Expression of RGC32 in human normal and preeclamptic placentas and its role in trophoblast cell invasion and migration

Wang, Q.-j.; Song, Bingfeng; Zhang, Y.-h.; Ma, Yuyan; Shao, Qianqian; Liu, J.; Qu, Xun

doi:10.1016/j.placenta.2014.12.012

Cited by 17 publications

(14 citation statements)

References 33 publications

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“…RGC32, a coactivator that mediates cellular proliferation and differentiation, was originally identified because of differential expression of RGC32 in response to complement activation (40). Recent studies showed that expression of RGC32 was significantly lower in human PE placentae (62). We found that expression of RGC32 was down‐regulated in BPH/5 implantation sites (E7.5) and midgestation placentae (E10.5), concurrent with onset of complement overexpression.…”

Section: Discussionmentioning

confidence: 99%

Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia

et al. 2018

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Preeclampsia (PE), a hypertensive disorder of pregnancy, is a leading cause of maternal and fetal morbidity and mortality. Although the etiology is unknown, PE is thought to be caused by defective implantation and decidualization in pregnancy. Pregnant blood pressure high (BPH)/5 mice spontaneously develop placentopathies and maternal features of human PE. We hypothesized that BPH/5 implantation sites have transcriptomic alterations. Next-generation RNA sequencing of implantation sites at peak decidualization, embryonic day (E)7.5, revealed complement gene up-regulation in BPH/5 vs. controls. In BPH/5, expression of complement factor 3 was increased around the decidual vasculature of E7.5 implantation sites and in the trophoblast giant cell layer of E10.5 placentae. Altered expression of VEGF pathway genes in E5.5 BPH/5 implantation sites preceded complement dysregulation, which correlated with abnormal vasculature and increased placental growth factor mRNA and VEGF expression at E7.5. By E10.5, proangiogenic genes were down-regulated, whereas antiangiogenic sFlt-1 was up-regulated in BPH/5 placentae. We found that early local misexpression of VEGF genes and abnormal decidual vasculature preceded sFlt-1 overexpression and increased complement deposition in BPH/5 placentae. Our findings suggest that abnormal decidual angiogenesis precedes complement activation, which in turn contributes to the aberrant trophoblast invasion and poor placentation that underlie PE.-Sones, J. L., Merriam, A. A., Seffens, A., Brown-Grant, D.-A., Butler, S. D., Zhao, A. M., Xu, X., Shawber, C. J., Grenier, J. K., Douglas, N. C. Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia.

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Section: Discussionmentioning

confidence: 99%

Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia

et al. 2018

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“…Mechanistically, RGC32 increases VEGF receptor 2 expression through activating nuclear factor (NF)-κB signaling pathway ( 20 ). Reduced RGC32 expression is also found in human preeclamptic placentas compared with normal controls ( 21 ), indicating the important role of RGC32 in placenta functions. These studies suggest that RGC32 may exert different roles in EC proliferation and angiogenesis in different physiological or pathological processes, which likely depends on the location of the ECs or the nature of the stimulus.…”

Section: Roles Of Rgc32 In Ecsmentioning

confidence: 98%

Response Gene to Complement 32 in Vascular Diseases

Cui

Chen

2018

Front. Cardiovasc. Med.

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Response gene to complement 32 (RGC32) is a protein that was identified in rat oligodendrocytes after complement activation. It is expressed in most of the organs and tissues, such as brain, placenta, heart, and the liver. Functionally, RGC32 is involved in various physiological and pathological processes, including cell proliferation, differentiation, fibrosis, metabolic disease, and cancer. Emerging evidences support the roles of RGC32 in vascular diseases. RGC32 promotes injury-induced vascular neointima formation by mediating smooth muscle cell (SMC) proliferation and migration. Moreover, RGC32 mediates endothelial cell activation and facilitates atherosclerosis development. Its involvement in macrophage phagocytosis and activation as well as T-lymphocyte cell cycle activation also suggests that RGC32 is important for the development and progression of inflammatory vascular diseases. In this mini-review, we provide an overview on the roles of RGC32 in regulating functions of SMCs, endothelial cells, and immune cells, and discuss their contributions to vascular diseases.

