Declined placental PLAC1 expression is involved in preeclampsia

Wan, Ling; Sun, Dandan; Xie, Jiamin; Du, Mengkai; Wang, Peng; Wang, Miaomiao; Yu, Lei; Wang, Huihua; Wang, Hanzhi; Dong, Minyue

doi:10.1097/md.0000000000017676

Cited by 10 publications

(8 citation statements)

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“…The function of trophoblasts is regulated by a group of genes, especially placenta-specific genes including PLAC1 and syncytin ( Rawn and Cross, 2008 ). These genes regulate trophoblastic migration, invasion, proliferation, apoptosis, and metabolism ( Bolze et al, 2017 ; Wan et al, 2019 ). Galectins are among these genes.…”

Section: Introductionmentioning

confidence: 99%

Galectin-14 Promotes Trophoblast Migration and Invasion by Upregulating the Expression of MMP-9 and N-Cadherin

Wang

et al. 2021

Front. Cell Dev. Biol.

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Galectin-14 is specifically expressed in placental trophoblasts, and its expression is reduced in trophoblasts retrieved from the cervix of women destined to develop early pregnancy loss. However, the roles of galectin-14 in regulating trophoblasts and in the pathogenesis of pregnancy complication have never been investigated. In the current research, we aimed to investigate the roles of galectin-14 in the regulation of trophoblasts. Tissues of the placenta and villi were collected. Primary trophoblasts and human trophoblast cell line HTR-8/SVneo were used. Western blotting and RT-PCR were used to quantify gene expression. The siRNA-mediated galectin-14 knockdown and lentivirus-mediated overexpression were performed to manipulate the gene expression in trophoblasts. Transwell migration and invasion assays were used to evaluate cell migration and invasion capacity. Gelatin zymography was used to determine the gelatinase activity. Galectin-14 was significantly decreased in the villi of early pregnancy loss and the placenta of preeclampsia. Knockdown of galectin-14 in primary trophoblasts inhibited cell migration and invasion, downregulated the expression of matrix metalloproteinase (MMP)-9 and N-cadherin, the activity of MMP-9, and decreased the phosphorylation of Akt. Meanwhile, the overexpression of galectin-14 in HTR-8/SVneo promoted cell migration and invasion, upregulated the expression of MMP-9 and N-cadherin, the activity of MMP-9, and increased the phosphorylation of Akt. Increased Akt phosphorylation promoted cell migration and invasion and upregulated the expression and activity of MMP-9, while decreased Akt phosphorylation inhibited cell migration and invasion and downregulated the expression and activity of MMP-9. Thus, galectin-14 promotes trophoblast migration and invasion by enhancing the expression of MMP-9 and N-cadherin through Akt phosphorylation. The dysregulation of galectin-14 is involved in the pathogenesis of early pregnancy loss and preeclampsia.

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Section: Introductionmentioning

confidence: 99%

Galectin-14 Promotes Trophoblast Migration and Invasion by Upregulating the Expression of MMP-9 and N-Cadherin

Wang

et al. 2021

Front. Cell Dev. Biol.

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“…However, a research found that H.pylori infection caused placental malfunction and is associated with preeclampsia 26 . PLAC1 is a protein mainly secreted by the placenta, and in another study by Wan et al showed that the expression of PLAC1 was reduced in the placenta of patients with eclampsia, and knockdown of PLAC1 expression attenuated the invasive ability of placental trophoblast cells 27 . These studies suggest a possible link between H. pylori infection and PLAC1 expression, but no relevant studies have been performed in tumors, and the exact mechanism and whether there is a direct correlation between them need to be further explored.…”

Section: Discussionmentioning

confidence: 99%

Placenta‐specific protein 1 promotes cell proliferation via the AKT/GSK‐3β/cyclin D1 signaling pathway in gastric cancer

Liu

Shi

et al. 2021

IUBMB Life

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Gastric cancer is a malignant tumor with a poor prognosis. Therefore, it is important to search for molecules that play a vital role in the development, diagnosis, and treatment of this disease. Placenta‐specific 1 (PLAC1) is one of the cancer‐testis antigens; it plays an important role in both placental development and tumorigenesis. However, the role of PLAC1 in gastric cancer has not been fully investigated, and its underlying mechanism needs further study. We first explored the expression and clinical relevance of PLAC1 in gastric cancer and performed gene set enrichment analysis of PLAC1‐related genes using online databases. Subsequently, we studied the function and mechanism of PLAC1 in gastric cancer cells through in vitro experiments. Our results showed that PLAC1 is highly expressed in gastric cancer, is associated with poor prognosis, and can promote gastric cancer cell proliferation through the AKT/GSK‐3β/cyclin D1 signaling pathway. Moreover, we discovered that AKTi attenuates the effect of PLAC1. Our study further revealed the role and mechanism of PLAC1 in gastric cancer and suggested that this antigen might be a useful molecular marker for gastric cancer diagnosis, prognosis, and treatment.

