Cyclin D1 regulates osteoarthritis chondrocyte apoptosis
            <i>via</i>
            WNT3/β-catenin signalling

Chen, Yi-Yue; You, Chun‐Xiang; Wang, Wan-Chuan; Tang, Qi; Wu, Runliu; Zhu, Wan; Li, Ding; Liao, Lele

doi:10.1080/21691401.2019.1593853

Cited by 15 publications

(14 citation statements)

References 26 publications

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“…All of them are highly expressed in TCam-2 in our previous RNA-Seq screens (Smialek et al, 2019 preprint). Our analysis showed that KIF18A knockdown caused a significant downregulation of the mRNA level of BCL2, an antiapoptotic gene (Petros et al, 2001), and upregulation of antiapoptotic (Chen et al, 2019;Singh et al, 2019) CCND1 and PIK3CA. Upregulation of the pro-apoptotic shorter isoforms of BCL2L1 mRNA occurring upon KIF18A knockdown was in line with the pro-apoptotic effect of KIF18A knockdown, as with downregulation of anti-apoptotic BCL2 (Fig.…”

Section: Knockdown Of Kif18a Causes a Decrease In Proliferation Of Tcmentioning

confidence: 70%

Kinesin KIF18A is a novel PUM-regulated target promoting mitotic progression and survival of a human male germ cell line

Smialek

Kuczyńska

Ilaslan

et al. 2020

Journal of Cell Science

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Regulation of proliferation, apoptosis and cell cycle is crucial for the physiology of germ cells. Their malfunction contributes to infertility and germ cell tumours. The kinesin KIF18A is an important regulator of those processes in animal germ cells. Post-transcriptional regulation of KIF18A has not been extensively explored. Owing to the presence of PUM-binding elements (PBEs), KIF18A mRNA is a potential target of PUM proteins, where PUM refers to Pumilio proteins, RNAbinding proteins that act in post-transcriptional gene regulation. We conducted RNA co-immunoprecipitation combined with RT-qPCR, as well as luciferase reporter assays, by applying an appropriate luciferase construct encoding wild-type KIF18A 3′-UTR, upon PUM overexpression or knockdown in TCam-2 cells, representing human male germ cells. We found that KIF18A is repressed by PUM1 and PUM2. To study how this regulation influences KIF18A function, an MTS proliferation assay, and apoptosis and cell cycle analysis using flow cytometry, was performed upon KIF18A mRNA siRNA knockdown. KIF18A significantly influences proliferation, apoptosis and the cell cycle, with its effects being opposite to PUM effects. Repression by PUM proteins might represent one of mechanisms influencing KIF18A level in controlling proliferation, cell cycle and apoptosis in TCam-2 cells.

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Section: Knockdown Of Kif18a Causes a Decrease In Proliferation Of Tcmentioning

confidence: 70%

Kinesin KIF18A is a novel PUM-regulated target promoting mitotic progression and survival of a human male germ cell line

Smialek

Kuczyńska

Ilaslan

et al. 2020

Journal of Cell Science

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“…Thus, more experiments are needed to explore the effect of WNT3 overexpression on trophoblast proliferation. Some researchers have found similar phenomena in breast cancer cell lines, esophageal squamous cell carcinoma cell lines, and osteoarthritic chondrocyte cell lines, in which expression of nuclear β-catenin was decreased and the Wnt/β-catenin signaling pathway was suppressed after knockdown of WNT3 [ 37 – 39 ]. Thus, WNT3 may be an activator of the Wnt/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 83%

WNT3 hypomethylation counteracts low activity of the Wnt signaling pathway in the placenta of preeclampsia

Zhang

Sang

et al. 2021

Cell. Mol. Life Sci.

