Regulation of osteoblast behaviors via cross-talk between Hippo/YAP and MAPK signaling pathway under fluoride exposure

Zhu, Wenqing; Yu, Yongqi; Xu, Lina; Ming, Pan-pan; Shao, Shui-yi; Qiu, Jing

doi:10.1007/s00109-019-01785-x

Cited by 17 publications

(15 citation statements)

References 43 publications

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“…In T cell acute lymphoblastic leukemia (T-ALL), short insertion mutations in noncoding intergenic region of TAL1-specific SE produce a de novo myeloblastosis oncogene (MYB) TF binding motif, followed by the recruitment of MYB and H3K27ac-binding CBP, which is important for SE initiation, seRNA transcription, and TAL1 oncogene expression [16]. Notably, focal amplification of enhancer elements frequently occurs in various cancers, which actually accelerates noncoding genes transcription [59]. The two different focal amplifications of SE 3′ to MYC in lung adenocarcinoma and endometrial carcinoma activate and boosts MYC promoter, which depends on lineage-specific chromatin loops and seRNA generation [7].…”

Section: Oncogenic Serna Formationmentioning

confidence: 99%

“…Interestingly, activation of mitogen-activated protein kinase (MAPK) signaling inhibits YAP phosphorylation and promotes YAP nuclear translocation via upregulating c-Jun N-terminal kinase (JNK) and extracellular signal regulated kinase (ERK). Hence, the crosstalk between Hippo-YAP and MAPK signaling pathway cooperatively takes part in the regulation of apoptosis behavior in cancer progress [59]. Upon apoptosis stimuli, Bak and Bax form complex, and the accumulation of Bak protein on mitochondrial outer membrane further boosts apoptosis by stimulating the release of proapoptotic proteins from mitochondria into cytosol [105].…”

Section: Serna Promotes Oncogene Expressionmentioning

confidence: 99%

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Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

Tan

Tang

2020

Mol Cancer

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seRNA is a noncoding RNA (ncRNA) transcribed from active super-enhancer (SE), through which SE exerts biological functions and participates in various physiological and pathological processes. seRNA recruits cofactor, RNA polymerase II and mediator to constitute and stabilize chromatin loop SE and promoter region, which regulates target genes transcription. In tumorigenesis, DNA insertion, deletion, translocation, focal amplification and carcinogen factor mediate oncogenic SE generation, meanwhile, oncogenic SE transcribes into tumor-related seRNA, termed as oncogenic seRNA. Oncogenic seRNA participates in tumorigenesis through activating various signal-pathways. The recent reports showed that oncogenic seRNA implicates in a widespread range of cytopathological processes in cancer progression including cell proliferation, apoptosis, autophagy, epithelial-mesenchymal transition, extracellular matrix stiffness and angiogenesis. In this article, we comprehensively summarized seRNA's characteristics and functions, and emphatically introduced inducible formation of oncogenic seRNA and its functional mechanisms. Lastly, some research strategies on oncogenic seRNA were introduced, and the perspectives on cancer therapy that targets oncogenic seRNA were also discussed.

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Section: Oncogenic Serna Formationmentioning

confidence: 99%

Section: Serna Promotes Oncogene Expressionmentioning

confidence: 99%

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

Tan

Tang

2020

Mol Cancer

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“…The phosphorylation process was transient within 60 min and would return to normal rapidly. Once activated, the MAPK signaling pathway would respond and induce further reaction, which was like a cascade, and affected the regulation of osteogenic markers in the end [40,41]. These results indicated that MAPK/ERK signaling pathway might participate in the osteoblast behavior under zinc ions exposure, but the speci c mechanism still needs further study.…”

Section: Discussionmentioning

confidence: 91%

Effects of Zinc Ions Released from Ti-NW-Zn Surface on Osteogenesis and Angiogenesis in Vitro and in an in Vivo Zebrafish Model

