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928965 occurrences (No.3 in the rank) during 5 years in the PubMed. [cache]
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928965 occurrences (No.3 in the rank) during 5 years in the PubMed. [cache]
| 122) Furthermore, systems analysis of IACS-010759-induced changes in RTS osteoblasts revealed that chemical inhibition of mitochondrial respiratory complex I impaired cell proliferation, induced senescence, and decreased MAPK signaling and cell cycle associated genes, but increased H19 and ribosomal protein genes. |
| PMID:34965247 DOI:10.1371/journal.pgen.1009971 |
| 2021 PLoS genetics |
| * Patient-derived iPSCs link elevated mitochondrial respiratory complex I function to osteosarcoma in Rothmund-Thomson syndrome. |
| - Rothmund-Thomson syndrome (RTS) is an autosomal recessive genetic disorder characterized by poikiloderma, small stature, skeletal anomalies, sparse brows/lashes, cataracts, and predisposition to cancer. Type 2 RTS patients with biallelic RECQL4 pathogenic variants have multiple skeletal anomalies and a significantly increased incidence of osteosarcoma. Here, we generated RTS patient-derived induced pluripotent stem cells (iPSCs) to dissect the pathological signaling leading to RTS patient-associated osteosarcoma. RTS iPSC-derived osteoblasts showed defective osteogenic differentiation and gain of in vitro tumorigenic ability. Transcriptome analysis of RTS osteoblasts validated decreased bone morphogenesis while revealing aberrantly upregulated mitochondrial respiratory complex I gene expression. RTS osteoblast metabolic assays demonstrated elevated mitochondrial respiratory complex I function, increased oxidative phosphorylation (OXPHOS), and increased ATP production. Inhibition of mitochondrial respiratory complex I activity by IACS-010759 selectively suppressed cellular respiration and cell proliferation of RTS osteoblasts. Furthermore, systems analysis of IACS-010759-induced changes in RTS osteoblasts revealed that chemical inhibition of mitochondrial respiratory complex I impaired cell proliferation, induced senescence, and decreased MAPK signaling and cell cycle associated genes, but increased H19 and ribosomal protein genes. In summary, our study suggests that mitochondrial respiratory complex I is a potential therapeutic target for RTS-associated osteosarcoma and provides future insights for clinical treatment strategies. |
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(1)23  death |
(18)5 differentiation |
(35)3 envelope |
(52)2 immunity |
| (2)15 lines |
(19)5 infiltration |
(36)3 function |
(53)2 informative |
| (3)15 types |
(20)5 membrane |
(37)3 growth |
(54)2 interactions |
| (4)14 proliferation |
(21)4 *null* | (38)3 lysis |
(55)2 is |
| (5)14 wall |
(22)4 activation |
(39)3 migration |
(56)2 killing |
| (6)8 carcinoma |
(23)4 apoptosis |
(40)3 mitochondrial |
(57)2 malignancies |
| (7)8 transplantation |
(24)4 culture |
(41)3 shape |
(58)2 manner |
| (8)7 line |
(25)4 cultures |
(42)3 therapy |
(59)2 marker |
| (9)7 lung |
(26)4 invasion |
(43)2 DNA |
(60)2 mass |
| (10)7 populations |
(27)4 metabolism |
(44)2 adhesion, |
(61)2 migration, |
| (11)7 proliferation, |
(28)4 receptor |
(45)2 behavior |
(62)2 mixture |
| (12)7 viability |
(29)4 responses |
(46)2 biology |
(63)2 morphology |
| (13)6 surface |
(30)4 type |
(47)2 cholesterol |
(64)2 nuclear |
| (14)6 survival |
(31)3 RNA |
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(32)3 adhesion |
(49)2 development |
(66)2 over-activation, |
| (16)5 and |
(33)3 cycle |
(50)2 fate |
(67)2 permeability |
| (17)5 cycle, |
(34)3 division |
(51)2 genes |
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