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Systemic transcriptome alternation under mtDNA depletion in 143B TK- osteosarcoma cells

ABSTRACT: The mitochondrial protein repertoire varies depending on cellular states, tissue type, species, and disease state. However, little is known about how this repertoire changes under different cellular or disease states. To gain a better understanding of dynamic mitochondrial proteomic changes, we compared alterations of mitochondrial proteome with transcriptome under mitochondrial DNA depletion.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22970 | GEO | 2010/07/17

SECONDARY ACCESSION(S): PRJNA127745

REPOSITORIES: GEO

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Systemic transcriptome alternation under mtDNA depletion in 143B TK- osteosarcoma cells

Project description:The mitochondrial protein repertoire varies depending on cellular states, tissue type, species, and disease state. However, little is known about how this repertoire changes under different cellular or disease states. To gain a better understanding of dynamic mitochondrial proteomic changes, we compared alterations of mitochondrial proteome with transcriptome under mitochondrial DNA depletion. Total RNA obtained from 143B TK- osteosarcoma ?+ cells or 143B TK- osteosarcoma ?° cells

2010-07-17 | E-GEOD-22970 | biostudies-arrayexpress

ChIP-seq analysis of 143B cells upon mtDNA depletion and metabolic intervention [ChIP-Seq 2]

Project description:The goal of the study was to understand whether mitochondrial-driven epigenetic changes regulate gene expression. Mitochondrial metabolism has been implicated in epigenetics but the extent to which this impacts gene expression is unclear. Here we show that loss of mitochondrial DNA (mtDNA) results in locus-specific alterations in histone acetylation, DNA methylation and expression of a subset of genes. Most of these changes are rescued by restoring mitochondrial electron transport in a way that maintains the oxidative tricarboxylic acid cycle, but not reactive oxygen species or ATP production, or by modulating the mitochondrial pool of acetyl-CoA. Changes in acetyl-CoA and histone acetylation precede overt mitochondrial dysfunction and significant changes in gene expression and DNA methylation. This suggests that acetyl-CoA levels signal mitochondrial status to the nucleus. Differentially expressed genes with altered histone marks or DNA methylation regulate amino acid degradation, which likely compensates for the changes in acetyl-CoA and one carbon metabolism. These have the potential to further affect methylation reactions, redox control and nucleotide levels. These results illustrate the extent to which mitochondria impact cell physiology through epigenetic remodeling.

2019-02-07 | GSE126138 | GEO

Expression profiling of 143B-shCtrl and 143B-shIRX1 stable osteosarcoma cell lines

Project description:Pulmonary metastasis is the main cause of medical failure and death of osteosarcoma patients. Our recent study identified IRX1 as a potential metastasis-driving gene in osteosarcoma. Studies showed that IRX1 can promote the migration, invasion and anoikis resistance of osteosarcoma cells. We generated 143B stable IRX1 knockdown and control cell lines, and found that IRX1 knockdown can inhibit the pulmonary metastasis of 143B cells in orthotopic mouse osteosarcoma model.

2015-08-25 | GSE55958 | GEO

Expression profiling of 143B-shCtrl and 143B-shIRX1 stable osteosarcoma cell lines

2015-08-25 | E-GEOD-55958 | biostudies-arrayexpress

RCCD1 also Resides in Mitochondria to Regulate mtDNA Dynamics and Mitochondrial Homeostasis

Project description:Regulator of chromosome condensation domain-containing protein 1 (RCCD1) plays an important role in chromosome segregation and microtubule stability in the nucleus and has been identified recently as a potential driver for breast cancer. We report here that, unexpectedly, RCCD1 is also localized in mitochondria. We show that RCCD1 resides in the mitochondrial inner membrane, where it interacts with the mitochondrial contact site/cristae organizing system (MICOS) and mitochondrial DNA (mtDNA) to regulate mitochondrial nucleoid organization, thereby influencing mtDNA transcription, oxidative phosphorylation, and the production of reactive oxygen species. Interestingly, RCCD1 is upregulated under hypoxic conditions, leading to decreased generation of reactive oxygen species and alleviated apoptosis favoring cancer cell survival. We show that RCCD1 promotes breast cancer cell proliferation in vitro and accelerates breast tumor growth in vivo. Indeed, RCCD1 is overexpressed in breast carcinomas, and its level of expression is associated with aggressive breast cancer phenotypes and poor patient survival. Our study reveals an additional dimension in RCCD1 functionality, indicating RCCD1 is an essential regulator of mtDNA dynamics and mitochondrial homeostasis, whose dysregulation inflicts pathologic states such as breast cancer.

