Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis for XBP1 overexpressing complete hydatidiform mole-derived cell lines

ABSTRACT: Transcriptome analysis for XBP1 overexpressing complete hydatidiform mole-derived cell lines

PROVIDER: PRJNA1063209 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27480505_1.fastq.gz	Fastqsanger.gz
	SRR27480505_2.fastq.gz	Fastqsanger.gz
	SRR27480506_1.fastq.gz	Fastqsanger.gz
	SRR27480506_2.fastq.gz	Fastqsanger.gz
	SRR27480507_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Transcriptome analysis for XBP1 overexpressing complete hydatidiform mole-derived cell lines

Project description:The trophoblastic disease is a general term for diseases that cause abnormal growth of trophoblasts, the most frequent form of which is called hydatidiform mole (CHM). CHM cell lines (Hmol1-3B and Hmol1-2C) were established in our laboratory (Yamamoto E, et al. Int J Mol Med. 2017 Sep; 40(3): 614–622). In this study, XBP1 was overexpressed, and RNA sequencing was performed to investigate the role of XBP1 in CHM.

2024-12-21 | GSE252905 | GEO

The gene expression profiles of complete hydatidiform mole which developed post molar gestational trophoblast neoplasia

Project description:A complete hydatidiform mole (CHM) is a common disease known to develop post-molar gestational trophoblast neoplasia (GTN). However, the details of the molecular biological mechanisms underlying the progression to post-molar GTN from hydatidiform moles are still largely unknown. In this study, we performed RNA sequencing (RNA-seq) using archival fresh frozen tissues of patients with CHM and compared the gene expression profiles of patients who achieved spontaneous remission and those who developed post-molar GTN after the evacuation.

2024-12-21 | GSE252906 | GEO

Gene expression profiles of complete hydatidiform moles and XBP1-overexpressing cell lines associated with progression to gestational trophoblastic tumors

Project description:Gene expression profiles of complete hydatidiform moles and XBP1-overexpressing cell lines associated with progression to gestational trophoblastic tumors

| PRJNA1063206 | ENA

Impaired DNA methylation in oocytes with a mutation in KHDC3L causing recurrent hydatidiform mole

Project description:Mutations in components of the subcortical maternal complex (SMC) of the human oocyte are enigmatically associated with DNA methylation abnormalities specifically at imprinted genes in conceptuses, but the developmental timing, genomic extent and mechanistic details of these defects are unknown. Here, we show, by single-cell bisulphite sequencing, that mutation in human KHDC3L that causes recurrent hydatidiform mole results in a genome-wide deficit of de novo methylation in oocytes.

2019-11-21 | GSE122872 | GEO

A KHDC3L mutation resulting in recurrent hydatidiform mole causes genome-wide DNA methylation loss in oocytes and persistent imprinting defects post-fertilisation.

Project description:Maternal-effect mutations in components of the subcortical maternal complex (SCMC) of the human oocyte can cause early embryonic failure, gestational abnormalities and recurrent pregnancy loss. Enigmatically, they are also associated with DNA methylation abnormalities at imprinted genes in conceptuses, in the devastating gestational abnormality biparental complete hydatidiform mole (BiCHM) or in multi-locus imprinting disease (MLID). However, the developmental timing, genomic extent and mechanistic basis of these imprinting defects are unknown. Here, we studied methylation level of a women reported with familial recurrent hydatidiform mole and multiple pregnancy loss. Genotype analysis revealed homozygous mutation in KHDC3L. We obtained biparental mole from patient (Patient D) and compared it’s whole-genome methylation profile with respect to control placentas and sporadic mole (AnCHM) using Infinium MethylationEPIC BeadChip (WG-317-1001, Illumina). We also used endometrium samples from their respective mother for the comparison purposes. Molar conceptuses were observed with methylation defects at genome-wide level and profound loss of methylation at multiple genome-derived differentially methylated regions (gDMRs) confirming MLID.