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“…CEBPB (CCAAT enhancer binding protein beta) [38], ACSL4 [39], MBD2 [40], ULK1 [41], NUCB2 [42], TWIST1 [43], HOOK2 [44], CLDN7 [45], TBK1 [46], YIPF6 [47], TFRC (transferrin receptor) [48], ENPP2 [49], SLIT2 [50], MFGE8 [51], FAT1 [52], GPC4 [53], COL6A3 [54], EGFL6 [55], AOC3 [56], CCN2 [57], LYVE1 [58], RARA (retinoic acid receptor alpha) [59], COL18A1 [60], THY1 [61], CD36 [62], PEMT (phosphatidylethanolamine N-methyltransferase) [63], AIF1L [64], OXTR (oxytocin receptor) [65], LMNA (lamin A/C) [66], CXCL14 [67], DKK3 [68], ANGPTL2 [69] and CMTM7 [70] were reported to be associated with obesity, but these genes might be linked with progression of GDM. AHR (aryl hydrocarbon receptor) [71], STS (steroid sulfatase) [72], PLAC1 [73], CYP11A1 [74], PSG11 [75], STAT5B [76], TLR3 [77], FOLR1 [78], HSPB1 [79], HSP90AA1 [80], ANXA4 [81], ATF3 [82], DAPK1 [83], ENTPD1 [84], ABL1 [85], VSIG4 [86], CD99 [87], VWF (von Willebrand factor) [88], PODXL (podocalyxin like) [89], PDPN (podoplanin) [90], RND3 [91], VCAN (versican) [92], AXL (AXL receptor tyrosine kinase) [93], PIEZO1 [94], GAS6 [93], LAMA4 [95], CAV1 [96], DLL1 [97], CD44 [98], CD81 [99], SMAD3 [100], NES (nestin) [101], DCN (decorin) [102], AGTR1 [103], SLIT3 [104], B2M [105], STAT3 [106], STC1 [107] and ADAMTS1 [108] were shown to participate in facilitating the preeclampsia. Majchrzak-Celiń ka et al [109] ...…”

Section: Discussionmentioning

confidence: 99%

Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus

Vastrad¹,

Vastrad²,

Tengli

2021

Preprint

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Gestational diabetes mellitus (GDM) is one of the metabolic diseases during pregnancy. The identification of the central molecular mechanisms liable for the disease pathogenesis might lead to the advancement of new therapeutic options. The current investigation aimed to identify central differentially expressed genes (DEGs) in GDM. The transcription profiling by array data (E-MTAB-6418) was obtained from the ArrayExpress database. The DEGs between GDM samples and non GDM samples were analyzed with limma package. Gene ontology (GO) and REACTOME enrichment analysis were performed using ToppGene. Then we constructed the protein-protein interaction (PPI) network of DEGs by the Search Tool for the Retrieval of Interacting Genes database (STRING) and module analysis was performed. Subsequently, we constructed the miRNA-hub gene network and TF-hub gene regulatory network by the miRNet database and NetworkAnalyst database. The validation of hub genes was performed through receiver operating characteristic curve (ROC). Finally, the candidate small molecules as potential drugs to treat GDM were predicted by using molecular docking. Through transcription profiling by array data, a total of 869 DEGs were detected including 439 up regulated and 430 down regulated genes. Biological process analysis of GO enrichment analysis showed these DEGs were mainly enriched in reproduction, nuclear outer membrane-endoplasmic reticulum membrane network, identical protein binding, cell adhesion, supramolecular complex and signaling receptor binding. Signaling pathway enrichment analysis indicated that these DEGs played a vital in cell surface interactions at the vascular wall and extracellular matrix organization. Ten genes, HSP90AA1, EGFR, RPS13, RBX1, PAK1, FYN, ABL1, SMAD3, STAT3, and PRKCA in the center of the PPI network, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network were associated with GDM, according to ROC analysis. Finally, the most significant small molecules were predicted based on molecular docking. Our results indicated that HSP90AA1, EGFR, RPS13, RBX1, PAK1, FYN, ABL1, SMAD3, STAT3, and PRKCA could be the potential novel biomarkers for GDM diagnosis, prognosis and the promising therapeutic targets. The current might be essential to understanding the molecular mechanism of GDM initiation and development.

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Declined placental PLAC1 expression is involved in preeclampsia

Cited by 10 publications

References 50 publications

Galectin-14 Promotes Trophoblast Migration and Invasion by Upregulating the Expression of MMP-9 and N-Cadherin

Galectin-14 Promotes Trophoblast Migration and Invasion by Upregulating the Expression of MMP-9 and N-Cadherin

Placenta‐specific protein 1 promotes cell proliferation via the AKT/GSK‐3β/cyclin D1 signaling pathway in gastric cancer

Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus

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