2023-12-01 | GSE219134 | GEO

Diallyl trisulfide inhibits osteosarcoma 143B cell migration, invasion and EMT by inducing autophagy

Project description: Not available

| S-EPMC10907726 | biostudies-literature

Expression data of osteosarcoma 143B and metastatic variants

Project description:To determine the key factor to select specifc organ to be metastasized, 143B+mCherryIRES-luciferase2 cells were injected into heart, and the metastasized cells were obtained from the kidney or lymph node. We repeated the intracardiac injections, the selection using puromycin, and finally the cells metastasized into kidney within 3 weeks.

2022-01-27 | GSE188984 | GEO

[Aurora kinase-B silencing promotes apoptosis of osteosarcoma 143B cells by ULK1 phosphorylation-induced autophagy].

Project description:OBJECTIVE:To investigate the effect of Aurora kinase B (AURKB) silencing-induced autophagy on apoptosis of osteosarcoma 143B cells and the underlying molecular mechanisms. METHODS:Human osteosarcoma 143B cells were transfected with Lv/shAURKB or the negative control vector Lv/shScrambled followed by treatment with chloroquine (CQ) for 24 h. Western blotting was performed to detect the protein expression levels of AURKB, P62, LC3, cleaved caspase-3, Bcl-2, and P-ULK1Ser555. Transmission electron microscopy and LC3 dual-label fluorescence method were used to trace the autophagosomes in 143B cells to assess cell autophagy, and the cell apoptosis was detected using flow cytometry and TUNEL assay. Co-immunoprecipitation assay was used to detect the interaction between AURKB and ULK1. RESULTS:The ratio of autophagy-related proteins LC3 II/I and the number of autophagosomes were significantly increased in 143B cells after transfection with Lv/shAURKB (P < 0.05), which significantly increased the expression of cleaved caspase-3 and reduced the expression of Bcl-2 (P < 0.05). Combined treatment of the cells with Lv/shAURKB and the autophagy inhibitor chloroquine obviously restored the expressions of caspase-3 and Bcl-2 (P < 0.05). Transfection with Lv/shAURKB significantly increased the apoptosis rate of 143B cells (P < 0.05), and this effect was significantly antagonized by combined treatment with chloroquine (P < 0.05). AURKB silencing strongly activated the phosphorylation of the autophagy-initiating protein ULK1Ser555 in 143B cells (P < 0.05). The results of co-immunoprecipitation assay confirmed when AURKB was immunoprecipitated, ULK1 also precipitated. CONCLUSIONS:Silencing AURKB can induce autophagy by activating ULK1Ser555 phosphorylation to promote apoptosis in 143B cells.

| S-EPMC7544570 | biostudies-literature

Gene delivery in a mouse xenograft of a retargeted retrovirus to a solid 143B osteosarcoma.

Project description:BackgroundOsteosarcomas are the most common primary bone malignancies found in children and adolescents. An optimized system was developed for efficient retroviral gene delivery into solid 143B osteosarcoma tumors in mice using a retargeted Env. In these studies, the viral Env CP was isolated from an in vitro screen of a library of feline leukemia virus Env randomized in the receptor-binding domain and maintained high titer on human 143B osteosarcoma cell line.FindingsThe vector developed to express the random Env libraries encoded the drug selectable marker neo. To adapt this for studies in live animals, the murine based vector was modified to express the luciferase gene. The bicistronic vector developed expressed both the CP Env and luciferase in the presence of either the MPMV CTE or a WPRE element. Virus bearing the CP FeLV Env variant maintained high titers after concentration allowing for direct visualization of delivery of the luciferase gene in subcutaneous 143B osteosarcoma tumors.ConclusionThis system serves as a proof-of-concept for the use of novel FeLV Env pseudotyped MLV particles for in vivo gene delivery. Gene delivery and expression of lucerifase from viral particles bearing the CP Env was readily detected in live mice after a single round of intratumor injection.

| S-EPMC3689073 | biostudies-literature

mtDNA-acquisition

Project description:Mitochondrial Genome Acquisition Restores Respiratory Function and Tumorigenic Potential of Cancer Cells without Mitochondrial DNA

| PRJEB8982 | ENA

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