Circ-Smad5 retards the G1/S transition of cell cycle via inhibiting the activity of wnt/lef/cyclind1 signaling in JB6 cells

Ma, Xiaogen; Fei, Xiang; Pei, Zhuo; Miao, Jiafeng; Wu, Pan; Song, Xiaofeng; Li, Yuhong; Zhang, Yiming

doi:10.1016/j.gendis.2020.01.001

Cited by 7 publications

(6 citation statements)

References 30 publications

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“…Bax, Bcl‐2 and Caspase‐3 were essential proteins for apoptosis, while CyclinD1 is crucial for the cell cycle's G1 to S phase transition. 40 , 41 , 42 Our western blot assay revealed that apoptosis‐associated proteins and cyclin D1 were consistent with the flow cytometry results. Therefore, we concluded that MEF2A affects RCC progression by influencing G1/S transition of cell cycle and cell apoptosis.…”

Section: Discussionsupporting

confidence: 84%

“…Through flow cytometry, we found that overexpression of MEF2A increased the cell number in the G1 phase and the cell apoptosis rate. Bax, Bcl‐2 and Caspase‐3 were essential proteins for apoptosis, while CyclinD1 is crucial for the cell cycle's G1 to S phase transition 40–42 . Our western blot assay revealed that apoptosis‐associated proteins and cyclin D1 were consistent with the flow cytometry results.…”

Section: Discussionsupporting

confidence: 81%

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Brusatol enhances MEF2A expression to inhibit RCC progression through the Wnt signalling pathway in renal cell carcinoma

Wang,

Zhou,

Bao

et al. 2023

J Cellular Molecular Medi

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Renal cell carcinoma (RCC) is the most aggressive subtype of kidney tumour with a poor prognosis and an increasing incidence rate worldwide. Brusatol, an essential active ingredient derived from Brucea javanica, exhibits potent antitumour properties. Our study aims to explore a novel treatment strategy for RCC patients. We predicted 37 molecular targets of brusatol based on the structure of brusatol, and MEF2A (Myocyte Enhancer Factor 2A) was selected as our object through bioinformatic analyses. We employed various experimental techniques, including RT‐PCR, western blot, CCK8, colony formation, immunofluorescence, wound healing, flow cytometry, Transwell assays and xenograft mouse models, to investigate the impact of MEF2A on RCC. MEF2A expression was found to be reduced in patients with RCC, indicating a close correlation with MEF2A deubiquitylation. Additionally, the protective effects of brusatol on MEF2A were observed. The overexpression of MEF2A inhibits RCC cell proliferation, invasion and migration. In xenograft mice, MEF2A overexpression in RCC cells led to reduced tumour size compared to the control group. The underlying mechanism involves the inhibition of RCC cell proliferation, invasion, migration and epithelial‐mesenchymal transition (EMT) through the modulation of Wnt/β‐catenin signalling. Altogether, we found that MEF2A overexpression inhibits RCC progression by Wnt/β‐catenin signalling, providing novel insight into diagnosis, treatment and prognosis for RCC patients.

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Section: Discussionsupporting

confidence: 84%

Section: Discussionsupporting

confidence: 81%

Brusatol enhances MEF2A expression to inhibit RCC progression through the Wnt signalling pathway in renal cell carcinoma

Wang,

Zhou,

Bao

et al. 2023

J Cellular Molecular Medi

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“…In the process of tissue development and differentiation, Tcf4 responds to the β-catenin signal and initiates the downstream Wnt signaling pathway, thus promoting cell proliferation and differentiation ( Cadigan, 2012 ). Disruption of Tcf4 or β-catenin can block the Wnt signaling pathway and lead to complete loss of cell proliferation ( Ma et al, 2020 ). Our previous studies have shown that Tcf4 was highly expressed in growing hair follicles and in DPCs cultured in vitro when its morphological features were still in the agglutinative growth mode ( Xiong et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Twist1 Contributes to the Maintenance of Some Biological Properties of Dermal Papilla Cells in vitro by Forming a Complex With Tcf4 and β-Catenin

Yang

et al. 2020

Front. Cell Dev. Biol.