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“…[8][9][10][11] Extensive researches have shown that RGC-32 induces cell proliferation, differentiation, invasion, migration, epithelial-mesenchymal transition (EMT) occurrence and metabolism. [12][13][14][15][16] A considerable amount of literatures have been published on regulatory effects of RGC-32 in a variety of non-cancerous diseases, concerning vascular diseases, [17][18][19] Alzheimer's Disease, 20 obesity, 21 diabetic retinopathy, 22 autoimmune encephalomyelitis, 23 renal ischemia reperfusion injury, 24 preeclampsia 25 and other non-tumour diseases. In addition to its mediating role in non-cancer, essential roles of it were identified to facilitate the progressions of numerous malignancies, namely ovarian cancer, 26,27 colon cancer, 28,29 prostate cancer, 30 lung cancer, 31,32 breast carcinoma 33 and pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

Oncogenic gene RGC‐32 is a direct target of miR‐26b and facilitates tongue squamous cell carcinoma aggressiveness through EMT and PI3K/AKT signalling

Yang

Chen

et al. 2020

Cell Biochemistry & Function

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Growing data have recognized the significance of Response Gene to Complement (RGC)-32 in numerous tumour developments. Notwithstanding, the functional role and underlying mechanism of it in tongue squamous cell carcinoma (TSCC) remain enigmatic. Here, to identify the impact of RGC-32 in TSCC, its expression in multiple TSCC cells was measured and loss-of-function experiments in cell lines were performed to illuminate the function of it induced TSCC progression, via si-RNA knockdown, CCK-8, colony formation, wound-healing, transwell, flow cytometry and western blot assays. To clarify potential mechanism, expressions of hallmarks in epithelial-mesenchymal transition (EMT) process and PI3K/AKT signalling were assessed, and the upstream miR regulator of RGC-32 was predicted and verified by applying bioinformatic approaches and dual-luciferase reporter assay, respectively. Finally, the rescue experiments were applied to better elucidate the effect of miR-26b/RGC-32 axis in TSCC behaviours. As a result, RGC-32 was upregulated in TSCC cells and knocking down of it abrogated cell proliferation, trans-migration and invasion, whilst promoted apoptosis in TSCC, which was regulated through repressing EMT and inactivation of PI3K/AKT signalling. Subsequently, miR-26b was predicted and identified as an upstream regulator of RGC-32, and the pro-tumorigenic effect of RGC-32 was reversed by miR-26b overexpression. Collectively, our results demonstrated that RGC-32 facilitated TSCC progression, which was modulated by activations of PI3K/AKT pathway and EMT process, and reduction of its negative regulator of miR-26b. These findings highlight a novel role of miR-26b/RGC-32 axis in TSCC and underlying mechanism, encouraging a potent usage in TSCC treatment. Significance of the study: We first uncovered that Response Gene to Complement-32 played a significantly pro-tumorigenic role in tongue squamous cell carcinoma (TSCC), which was closely regulated by downregulation of miR-26b and activations of epithelial-mesenchymal transition process and PI3K/AKT signalling. These findings contribute to better understand the molecular mechanism in carcinogenesis of TSCC, and shed some light on promising strategy for TSCC therapeutics.

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Expression of RGC32 in human normal and preeclamptic placentas and its role in trophoblast cell invasion and migration

Cited by 17 publications

References 33 publications

Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia

Angiogenic factor imbalance precedes complement deposition in placentae of the BPH/5 model of preeclampsia

Response Gene to Complement 32 in Vascular Diseases

Oncogenic gene RGC‐32 is a direct target of miR‐26b and facilitates tongue squamous cell carcinoma aggressiveness through EMT and PI3K/AKT signalling

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