PI3K, AKT, and P-AKT levels in thin endometrium

Le, Aiwen; Shan, Lili; Dai, X Y; Xiao, Tian; Li, X R; Wang, Z H; J, Zhang; Chen, X Y

doi:10.4238/gmr.15017184

Cited by 9 publications

(4 citation statements)

References 23 publications

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“…For example, rapid activation of PI3K/Akt signaling cascades by growth factors and estrogen is involved in the migration of normal endometrial stromal cells (Gentilini et al, 2007). However, the expression of DEGs in the PI3K/AKT pathway, including EFNA1, FGF9, LPAR1, CCNE2, SGK1, MET, IL6R, and PDGFRA, was decreased in thin endometrium, which suggests that the repair ability of the thin endometrium was impaired during the proliferative phase (Le et al, 2016). Similarly, the abnormal Wnt/beta-catenin signal pathway would also impair the proliferation of estrogendependent endometrial cells (Tepekoy et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium

et al. 2021

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Although the thin endometrium (TE) has been widely recognized as a critical factor in implantation failure, the contribution of miRNA–mRNA regulatory network to the development of disease etiology remains to be further elucidated. This study performed an integrative analysis of the miRNA–mRNA expression profiles in the thin and adjacent normal endometrium of eight patients with intrauterine adhesion to construct the transcriptomic regulatory networks. A total of 1,093 differentially expressed genes (DEGs) and 72 differentially expressed miRNAs (DEMs) were identified in the thin adhesive endometrium of the TE group compared with the control adjacent normal endometrial cells. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed that the DEGs and the target genes of DEM were significantly enriched in angiogenesis, cell growth regulation, and Wnt signaling pathway. Multiple hub genes (CAV1, MET, MAL2, has-mir-138, ARHGAP6, CLIC4, RRAS, AGFG1, has-mir-200, and has-mir-429) were identified by constructing the miRNA–mRNA regulatory networks. Furthermore, a miRNA–mRNA pathway function analysis was conducted, and the hub genes were enriched in the FoxO signaling pathway, cell growth regulation, inflammatory response regulation, and regulation of autophagy pathways. Our study is the first to perform integrated mRNA-seq and miRNA-seq analyses in the thin adhesive endometrium and the control adjacent normal endometrial cells. This study provides new insights into the molecular mechanisms underlying the formation of thin endometrium.

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Section: Discussionmentioning

confidence: 99%

Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium

et al. 2021

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“…The resulting production of SOD, CAT, GSH, and GSH-Px reduces oxidative stress damage to cells (Wen et al, 2018). Therefore, the activity of PI3K/Akt signaling pathway is usually expressed by the level of downstream p-Akt, where high expression of p-Akt indicates that the pathway is activated (Le et al, 2016). In our study, we found that the protein expression of PI3K, p-Akt, and Nrf2 was significantly reduced in the NTDs mouse embryonic model induced by atRA, suggesting that the PI3K/Akt signaling pathway was inhibited.…”

Section: Discussionmentioning

confidence: 99%

Wuzi Yanzong Pill protects neural tube defects by activating PI3K/Akt signaling pathway

Wang

Yang

et al. 2023

Intl J of Devlp Neuroscience

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Neural tube defects (NTDs) are severe congenital malformations that can lead to lifelong disability. Wuzi Yanzong Pill (WYP) is an herbal formula of traditional Chinese medicine (TCM) that has been shown to have a protective effect against NTDs in a rodent model induced by all‐trans retinoic acid (atRA), but the mechanism remains unclear. In this study, the neuroprotective effect and mechanism of WYP on NTDs were investigated in vivo using an atRA‐induced mouse model and in vitro using cell injury model induced by atRA in Chinese hamster ovary (CHO) cells and Chinese hamster dihydrofolate reductase‐deficient (CHO/dhFr) cells. Our findings suggest that WYP has an excellent preventive effect on atRA‐induced NTDs in mouse embryos, which may be related to the activation of the PI3K/Akt signaling pathway, improved embryonic antioxidant capacity, and anti‐apoptotic effects, and this effect is not dependent on folic acid (FA). Our results demonstrated that WYP significantly reduced the incidence of NTDs induced by atRA; increased the activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and content of glutathione (GSH); decreased the apoptosis of neural tube cells; up‐regulated the expression of phosphatidylinositol 3 kinase (PI3K), phospho protein kinase B (p‐Akt), nuclear factor erythroid‐2 related factor (Nrf2), and b‐cell lymphoma‐2 (Bcl‐2); and down‐regulated the expression of bcl‐2‐associated X protein (Bax). Our in vitro studies suggested that the preventive effect of WYP on atRA‐treated NTDs was independent of FA, which might be attributed to the herbal ingredients of WYP. The results suggest that WYP had an excellent prevention effect on atRA‐induced NTDs mouse embryos, which may be independent of FA but related to the activation of the PI3K/Akt signaling pathway and improvement of embryonic antioxidant capacity and anti‐apoptosis.

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“…In present study, we evaluated the function of AKT and AKT1 in renal cell carcinoma. In addition, it was reported that the expression of AKT was positively correlated with the expression of p-AKT [ 20 ], which suggested AKT and p-AKT had the similar research value. In present study the antibody of total AKT was used in cellular experiments, based on the findings of in vitro experiments and previous studies, AKT1 was involved in regulating cell growth and proliferation, so we explored expression of AKT1 in human tissues by IHC staining.…”

Section: Discussionmentioning

confidence: 99%

Effect of AKT silence on malignant biological behavior of renal cell carcinoma cells

Nong

et al. 2022

BMC Urol

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Background As the most common malignant tumor of primary renal tumor, renal cell carcinoma (RCC) is the highly invasive disease with high mortality. AKT is a serine/threonine kinase that play a critical role in the phosphoinositide 3-kinase (PI3K) signaling pathway, and it is an attractive target for RCC treatment. The aim of present study was to investigate the effect of AKT silence on malignant behavior of renal cell carcinoma cells. Methods AKT expression was quantified by immunohistochemistry in tumor tissues and normal tissues. The human RCC cell lines Caki-2 cell were chosen for this study. The optimal silencing siRNA was subsequently selected by RT-qPCR and western blot. The effect of AKT silence on RCC cells was investigated by CCK8 assay, transwell assay, scratch test and flow cytometry. The AKT1 expression in human renal cell carcinoma tissue was detected by immunohistochemical staining. Results The AKT in Caki-2 cells was silenced successfully. The results shown AKT silence could inhibit cell proliferation, invasion, and, migration. In addition, AKT silence could promote Caki-2 cell apoptosis with prevention of RCC cells move from G1 phase to S phase. Immunohistochemical staining revealed significant difference of expression of AKT1 in RCC tissues and normal renal tissues. Taken together, AKT family members might involve in malignant growth of RCC, and might be a potential therapeutic target. Conclusion Our data show that AKT silence inhibited cell proliferation, invasion, and, migration of Caki-2 cell, and promoted Caki-2 cell apoptosis. Moreover, AKT silence prevented RCC cells move from G1 phase to S phase. Therefore, AKT may act as an effective therapeutic target for RCC.

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PI3K, AKT, and P-AKT levels in thin endometrium

Cited by 9 publications

References 23 publications

Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium

Integrated Transcriptomic Analysis of the miRNA–mRNA Interaction Network in Thin Endometrium

Wuzi Yanzong Pill protects neural tube defects by activating PI3K/Akt signaling pathway

Effect of AKT silence on malignant biological behavior of renal cell carcinoma cells

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