LncRNA XIST facilitates S1P-mediated osteoclast differentiation via interacting with FUS

Zhang, Dawei; Wang, Honggang; Zhang, Kuibo; Guo, Yuanqing; Yang, Lianjun; Lv, Hai

doi:10.1007/s00774-021-01294-3

Cited by 12 publications

(6 citation statements)

References 30 publications

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“…Although it has been reported that FUS can regulate the mRNA stability of downstream target genes, the downstream molecules are not well understood [ 32 – 34 ]. StarBase was used to predict possible binding targets.…”

Section: Resultsmentioning

confidence: 99%

CircZNF367 promotes osteoclast differentiation and osteoporosis by interacting with FUS to maintain CRY2 mRNA stability

Deng

Wang

Luo³

et al. 2023

J Orthop Surg Res

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Background Osteoporosis, characterized by reduced bone mass and deterioration of bone quality, is a significant health concern for postmenopausal women. Considering that the specific role of circRNAs in osteoporosis and osteoclast differentiation remains poorly understood, this study aims to shed light on their involvement in these processes to enhance our understanding and potentially contribute to improved treatment strategies for osteoporosis. Methods An osteoporotic model was constructed in vivo in ovariectomized mouse. In vitro, we induced osteoclast formation in bone marrow-derived macrophages (BMDMs) using M-CSF + RANKL. To assess osteoporosis in mice, we conducted HE staining. We used MTT and TRAP staining to measure cell viability and osteoclast formation, respectively, and also evaluated their mRNA and protein expression levels. In addition, RNA pull-down, RIP and luciferase reporter assays were performed to investigate interactions, and ChIP assay was used to examine the impact of circZNF367 knockdown on the binding between FUS and CRY2. Results We observed increased expression of CircZNF367, FUS and CRY2 in osteoporotic mice and M-CSF + RANKL-induced BMDMs. Functionally, knocking down circZNF367 inhibited osteoporosis in vivo. Furthermore, interference with circZNF367 suppressed osteoclast proliferation and the expression of TRAP, NFATc1, and c-FOS. Mechanistically, circZNF367 interacted with FUS to maintain CRY2 mRNA stability. Additionally, knocking down CRY2 rescued M-CSF + RANKL-induced osteoclast differentiation in BMDMs promoted by circZNF367 and FUS. Conclusion This study reveals that the circZNF367/FUS axis may accelerate osteoclasts differentiation by upregulating CRY2 in osteoporosis and suggests that targeting circZNF367 may have potential therapeutic effects on osteoporosis.

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Section: Resultsmentioning

confidence: 99%

CircZNF367 promotes osteoclast differentiation and osteoporosis by interacting with FUS to maintain CRY2 mRNA stability

Deng

Wang

Luo³

et al. 2023

J Orthop Surg Res

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“…Online bioinformatic tools was used to predict the interaction with LINC01133 [21], which was supported by results of high throughput sequencing [22]. FUS (Fused in Sarcoma) was chosen due to FUS was an RNA-binding protein that involved in the export of mRNA from the nucleus to the cytoplasm and plays a role in mRNA stability and turnover [40]. LncRNA XIST was reported to interact with FUS and increased the stability of SPHK1 to promote osteoclast differentiation through SPHK1/S1P/ERK signaling pathway [40].…”

Section: Discussionmentioning

confidence: 99%

“…FUS (Fused in Sarcoma) was chosen due to FUS was an RNA-binding protein that involved in the export of mRNA from the nucleus to the cytoplasm and plays a role in mRNA stability and turnover [40]. LncRNA XIST was reported to interact with FUS and increased the stability of SPHK1 to promote osteoclast differentiation through SPHK1/S1P/ERK signaling pathway [40]. LncRNA GAS6-AS1 regulated colorectal cancer (CRC) proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) via recruiting FUS to stable TRIM14 mRNA stability [41].…”

Section: Discussionmentioning

confidence: 99%

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

黄,

Wang,

Sun

et al. 2024

Preprint

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Intermittent hypoxia has been reported to contribute beneficial effects on fracture healing depending on various factors like duration, frequency, and severity. Yet, little is known about the underlying molecular mechanism. Our previous study found that LINC00323 was up-regulated under hypoxic conditions, suggesting that it might play a final role in hypoxia-induced fracture repair. The present study is to investigate the osteogenic effect of LINC00323 in vitro and in vivo. Upregulation of LINC00323 enhanced the mineralization and activity ALP and increased the expression of osteogenic markers. Further analysis revealed that LINC00323 promoted PDGFB expression by binding FUS to regulate the growth and osteogenic differentiation of MC3T3-E1. Lentivirus mediated LINC00323 particles were injected into the fracture site of the tibia of mice, and fracture healing was evaluated by X-rays, micro-CT examination, biomechanical test and histological staining. Local injection of Lentivirus-LINC00323 increased bone mass, biomechanical strength and cartilage callus formation. These findings indicated that LINC00323 induced the differentiation of osteoblast-like cells via regulation of the expression of PDGFB, represents a theoretical basis to accelerate fracture healing.

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“…lncRNAs are involved in modulating osteoclast differentiation. For instance, lncRNA-XIST promotes osteoclast differentiation by interacting with fused in sarcoma (FUS) [12] . lncRNA-SOX2OT regulates osteoclast differentiation by functioning as a ceRNA via the miR-194-5p/Rac family small GTPase 1 (RAC1) axis [13] .…”

Section: Discussionmentioning

confidence: 99%

lncRNA-Gm5532 regulates osteoclast differentiation through the miR-125a-3p/TRAF6 axis

Zhang,

Yao

et al. 2023

ABBS

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Long noncoding RNAs (lncRNAs) are important regulators of bone metabolism. In this study, lncRNA microarray analysis was used to identify differentially expressed lncRNAs in differentiated osteoclasts. lncRNA-Gm5532 is highly expressed during osteoclast differentiation. lncRNA-Gm5532 knockdown impairs osteoclast formation and bone resorption. Mechanistic experiments show that lncRNA-Gm5532 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-125a-3p, which promotes TNF receptor-associated factor 6 (TRAF6) expression. miR-125a-3p mimics suppress osteoclast differentiation and TAK1/NF-κB/MAPK signaling. The miR-125a-3p inhibitor reverses the negative effects of siGm5532 on osteoclast differentiation. In summary, our study reveals that lncRNA-Gm5532 functions as an activator in osteoclast differentiation by targeting the miR-125a-3p/TRAF6 axis, making it a novel biomarker and potential therapeutic target for osteoporosis.

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LncRNA XIST facilitates S1P-mediated osteoclast differentiation via interacting with FUS

Cited by 12 publications

References 30 publications

CircZNF367 promotes osteoclast differentiation and osteoporosis by interacting with FUS to maintain CRY2 mRNA stability

CircZNF367 promotes osteoclast differentiation and osteoporosis by interacting with FUS to maintain CRY2 mRNA stability

LINC00323 induced by hypoxia promote cartilage callus by interacting with FUS to regulate PDGFB expression

lncRNA-Gm5532 regulates osteoclast differentiation through the miR-125a-3p/TRAF6 axis

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