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Objective: During hair follicle regeneration, hair follicle stem cells (HFSCs) are regulated by signals from dermal papilla cells (DPCs). Previously we found that Tcf4 could promote the proliferation of DPCs. In this study, we focused on whether and how the biological properties of Tcf4-induced DPCs were regulated by Twist1. Methods: Twist1 was overexpressed or knocked down in DPCs following different adenovirus or lentivirus infection. Phase-contrast microscopy was used to observe the agglutinative growth of DPCs. The CCK-8 assay was used to test the proliferation of DPCs. Western blot and qPCR experiments were used to determine the expression of HGF, IGF-1, VEGF, c-myc, survivin, and CyclinD1 in DPCs. ELISAs were used to test the growth factors secreted by DPCs. Conditional medium culture was used to detect the inductive ability of DPCs. Co-immunoprecipitation and immunofluorescence were used to test the binding of Twist1, Tcf4, and β-catenin in DPCs. Immunofluorescence was also used to test the expression of Twist1, Tcf4, and KRT15 in hair follicles. Results: Twist1 induced DPC agglutinative growth and proliferation. Twist1 upregulated the expression of downstream target genes downstream of Tcf4, c-myc, survivin, in Tcf4-induced DPCs, as well as the expression and secretion of growth factors HGF, IGF-1, VEGF, which had the ability to induce hair follicle growth. The conditional medium from Twist1-treated DPCs increased the expression of KRT40 and MSX2 in HaCaT cells. Twist1 and Tcf4 co-localized in DPCs both in vitro and in vivo. Anti-Twist1 precipitated Tcf4 and β-catenin. Conclusion: These results indicate that Tcf4 and Twist1 play a synergistic role in regulating the hair follicle induction ability of DPCs. Twist1 functions by forming a ternary complex with Tcf4 and β-catenin. Thus, we report new data that elucidate whether and how Twist1 regulates some biological properties of DPCs.

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“…The translocation of β-catenin from the cytoplasm to the nucleus is a sign of the activation of the canonical Wnt signalling pathway [ 18 , 19 ]. β-Catenin binds with Tcf/Lef and activates the transcription of downstream molecules such as cyclinD1 [ 20 ]. The noncanonical Wnt signalling pathway consists of several pathways, including the Wnt/Ca 2+ , Wnt/PCP and Wnt/Ror2 signalling pathways [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Wnt4 increases the thickness of the epidermis in burn wounds by activating canonical Wnt signalling and decreasing the cell junctions between epidermal cells

et al. 2023

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Background Burn wound healing is a complex process and the role of Wnt ligands varies in this process. Whether and how Wnt4 functions in burn wound healing is not well understood. In this study, we aim to reveal the effects and potential mechanisms of Wnt4 in burn wound healing. Methods First, the expression of Wnt4 during burn wound healing was determined by immunofluorescence, Western blotting and qPCR. Then, Wnt4 was overexpressed in burn wounds. The healing rate and healing quality were analysed by gross photography and haematoxyline and eosin staining. Collagen secretion was observed by Masson staining. Vessel formation and fibroblast distribution were observed by immunostaining. Next, Wnt4 was knocked down in HaCaT cells. The migration of HaCaT cells was analysed by scratch healing and transwell assays. Next, the expression of β-catenin was detected by Western blotting and immunofluorescence. The binding of Frizzled2 and Wnt4 was detected by coimmunoprecipitation and immunofluorescence. Finally, the molecular changes induced by Wnt4 were analysed by RNA sequencing, immunofluorescence, Western blotting and qPCR in HaCaT cells and burn wound healing tissues. Results The expression of Wnt4 was enhanced in burn wound skin. Overexpression of Wnt4 in burn wound skin increased the thickness of epidermis. Collagen secretion, vessel formation and fibroblast distribution were not significantly impacted by Wnt4 overexpression. When Wnt4 was knocked down in HaCaT cells, the ratio of proliferating cells decreased, the ratio of apoptotic cells increased and the ratio of the healing area in the scratch healing assay to the number of migrated cells in the transwell assay decreased. The nuclear translocation of β-catenin decreased in shRNA of Wnt4 mediated by lentivirus-treated HaCaT cells and increased in Wnt4-overexpressing epidermal cells. RNA-sequencing analysis revealed that cell junction-related signalling pathways were significantly impacted by Wnt4 knockdown. The expression of the cell junction proteins was decreased by the overexpression of Wnt4. Conclusions Wnt4 promoted the migration of epidermal cells. Overexpression of Wnt4 increased the thickness of the burn wound. A potential mechanism for this effect is that Wnt4 binds with Frizzled2 and increases the nuclear translocation of β-catenin, thus activating the canonical Wnt signalling pathway and decreasing the cell junction between epidermal cells.

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Circ-Smad5 retards the G1/S transition of cell cycle via inhibiting the activity of wnt/lef/cyclind1 signaling in JB6 cells

Cited by 7 publications

References 30 publications

Brusatol enhances MEF2A expression to inhibit RCC progression through the Wnt signalling pathway in renal cell carcinoma

Brusatol enhances MEF2A expression to inhibit RCC progression through the Wnt signalling pathway in renal cell carcinoma

Twist1 Contributes to the Maintenance of Some Biological Properties of Dermal Papilla Cells in vitro by Forming a Complex With Tcf4 and β-Catenin

Wnt4 increases the thickness of the epidermis in burn wounds by activating canonical Wnt signalling and decreasing the cell junctions between epidermal cells

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