Zhu

et al. 2021

Preprint

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Objective: Zinc-modified titanium materials have been widely applied in oral implants, among them, our previous studies have also successfully prepared a novel acid-etched micro-structured titanium surface modified with zinc-containing nanowires (Ti-NW-Zn). However, there are very few reports concerned about the biological safeties of zinc ions released from material surface and the appropriate concentration range of released zinc ions which was more conducive to angiogenesis and bone regeneration. Danio rerio (Zebrafish) represents a powerful alternative in vivo model to study both angiogenesis and osteogenesis. Then, the aim of this study is to investigate the effects of zinc ions released from Ti-NW-Zn surfaces on angiogenesis and osteogenesis via zebrafish model, and further revealed the relationship between angiogenesis and osteogenesis via HUVECs and MC3T3-E1s in vitro models.Materials and methods: Tg (Fli‐1:EGFP)y1 zebrafish embryos were used to investigate the in vivo angiogenesis exposure to zinc ions, Wild-type Zebrafish (Danio rerio) adult fish and their embryos were used to investigate the in vivo bone regeneration and survival rate. Cell experiments including proliferation, adhesion, osteogenic differentiation and signaling pathway experiments were carried out by CCK-8, Laser scanning confocal microscope and Western blot, etc. Zinc ion release assay was detected by a Zinc assay kit.Results: The zinc ions released from Ti-NW-Zn surfaces were far lower than median lethal concentrations (LCs) of both embryos and adult fish, which was beneficial to osteogenesis and angiogenesis promotion of zebrafish model. Moreover, the appropriate concentration range of zinc ions was 1-2 ppm in vitro models, which could induce HUVECs proliferations, and the conditioned medium (CM) collected from the supernatant of 1-2 ppm zinc ions-induced HUVECs medium could obviously promote MC3T3-E1 osteoblasts behaviors via activated the MAPK/ERK signaling pathway.Conclusion: Zinc ions released from Ti-NW-Zn surfaces was at a biological safe and appropriate concentration, which could promote the angiogenesis and osteogenesis in vivo and vitro. The positive effects of the appropriate concentration of zinc ions on osteoblast behaviors might be regulated by activating the MAPK/ERK signaling pathway.

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“…The role of the MaPK signaling pathway on osteogenic function is garnering increasing research attention (53). a previous study has also demonstrated that JnK and erK, which are key components of the MaPK signaling pathway, could serve as regulators of osteoblast physiology following fluoride exposure (26).…”

Section: Discussionmentioning

confidence: 99%

“…Many signaling pathways and key signaling molecules have been reported to regulate osteogenic differentiation. Bone morphogenetic protein, Wnt, Hippo and MaPK signaling pathways have all been previously demonstrated to serve important roles in regulating osteoblast physiology (21)(22)(23)(24)(25)(26). among these, the MaPK signaling cascade pathway is particularly important for processes including cell proliferation, apoptosis and differentiation by activating nuclear transcription factors (27).…”

Section: Role Of Mapk/jnk Signaling Pathway On the Regulation Of Biolmentioning

confidence: 99%

Role of MAPK/JNK signaling pathway on the regulation of biological behaviors of MC3T3‑E1 osteoblasts under titanium ion exposure

et al. 2020

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The oral cavity is a complex environment that is constantly undergoing remodeling. This provides a favorable electrolytic aqueous condition, which causes the corrosion of titanium implants and the release of titanium (Ti) ions. The accumulation of Ti ions in the peri-implant tissues may affect the osteogenesis process. Therefore, the present study aimed to investigate the possible effects of Ti ions on osteoblast physiology and its underlying mechanism, specifically the MaPK/JnK signaling pathway. in the present study, Mc3T3-e1 osteoblasts were cultured the medium containing 10 ppm Ti ions. confocal laser scanning microscopy was used to analyze cell morphology and adhesion. alkaline phosphatase (alP) activity assay and western blotting were performed to evaluate the expression of proteins associated with osteogenesis such as runx2 and osterix. nuclear translocation of JnK, a key factor of the MaPK signaling pathway, was visualized and analyzed using immunofluorescence staining. The results showed that 10 ppm Ti ions exerted negative effects on the biological behaviors of Mc3T3-e1 cells, which exhibited reduced adhesion, alP activity and osteogenic differentiation. it was also found that 10 ppm Ti ions activated the MaPK/JnK signaling pathway by promoting the nuclear translocation of JnK via phosphorylation. in addition, the inhibitory effects of 10 ppm Ti ions on Mc3T3-e1 cells was found to be reversed by the JnK inhibitor SP600125. in conclusion, the preset study suggests that the MaPK/JnK signaling pathway serves a key role in the molecular mechanism underlying the changes in osteoblast behavior following Ti ion exposure. These findings may serve as a valuable reference point for the further in-depth exploration of peri-implant bone loss.

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Regulation of osteoblast behaviors via cross-talk between Hippo/YAP and MAPK signaling pathway under fluoride exposure

Cited by 17 publications

References 43 publications

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

Oncogenic seRNA functional activation: a novel mechanism of tumorigenesis

Effects of Zinc Ions Released from Ti-NW-Zn Surface on Osteogenesis and Angiogenesis in Vitro and in an in Vivo Zebrafish Model

Role of MAPK/JNK signaling pathway on the regulation of biological behaviors of MC3T3‑E1 osteoblasts under titanium ion exposure

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