[Clinical characterization of testicular yolk sac tumor in children and adults].

OBJECTIVE: To compare the clinical characteristics of simple testicular yolk sac tumor (YST) in children with those in adults so as to improve the diagnosis and treatment of the malignance. METHODS: This study included 75 cases of simple testicular YST pathologically confirmed between May 2008 and July 2018, which were divided into groups A (aged <18 years, n = 64) and B (aged ≥18 years, n = 11). We analyzed the clinical data on all the cases and compared the clinical manifestations, laboratory results, pathological findings, clinical stages, treatment methods and prognostic outcomes between the two groups of patients. RESULTS: The patients of group A ranged in age from 6 months to 5 years (ï¼»1.38 ± 0.89ï¼½ yr), with the tumor diameter of 0.9－6.0 (2.48 ± 1.12) cm, while those of group B from 25 to 49 years (median 34 years), with the tumor diameter of 3.5－6.3 (5.16 ± 1.32) cm, most presenting with a painless scrotal mass, 4 (6.2%) in group A and 5 (45.5%) in group B with testis pain. There were statistically significant differences between the two groups in the tumor diameter and initial manifestations (P < 0.05). All the patients were treated by radical high-level spermatectomy and orchiectomy and, in addition, 1 in group A and 3 in group B by retroperitoneal lymph node dissection (RPLND), 24 in the former and 5 in the latter group followed by chemotherapy. Elevated levels of serum alpha-fetoprotein (AFP) were observed in all the cases. Sixty-five of the patients were followed up for 10－78 (52.00 ± 23.78) months, during which 2 cases of simple metastasis, 3 cases of simple relapse, 3 cases of relapse with metastasis and 5 cases of death were found in group A, and 5 cases of simple metastasis, 1 case of simple relapse, 1 case of relapse with metastasis and 4 cases of death in group B. CONCLUSIONS: There are significant differences in the clinical manifestation, biological behavior, treatment and prognosis of testicular YST between children and adults. In children, most of the testicular YST cases are at clinical stage I and preferably treated by radical high-level spermatectomy and orchiectomy with favorable prognosis. In adults, however, the tumor is highly malignant, with high incidences of recurrence and metastasis and poor prognosis, for the treatment of which the first choice is radical high-level spermatectomy and orchiectomy combined with RPLND and chemotherapy.

Over-expression of testis-specific expressed gene 1 attenuates the proliferation and induces apoptosis of GC-1spg cells.

The effects of over-expression of testis-specific expressed gene 1 (TSEG-1) on the viability and apoptosis of cultured spermatogonial GC-1spg cells were investigated, and the immortal spermatogonial cell line GC-1spg (CRL-2053™) was obtained as the cell model in order to explore the function of TSEG-1. We transfected the eukaryotic vector of TSEG-1, named as pEGFP-TSEG-1 into cultured spermatogonial GC-1spg cells. Over-expression of TSEG-1 inhibited the proliferation of GC-1spg cells, and arrested cell cycle slightly at G0/G1 phase. Transfection of TSEG-1 attenuated the transcript levels of Ki-67, PCNA and cyclin D1. In addition, over-expression of TSEG-1 induced early and late apoptosis, and reduced the mitochondrial membrane potential of GC-1spg cells. Moreover, transfection of TSEG-1 significantly enhanced the ratio of Bax/Bcl-2 and transcript levels of caspase 9, and decreased the expression of Fas and caspase 8 in GC-1spg cells. These results indicated over-expression of TSEG-1 suppresses the proliferation and induces the apoptosis of GC-1spg cells, which establishes a basis for further study on the function of TSEG-1.

[Cloning and sequence analysis of TSEG-1, a novel gene specifically expressed in mouse testis].

The expressed sequence tags (ESTs) of normal mouse testis were obtained from online EST database ZooDDD. Their highly homologous EST sequences were found through the dbEST database to construct contigs, and spliced by the biomedical software Biolign. The corresponding exons and introns within genome sequences were predicted by software GeneScan. According to the open reading frame, the primers were designed. RT-PCR was applied in the cloning of novel gene from mouse testis and analyzing its expression pattern in various mouse tissues. The bioinformatics analysis on the sequencing results of TSEG-1 was conducted. Results indicated that a novel gene TSEG-1 was cloned from 1 668-2 011 kb of mouse X chromosome, with full-length sequence of 510 bp. The open reading frame (ORF) is 336 bp in length and en-codes a deduced amino acid sequence of 111 residues. The molecular weight of TSEG-1 protein is 12.84258 kDa, and its pI is 11.4000. RT-PCR demonstrated the correctness of its ORF. TSEG-1 was distinctively expressed in testis, but not in other tissues of mouse. No obvious homology with other mouse cDNA was found for TSEG-1. The GenBank accession number EU079024 was achieved. It was predicted that TSEG-1 is a kind of transmembrane protein, and the transmembrane domain is from 41 amino acid residue to 61 amino acid residue. Blastn analysis revealed its high homology to human testis-specific gene H2AX. Computational prediction of the 5'-untranslated region of TSEG-1 gene revealed a 680 bp-length promoter region. There are four antigen binding sites and two phosphorylation sites of specific protein kinase in TSEG-1 protein, with subcellular localization in mitochondria. The cloning of mouse testis specific gene TSEG-1 laid a foundation for subsequent research of its biological function and expression regulation.

LncRNA MIAT facilitated BM-MSCs differentiation into endothelial cells and restored erectile dysfunction via targeting miR-200a in a rat model of erectile dysfunction.

BACKGROUND: Bone-marrow derived mesenchymal stem cells (BM-MSCs) implantation effectively restored rats' erectile dysfunction (ED). Long noncoding RNA (LncRNA)-myocardial infarction-associated transcript (MIAT) has been reported to play an important role in regulating endothelial cells (ECs) function via vascular endothelial growth factor (VEGF) that induced BM-MSCs differentiation into ECs. However, the molecular functions and biological roles of lncRNA MIAT in ED remained unclear. METHODS: The rat model of ED was established. Quantitative real-time PCR (qRT-PCR) and western blotting were used to detect the expression of lncRNA MIAT, von Willebrand factor (vWF), vascular endothelial cadherin (VE-cadherin), endothelial NO synthase (eNOS) and VEGF following BM-MSCs transfection. Erectile function was evaluated by intra-cavernous pressure/mean artery pressure (ICP/MAP). Furthermore, RNA immunoprecipitation (RIP) assay and RNA pull down as well as luciferase reporter assay were carried out to examine the interaction among lncRNA MIAT, miR-200a and VEGF. RESULTS: BM-MSCs restored ED by upregulating lncRNA MIAT. LncRNA MIAT was upregulated in a time-dependent manner during BM-MSCs differentiation into ECs. LncRNA MIAT regulated VEGF via targeting miR-200a, thereby promoting BM-MSCs differentiation into ECs. LncRNA MIAT knockdown in vivo abolished the effect of BM-MSCs on ED. CONCLUSION: LncRNA MIAT promoted BM-MSCs differentiation into ECs and restored ED via miR-200a.