAC organoids and bystander efficacy on CEACAM6-negative PDAC cells and cancer-associated fibroblasts. In mouse studies, a single injection of 84-EBET induces marked tumor regression in various PDAC-patient-derived xenografts, with a decrease in the inflammatory phenotype of stromal cells and without significant body weight loss. Combination with standard chemotherapy or PD-1 antibody induces more profound and sustained regression without toxicity enhancement. Our preclinical evidence demonstrates potential efficacy by delivering BET protein degrader to PDAC and its microenvironment via CEACAM6-targeted ADC. Subject terms: Pancreatic cancer, Drug development, Targeted therapiesCatalog #: Product Name: 09600 StemSpanâ„¢ SFEM 09605 StemSpanâ„¢ SFEM II 05001 PneumaCultâ„¢-ALI Medium 10981 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium 100-0956 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Catalog #: 09600 Product Name: StemSpanâ„¢ SFEM Catalog #: 09605 Product Name: StemSpanâ„¢ SFEM II Catalog #: 05001 Product Name: PneumaCultâ„¢-ALI Medium Catalog #: 10981 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium Catalog #: 100-0956 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Safety Data SheetCatalog #: Product Name: 60074AD Rat IgM, kappa Isotype Control Antibody, Clone RTK2118, Alexa Fluor® 488 Catalog #: 60074AD Product Name: Rat IgM, kappa Isotype Control Antibody, Clone RTK2118, Alexa Fluor® 488 ReferenceT. Baba et al. (Mar 2024) Cancer Research Communications 4 3Autophagy Inhibition–induced Cytosolic DNA Sensing Combined with Differentiation Therapy Induces Irreversible Myeloid Differentiation in Leukemia Cells
Accumulating evidence indicates that various oncogenic mutations interfere with normal myeloid differentiation of leukemogenic cells during the early process of acute myeloid leukemia (AML) development. Differentiation therapy is a therapeutic strategy capable of terminating leukemic expansion by reactivating the differentiation potential; however, the plasticity and instability of leukemia cells counteract the establishment of treatments aimed at irreversibly inducing and maintaining their differentiation states. On the basis of our previous observation that autophagy inhibitor treatment induces the accumulation of cytosolic DNA and activation of cytosolic DNA-sensor signaling selectively in leukemia cells, we herein examined the synergistic effect of cytosolic DNA-sensor signaling activation with conventional differentiation therapy on AML. The combined treatment succeeded in inducing irreversible differentiation in AML cell lines. Mechanistically, cytosolic DNA was sensed by absent in melanoma 2 (AIM2), a cytosolic DNA sensor. Activation of the AIM2 inflammasome resulted in the accumulation of p21 through the inhibition of its proteasomal degradation, thereby facilitating the myeloid differentiation. Importantly, the combined therapy dramatically reduced the total leukemia cell counts and proportion of blast cells in the spleens of AML mice. Collectively, these findings indicate that the autophagy inhibition-cytosolic DNA-sensor signaling axis can potentiate AML differentiation therapy. Clinical effects on AML therapy are closely associated with reactivating the normal myeloid differentiation potential in leukemia cells. This study shows that autophagosome formation inhibitors activate the cytosolic DNA-sensor signaling, thereby augmenting conventional differentiation therapy to induce irreversible differentiation and cell growth arrest in several types of AML cell lines.Catalog #: Product Name: 03534 MethoCult™ GF M3534 Catalog #: 03534 Product Name: MethoCult™ GF M3534 ReferenceJ. Jahan et al. (Mar 2024) Biochemical pharmacology 222The role of telomerase reverse transcriptase in the mitochondrial protective functions of Angiotensin-(1–7) in diabetic CD34 + cells
Angiotensin (Ang)-(1–7) stimulates vasoprotective functions of diabetic (DB) CD34 + hematopoietic stem/progenitor cells partly by decreasing reactive oxygen species (ROS), increasing nitric oxide (NO) levels and decreasing TGFβ1 secretion. Telomerase reverse transcriptase (TERT) translocates to mitochondria and regulates ROS generation. Alternative splicing of TERT results in variants α-, β- and α-β-TERT, which may oppose functions of full-length (FL) TERT. This study tested if the protective functions of Ang-(1–7) or TGFβ1-silencing are mediated by mitoTERT and that diabetes decreases FL-TERT expression by inducing splicing. CD34 + cells were isolated from the peripheral blood mononuclear cells of nondiabetic (ND, n = 68) or DB (n = 74) subjects. NO and mitoROS levels were evaluated by flow cytometry. TERT splice variants and mitoDNA-lesions were characterized by qPCR. TRAP assay was used for telomerase activity. Decoy peptide was used to block mitochondrial translocation (mitoXTERT). TERT inhibitor or mitoXTERT prevented the effects of Ang-(1–7) on NO or mitoROS levels in DB-CD34 + cells. FL-TERT expression and telomerase activity were lower and mitoDNA-lesions were higher in DB cells compared to ND and were reversed by Ang-(1–7) or TGFβ1-silencing. The prevalence of TERT splice variants, with predominant β-TERT expression, was higher and the expression of FL-TERT was lower in DB cells (n = 25) compared to ND (n = 30). Ang-(1–7) or TGFβ1-silencing decreased TERT-splicing and increased FL-TERT. Blocking of β-splicing increased FL-TERT and protected mitoDNA in DB-cells. The findings suggest that diabetes induces TERT-splicing in CD34 + cells and that β-TERT splice variant largely contributes to the mitoDNA oxidative damage.Catalog #: Product Name: 09600 StemSpan™ SFEM Catalog #: 09600 Product Name: StemSpan™ SFEM ReferenceD. Shi et al. (Feb 2024) iScience 27 3Pseudouridine synthase 1 regulates erythropoiesis via transfer RNAs pseudouridylation and cytoplasmic translation
Pseudouridylation plays a regulatory role in various physiological and pathological processes. A prime example is the mitochondrial myopathy, lactic acidosis, and sideroblastic anemia syndrome (MLASA), characterized by defective pseudouridylation resulting from genetic mutations in pseudouridine synthase 1 (PUS1). However, the roles and mechanisms of pseudouridylation in normal erythropoiesis and MLASA-related anemia remain elusive. We established a mouse model carrying a point mutation (R110W) in the enzymatic domain of PUS1, mimicking the common mutation in human MLASA. Pus1 -mutant mice exhibited anemia at 4 weeks old. Impaired mitochondrial oxidative phosphorylation was also observed in mutant erythroblasts. Mechanistically, mutant erythroblasts showed defective pseudouridylation of targeted tRNAs, altered tRNA profiles, decreased translation efficiency of ribosomal protein genes, and reduced globin synthesis, culminating in ineffective erythropoiesis. Our study thus provided direct evidence that pseudouridylation participates in erythropoiesis in vivo. We demonstrated the critical role of pseudouridylation in regulating tRNA homeostasis, cytoplasmic translation, and erythropoiesis. Subject areas: Molecular biology, Cell biologyCatalog #: Product Name: 03334 MethoCult™ M3334 03436 MethoCult™ SF M3436 Catalog #: 03334 Product Name: MethoCult™ M3334 Catalog #: 03436 Product Name: MethoCult™ SF M3436 Items 913 to 924 of 13914 total
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