Pre-Eclampsia-Associated Reduction in Placental Growth Factor Impaired Beta Cell Proliferation Through PI3k Signalling

Li, Jun; Ying, Huanchun; Cai, Guiyang; Guo, Quan; Chen, Lizhu

doi:10.1159/000374051

Cited by 11 publications

(8 citation statements)

References 29 publications

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“…Meanwhile, the invasion-promoting effect of PTP4A1 was also revealed in colorectal cancer [16], lung cancer [17] and HCC [19]. Third, we demonstrated that PTP4A1 promoted cell proliferation via PI3K/AKT signaling pathway and downstream molecules, such as GSK3β and CyclinD1, consistently with a recent report that activation of PI3K/AKT signaling in beta cells may promote beta-cell proliferation through increased cellular level of cell-cycle regulator CyclinD1 [26]. …”

Section: Discussionsupporting

confidence: 86%

Protein tyrosine phosphatase PTP4A1 promotes proliferation and epithelial-mesenchymal transition in intrahepatic cholangiocarcinoma via the PI3K/AKT pathway

Liu

Dong

et al. 2016

Oncotarget

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The protein tyrosine phosphatase PTP4A1 is a key molecule that activates tyrosine phosphorylation, which is important for cancer progression and metastasis. However, the clinical implications and biological function of PTP4A1 in intrahepatic cholangiocarcinoma (ICC) remains unknown. Here, we showed that PTP4A1 was frequently overexpressed in ICC versus adjacent non-tumor tissues. This overexpression significantly correlated with aggressive tumor characteristics like the presence of lymph node metastasis and advanced tumor stages. Survival analysis further indicated that high PTP4A1 expression was significantly and independently associated with worse survival and increased recurrence in ICC patients. Moreover, through forced overexpression and knock-down of PTPT4A1, we demonstrated that PTP4A1 could significantly promote ICC cells proliferation, colony formation, migration, and invasion in vitro, and markedly enhance tumor progression in vivo. Mechanistically, PTP4A1 was involved in PI3K/AKT signaling and its downstream molecules, such as phosphorylation level of GSK3β and up-regulation of CyclinD1, in ICC cells to promote proliferation. Importantly, PTP4A1 induced ICC cells invasion was through activating PI3K/AKT signaling controlled epithelial-mesenchymal transition (EMT) process by up-regulating Zeb1 and Snail. Thus, PTP4A1 may serve as a potential oncogene that was a valuable prognostic biomarker and therapeutic target for ICC.

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Section: Discussionsupporting

confidence: 86%

Protein tyrosine phosphatase PTP4A1 promotes proliferation and epithelial-mesenchymal transition in intrahepatic cholangiocarcinoma via the PI3K/AKT pathway

Liu

Dong

et al. 2016

Oncotarget

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“…Finally, gestational PLGF may stimulate endothelial cells within the pancreatic islets to release growth factors that activate the PI3K-AKT pathway ( Fig. 2 ), thus enhancing β-cell proliferation ( 73 ). A previous study demonstrated that Pref-1 independently facilitated the phosphorylation of AKT and ERK1/2, and triggered alterations in the expression of FOXO1 and Pdx1 ( Fig.…”

Section: Growth Factor Signaling Pathwaysmentioning

confidence: 99%

Cellular signaling pathways regulating β‑cell proliferation as a promising therapeutic target in the treatment of diabetes (Review)

2018

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It is established that a decrease in β-cell number and deficiency in the function of existing β-cells contribute to type 1 and type 2 diabetes mellitus. Therefore, a major focus of current research is to identify novel methods of improving the number and function of β-cells, so as to prevent and/or postpone the development of diabetes mellitus and potentially reverse diabetes mellitus. Based on prior knowledge of the above-mentioned causes, promising therapeutic approaches may include direct transplantation of islets, implantation and subsequent induced differentiation of progenitors/stem cells to β-cells, replication of pre-existing β-cells, or activation of endogenous β-cell progenitors. More recently, with regards to cell replacement and regenerative treatment for diabetes patients, the identification of cellular signaling pathways with related genes or corresponding proteins involved in diabetes has become a topic of interest. However, the majority of pathways and molecules associated with β-cells remain unresolved, and the specialized functions of known pathways remain unclear, particularly in humans. The current article has evaluated the progress of research on pivotal cellular signaling pathways involved with β-cell proliferation and survival, and their validity for therapeutic adult β-cell regeneration in diabetes. More efforts are required to elucidate the cellular events involved in human β-cell proliferation in terms of the underlying mechanisms and functions.

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“…It has been estimated that 5%–7% of pregnancies worldwide are complicated by this disorder, resulting in a very large disease burden [1]. Although much research has been devoted toward this topic, its pathogenesis is still incompletely understood yet [2-5]. …”

Section: Introductionmentioning

confidence: 99%

MiR-495 Promotes Senescence of Mesenchymal Stem Cells by Targeting Bmi-1

Song

Liú

et al. 2017

Cell Physiol Biochem

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Background/Aims: Mesenchymal stem cells (MSCs) play an important role in regulating angiogenesis and immune balance. Abnormal proliferation and function of MSCs were reported at maternal fetal interface in patients with pre-eclampsia (PE). Micro-RNA-495 was known to be upregulated in the MSCs derived from patients with PE. However, it is not clear whether the up-regulated miR-495 is related to the pathogenesis of PE. Methods: We analyzed the expression of miR-495 in MSCs and umbilical cords derived from healthy pregnancies (NC) and PE, then we upregulated or downregulated the expression of miR-495 in MSCs derived from NC and tested the proliferation, apoptosis, migration, invasion, tube formation and senescence. Results: In the current study, we found that the expression of miR-495 was significantly increased in both umbilical cord tissues and MSCs in patients with severe PE. Overexpressing miR-495 arrested cell cycle in S phase and promoted cell apoptosis. The supernatants from miR-495-overexpressed-MSCs inhibited the migration of MSCs and HTR-8/SVneo, invasion of HTR-8/SVneo and tube formation of HUVEC, while si-miR-495 had the opposite effects. Furthermore, we analyzed the senescence related β-galactosidase activity and CD146 and found that miR-495 induced the senescence of MSCs. Molecular mechanism studies confirmed that Bmi-1 mediated these effects of miR-495 on MSCs. Conclusion: Taken together, our data demonstrated that miR-495 induced senescence of MSCs may be involved in the pathogenesis of PE.

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Pre-Eclampsia-Associated Reduction in Placental Growth Factor Impaired Beta Cell Proliferation Through PI3k Signalling

Cited by 11 publications

References 29 publications

Protein tyrosine phosphatase PTP4A1 promotes proliferation and epithelial-mesenchymal transition in intrahepatic cholangiocarcinoma via the PI3K/AKT pathway

Protein tyrosine phosphatase PTP4A1 promotes proliferation and epithelial-mesenchymal transition in intrahepatic cholangiocarcinoma via the PI3K/AKT pathway

Cellular signaling pathways regulating β‑cell proliferation as a promising therapeutic target in the treatment of diabetes (Review)

MiR-495 Promotes Senescence of Mesenchymal Stem Cells by Targeting Bmi-1

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