2019-11-21 | GSE138864 | GEO

Establishment and characterization of cell lines derived from complete hydatidiform mole.

Project description:Gestational trophoblastic diseases (GTDs) are a group of diseases characterized by abnormal cellular proliferation of atypical trophoblasts. A hydatidiform mole is an abnormal pregnancy caused by genetic fertilization disorders, and it can be classified as a complete hydatidiform mole (CHM) or a partial hydatidiform mole. The aim of this study was to establish cell lines from CHMs and to characterize the cells for future studies concerning GTD. HMol1-2C, HMol1-3B, HMol1-8 and HMol3-1B were established from primary cultures of CHM explants following the introduction of different combinations of genes including human telomerase reverse transcriptase (hTERT), a mutant form of CDK (CDK4R24C), cyclin D1, p53C234, MYC and HRAS. HMol1-2C, HMol1-3B, and HMol3-1B were confirmed to originate from trophoblasts of androgenic, homozygous CHMs. These three cell lines exhibited low human chorionic gonadotropin secretion, low migration and invasion abilities, and the potential to differentiate into syncytiotrophoblastic cells via forskolin treatment. These results suggest that these cells exhibit characteristics of trophoblastic cells, especially cytotrophoblastic cells. HMol1-8 was found to consist of diploid cells and originated from maternal cells, suggesting that they were derived from decidual cells. In conclusion, we successfully established three cell lines from CHMs by introduction of hTERT and other genes. Analysis revealed that the genetic origin of each cell line was identical with that of the original molar tissue, and the cell lines exhibited characteristics of trophoblastic cells, which are similar to undifferentiated cytotrophoblasts.

| S-EPMC5547987 | biostudies-other

The gene expression profiles of complete hydatidiform mole which developed post molar gestational trophoblast neoplasia

Project description:The gene expression profiles of complete hydatidiform mole which developed post molar gestational trophoblast neoplasia

| PRJNA1063208 | ENA

Definitive SNP/CNV haplotype map of Asians determined using a collection of complete hydatidiform moles

Project description:This SuperSeries is composed of the following subset Series: GSE18642: Definitive SNP/CNV haplotype map of Asians determined using a collection of complete hydatidiform moles (Affymetrix) GSE18663: Definitive SNP/CNV haplotype map of Asians determined using a collection of complete hydatidiform moles (Illumina) Refer to individual Series

2010-05-17 | E-GEOD-18701 | biostudies-arrayexpress

A Patient specific iPSC-based model of Hydatidiform mole reveals abnormal BMP4 signaling caused by NLRP7 deficiency

Project description:Complete Hydatidiform Mole (HM) is a gestational trophoblastic disease resulting in hyper proliferation of trophoblast cells and absence of embryo development. Mutations in NLRP7 gene is a major cause of familial recurrent complete HM, where no embryonic tissue is present during the pregnancy. NLRP7 is a novel protein and its function is poorly understood. Lack of NLRP7 in the mouse genome and challenges in studying human embryogenesis as well as human trophoblast differentiation has prevented elucidation of the pathophysiology of this disease and the function of NLRP7 in HM. Here, we established an in vitro model of HM using NLRP7 deficient patient-derived human induced pluripotent stem cells (iPSCs). Whole transcriptome profiling during trophoblast differentiation revealed that NLRP7 deficiency results in precocious downregulation of pluripotency factors, activation of trophoblast genes and promotes maturation of differentiated extraembryonic cell types such as syncytiotrophoblasts. We further showed that these phenotypes are dependent on BMP4 signaling and BMP pathway inhibition prevented excessive trophoblast differentiation of HM-iPSCs. Taken together, this novel human iPSC model of a genetic placental disease recapitulates aspect of trophoblast biology and sheds light on early human embryogenesis by identifying NLRP7 as an important regulator of this process.

2021-09-09 | GSE125592 | GEO

Gene expression profiles of complete hydatidiform moles and XBP1-overexpressing cell lines associated with progression to gestational trophoblastic tumors

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-22 | GSE252907 | GEO