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Preeclampsia is a hypertensive disorder of pregnancy. Many studies have shown that epigenetic mechanisms may play a role in preeclampsia. Moreover, our previous study indicated that the differentially methylated genes in preeclampsia were enriched in the Wnt/β-catenin signaling pathway. This study aimed to identify differentially methylated Wnt/β-catenin signaling pathway genes in the preeclamptic placenta and to study the roles of these genes in trophoblast cells in vitro. Using an Illumina Infinium HumanMethylation 850 K BeadChip, we found that the Wnt signaling pathway was globally hypermethylated in the preeclamptic group compared with the term birth group, but hypomethylated in the preeclamptic group compared with the preterm birth group. Among all Wnt/β-catenin signaling pathway factors, WNT3 was the most significantly differentially expressed gene and was hypomethylated in the preeclamptic group compared to the nonhypertensive groups, namely, the preterm birth group and term birth group. This result was confirmed by pyrosequencing. Through quantitative real-time PCR and western blot analysis, the WNT3 gene was found to be highly expressed in preeclamptic placental tissues, in contrast to other WNT factors, which were previously reported to be expressed at low levels in placental tissues. Additionally, in the HTR8/SVneo cell line, knockdown of WNT3 suppressed the Wnt/β-catenin signaling pathway, consistent with the findings for other WNT factors. These results prompted us to speculate that the WNT3 gene counteracts the low activation state of the Wnt signaling pathway in the preeclamptic placenta through methylation modification.

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“…10b). Some researchers have found similar phenomena in breast cancer cell lines, esophageal squamous cell carcinoma cell lines and osteoarthritic chondrocyte cell lines, in which expression of nuclear β-catenin was decreased and the Wnt/β-catenin signaling pathway was suppressed after knockdown of WNT3 [37][38][39]. Thus, WNT3 may be an activator of the Wnt/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 79%

WNT3 Hypopethylation Counteracts low Activity of the Wnt Signaling Pathway in the Placenta of Preeclampsia

Zhang

Sang

et al. 2021

Preprint

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Preeclampsia is a hypertensive disorder of pregnancy. Many studies have shown that epigenetic mechanisms may play a role in preeclampsia. Moreover, our previous study indicated that the differentially methylated genes in preeclampsia were enriched in the Wnt/β-catenin signaling pathway. This study aimed to identify differentially methylated Wnt/β-catenin signaling pathway genes in the preeclamptic placenta and to study the roles of these genes in trophoblast cells in vitro. Using an Illumina Infinium HumanMethylation 850K BeadChip, we found that the Wnt signaling pathway was globally hypermethylated in the preeclamptic group compared with the term birth group but hypomethylated in the preeclamptic group compared with the preterm birth group. Among all Wnt/β-catenin signaling pathway factors, WNT3 was the most significantly differentially expressed gene and was hypomethylated in the preeclamptic group compared to the nonhypertensive groups, namely, the preterm birth group and term birth group. This result was confirmed by pyrosequencing. Through quantitative real-time PCR and western blot analysis, the WNT3 gene was found to be highly expressed in preeclamptic placental tissues, in contrast to other WNT factors, which were previously reported to be expressed at low levels in placental tissues. Additionally, in the HTR8/SVneo cell line, knockdown of WNT3 suppressed the Wnt/β-catenin signaling pathway, consistent with the findings for other WNT factors. These results prompted us to speculate that the WNT3 gene counteracts the low activation state of the Wnt signaling pathway in the preeclamptic placenta through methylation modification.

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Cyclin D1 regulates osteoarthritis chondrocyte apoptosis via WNT3/β-catenin signalling

Cited by 15 publications

References 26 publications

Kinesin KIF18A is a novel PUM-regulated target promoting mitotic progression and survival of a human male germ cell line

Kinesin KIF18A is a novel PUM-regulated target promoting mitotic progression and survival of a human male germ cell line

WNT3 hypomethylation counteracts low activity of the Wnt signaling pathway in the placenta of preeclampsia

WNT3 Hypopethylation Counteracts low Activity of the Wnt Signaling Pathway in the Placenta of Preeclampsia

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