E2F1‐Ror2 signaling mediates coordinated transcriptional regulation to promote G1/S phase transition in bFGF‐stimulated NIH/3T3 fibroblasts

Endo, Mitsuharu; Tanaka, Yuki; Minami, Yasuhiro

doi:10.1096/fj.201902849r

Cited by 19 publications

(23 citation statements)

References 49 publications

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“…P21 CIP1 , encoded by CDKN1A, is one of the key factors in cell cycle regulation. Several studies have pointed out that P21 CIP1 is involved in the G1-S phase cell cycle transition [30][31][32]. In our study, P21 CIP1 was predicted as a target of miR-370-3p by TargetScan.…”

Section: Discussionsupporting

confidence: 52%

circITGA7 Acts As miR-370-3p Sponge to Suppress The Proliferation of Prostate Cancer

Guo¹,

Li²,

Wan³

et al. 2021

Preprint

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Objective: Prostate cancer (PCa) refers to one of the most common tumors in male’s genitourinary system. Emerging research has confirmed that circRNAs play an important role in the occurrence and development of tumors. However, the correlation between circular RNA circITGA7 and PCa still remains unclear. Here, the role of circITGA7 in PCa was explored and the underlying mechanism was investigated as well.Methods: The circRNA expression profiles in PCa and the paracancerous tissues were established by high-throughput sequencing. The expression levels of circITGA7 in PCa tissues and cells were detected by qRT-PCR. Cell Counting Kit-8, colony formation, EdU and flow cytometry assays were used to detect the effects of circITGA7 on PCa cell proliferation. To further explore the underlying mechanisms, bioinformatics analysis on downstream target genes was carried out. RNA immunoprecipitation and dual-luciferase reporter assays were used to verify the direct relationship between miR-370-3p and circITGA7 or P21CIP1.Results: circITGA7 was downregulated in PCa tissues and cells. Gain- or loss-of-function assays showed that circITGA7 inhibited the proliferation of PCa cells in vivo and in vitro. Mechanically, circITGA7 served as a sponge for miR-370-3p and miR-370-3p could target P21CIP1 in PCa cells. The inhibition of cell proliferation induced by circITGA7 could be reversed by transfecting miR-370-3p mimic. Conclusion: Our data indicated that circITGA7 played an important role in inhibiting tumor proliferation in PCa and might be a potential therapeutic target.

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Section: Discussionsupporting

confidence: 52%

circITGA7 Acts As miR-370-3p Sponge to Suppress The Proliferation of Prostate Cancer

Guo¹,

Li²,

Wan³

et al. 2021

Preprint

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“…Results of the RT‐qPCR also confirmed that DPSCs at passage twelve had much higher expression of senescence marker genes, such as p21 and p53 (Figure 1c ). A recent study had reported that the knockdown of ROR2 lead to the upregulation of cell senescence marker genes, such as p21 and the cell cycle resistance cyclin‐dependent kinase inhibitor 1B (p27) (Endo et al, 2020 ). We determined whether ROR2 and its ligand Wnt5a were involved in the senescence of DPSCs by performing cell passaging.…”

Section: Resultsmentioning

confidence: 99%

“…ROR2 is expressed in neural stem/progenitor cells (NPC) and participates in the regulation of its proliferation (Zhang et al, 2019 ). The suppressed ROR2 expression in bFGF‐stimulated NIH/3T3 cells results in an increased expression of senescence‐associated genes, such as p21 Cip1 (Endo et al, 2020 ). However, the role of ROR2 in the aging process in DPSCs is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Downregulation of ROR2 promotes dental pulp stem cell senescence by inhibiting STK4‐FOXO1/SMS1 axis in sphingomyelin biosynthesis

et al. 2021

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Dental pulp stem cells (DPSCs) play a vital role in tooth restoration, regeneration, and homeostasis. The link between DPSC senescence and tooth aging has been well‐recognized. ROR2 plays an important role in aging‐related gene expression. However, the expression and function of ROR2 in DPSC aging remain largely unknown. In this study, we found that ROR2 expression was significantly decreased in aged pulp tissues and DPSCs. The depletion of ROR2 in young DPSCs inhibits their self‐renewal capacity, while its overexpression in aged DPSCs restores their self‐renewal capacity. Interestingly, we found that sphingomyelin (SM) is involved in the senescence of DPSCs regulated by ROR2. Mechanistically, we confirmed that ROR2 inhibited the phosphorylation of STK4, which promoted the translocation of Forkhead Box O1 (FOXO1) to the nucleus. STK4 inhibition or knockdown of FOXO1 markedly increased the proliferation of DPSCs and upregulated the expression of SMS1, which catalyzed SM biogenesis. Moreover, FOXO1 directly bound to the SMS1 promoter, repressing its transcription. Our findings demonstrated the critical role of the ROR2/STK4‐FOXO1/SMS1 axis in the regulation of SM biogenesis and DPSC senescence, providing a novel target for antagonizing tooth aging.

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“…On the other hand, p27 Kip1 is a cell cycle regulator first identified as a cyclin-dependent kinase antagonist [ 22 ]. It has been reported that E2F1-Ror2 signaling promotes G1/S phase transition in bFGF-stimulated NIH/3T3 fibroblasts via p27 Kip1 [ 23 ]. Additionally, Yang et al reported that pentoxifylline inhibits the progression of fibrosis by modulating FOXO1/p27 Kip1 signaling [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-27a-3p suppresses cerebral ischemia-reperfusion injury by targeting FOXO1

Zhu

et al. 2021

Aging

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Cerebral ischemia-reperfusion (CI/R) injury is a serious complication when treating patients experiencing ischemic stroke. Although the microRNA miR-27a-3p reportedly participates in ischemia/reperfusion (I/R) injury, its actions in CI/R remain unclear. To mimic CI/R in vitro , HT22 cells were subjected to oxygen glucose deprivation/reoxygenation (OGD/R). The results indicate that OGD inhibited growth and induced apoptosis among HT22 cells. The apoptosis was accompanied by increases in activated caspases 3 and 9 and decreases in Bcl-2. Oxidative stress was also increased, as indicated by increases in ROS and malondialdehyde and decreases in glutathione and superoxide dismutase. In addition, OGD induced G1 arrest in HT22 cells with corresponding upregulation of FOXO1 and p27 Kip1, suggesting the cell cycle arrest was mediated by FOXO1/p27 Kip1 signaling. Notably, FOXO1 was found to be the direct target of miR-27a-3p in HT22 cells. MiR-27a-3p was downregulated in OGD/R-treated HT22 cells, and miR-27a-3p mimics partially or entirely reversed all of the in vitro effects of OGD. Moreover, miR-27a-3p agomir significantly alleviated the symptoms of CI/R in vivo in a rat model of CI/R. Thus, MiR-27a-3p appears to suppress CI/R injury by targeting FOXO1.

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E2F1‐Ror2 signaling mediates coordinated transcriptional regulation to promote G1/S phase transition in bFGF‐stimulated NIH/3T3 fibroblasts

Cited by 19 publications

References 49 publications

circITGA7 Acts As miR-370-3p Sponge to Suppress The Proliferation of Prostate Cancer

circITGA7 Acts As miR-370-3p Sponge to Suppress The Proliferation of Prostate Cancer

Downregulation of ROR2 promotes dental pulp stem cell senescence by inhibiting STK4‐FOXO1/SMS1 axis in sphingomyelin biosynthesis

MiR-27a-3p suppresses cerebral ischemia-reperfusion injury by targeting FOXO1

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