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Cervical cancer is one of the most common gynecological cancers worldwide. Aberrant expression of E3 ubiquitin ligase isolated by differential display (EDD) has been detected in various types of tumor and has been demonstrated to have an important role in carcinogenesis, tumor growth and drug resistance. However, the role of EDD in cervical cancer and its underlying molecular mechanisms remains unknown. The present study aimed to investigate the role of EDD in the tumorigenicity of cervical cancer. EDD expression levels were measured using reverse transcription-quantitative polymerase chain reaction and western blotting in SiHa, HeLa, CaSki, c-41 and c-33A cervical cancer cell lines and cervical cancer tissue specimens. A functional study was performed using cell proliferation, colony formation, cell apoptosis assays in vitro and tumor growth assays in vivo with EDD either overexpressed or silenced. In the present study, EDD expression levels were significantly upregulated in cervical cancer cell lines and tissue samples. EDD knockdown significantly inhibited colony formation, cell proliferation and tumor growth and accelerated cell apoptosis in the cervical cancer cell lines and tissue samples. Furthermore, microRNA (miR)-143 expression levels were low in cervical cancer tissue samples and were negatively correlated with EDD expression. miR-143 silencing eliminated the effect of EDD on cell proliferation, colony formation and cell apoptosis in the cervical cancer cells, which suggested that miR-143 is critical for EDD-mediated regulation of cervical cancer cell growth. The results of the present study indicated that EDD may promote cervical cancer growth in vivo and in vitro by targeting miR-143. In conclusion, EDD may have an oncogenic role in cervical cancer and may serve as a potential therapeutic target for the treatment of patients with cervical cancer.

BackgroundWith the development of whole-genome sequencing, small chromosomal deletions and duplications could be found by NIPT. This study is to evaluate the clinical significance of fetal chromosomal karyotype analysis and chromosomal microarray analysis (CMA) to clarify the clinical significance of 528 cases of high-throughput sequencing noninvasive prenatal screening suggesting high-risk cases. MethodsNon-invasive prenatal screening showed that the fetus 21, 18, 13, sex chromosomes, and other chromosomes are at high risk of aneuploidy and fetal chromosome copy number variations (CNVs) are at high risk, requiring prenatal diagnosis Pregnant women are the research objects. After obtaining informed consent, fetal cells were obtained by amniocentesis or umbilical vein puncture for chromosomal karyotype and CMA analysis. All cases of childbirth were followed up by telephone over a period of 1 year.Results Among 528 fetuses, 447 were at high risk of aneuploidy. The positive predictive value (PPV) for trisomy 21(T21), trisomy 18 (T18), trisomy 13 (T13), sex chromosome aneuploidies (SCAs), and other chromosome aneuploidy was 85.24%, 51.52%, 12.5%, 50.82%, and 5.88% respectively. Another 81 cases of non-invasive prenatal screening suggest CNVs High risk. The PPV for CNVs was 34.57% .Among them, CNVs has a clear pathogenic significance can reach 24.69% . Follow-up of childbirth cases: Of the 62 pregnant women diagnosed with fetal SCA, 13 chose to continue their pregnancy, and the overall continued pregnancy rate was 20.97% (13/62); CNVs has no clear significance/no disease reported in 8 cases, 1 case After being lost to follow-up, all 7 cases chose to continue their pregnancy. One of the children was not informed about the specific situation; one girl had six fingers on both hands, and the rest had no abnormal growth; the remaining five children developed normally. ConclusionThis study has obtained relatively reliable PPV data for NIPT screening for chromosomal aneuploidy, which provides a reliable basis for clinical genetic counseling and treatment; it is recommended to perform prenatal diagnosis and perform chromosomal nucleus when non-invasive and high-risk prompts suspicious chromosomal abnormalities (over/under/microdeletion/microduplication). Type and CMA inspection, so that the inspection is more comprehensive and not easy to miss the diagnosis.

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Complex chromosomal rearrangements (CCR) are rare chromosomal structural abnormalities. The chromosomal structural variants in CCR carriers are one of the factors contributing to a history of adverse pregnancy and childbirth. In this study, we report a patient with a history of adverse pregnancy and childbirth who exhibited complex balanced chromosomal translocations. The female patient was phenotypically and intellectually normal; in her first pregnancy, the embryo was damaged, and a histological examination of the chromosomes of the embryos revealed a deletion of approximately 4.66 Mb at 1p32.3p32.2, a duplication of approximately 1.02 Mb at 1p22.2p22.1, a duplication of approximately 1.46 Mb at 6q27 and a deletion of approximately 7.78 Mb at 9p24.3p24.1. Chromosomal examinations of the patient revealed the karyotype to be 46,XX,(1;9)(p32; p34). In the second pregnancy, the foetus was diagnosed prenatally with three or more positive ultrasound soft indicators. The patient's karyotype was re-examined and further confirmed by fluorescence in situ hybridisation as 46,XX,t(1;9;6)(p31;p22;q27), revealing this patient was a carrier of complex balanced chromosomal translocations. Carriers of CCR have a higher risk of spontaneous abortion, and genetic counselling clinicians should consider the karyotype analyses of such patients in clinical practice and recheck their chromosomes if necessary.