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lopment of early indication technologies for rapid disease diagnosis.In vitro fertilization (IVF) is associated with DNA methylation abnormalities and a higher incidence of adverse pregnancy outcomes. However, which exposure(s), among the many IVF interventions, contributes to these outcomes remains unknown. Frozen embryo transfer (ET) is increasingly utilized as an alternative to fresh ET, but reports suggest a higher incidence of pre-eclampsia and large for gestational age infants. This study examines DNA methylation in human placentas using the 850K Infinium MethylationEPIC BeadChip array obtained after 65 programmed frozen ET cycles, 82 fresh ET cycles and 45 unassisted conceptions. Nine patients provided placentas following frozen and fresh ET from consecutive pregnancies for a paired subgroup analysis. In parallel, eight mouse placentas from fresh and frozen ET were analyzed using the Infinium Mouse Methylation BeadChip array. Human and mouse placentas were significantly hypermethylated after frozen ET compared with fresh. Paired analysis showed similar trends. Sex-specific analysis revealed that these changes were driven by male placentas in humans and mice. Frozen and fresh ET placentas were significantly different from controls, with frozen samples hypermethylated compared with controls driven by males and fresh samples being hypomethylated compared with controls, driven by females. Sexually dimorphic epigenetic changes could indicate differential susceptibility to IVF-associated perturbations, which highlights the importance of sex-specific evaluation of adverse outcomes. Similarities between changes in mice and humans underscore the suitability of the mouse model in evaluating how IVF impacts the epigenetic landscape, which is valuable given limited access to human tissue and the ability to isolate specific interventions in mice.

Circular RNAs (circRNAs) are identified as key modulators in cancer biology. Nonetheless, the role of

in non-small cell lung cancer (NSCLC) and its modulatory mechanism are undefined. This study aimed to investigate the potential function and mechanism of

in NSCLC.

In this experimental study,

,

and vestigial like family member 4 (VGLL4) mRNA expressions were analyzed in NSCLC tissues and cells, using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Multiplication, migration and invasion of NSCLC cells were examined using the CCK-8 method and Transwell experiment, respectively. Dual-luciferase reporter gene experiments were conducted to identify the paring relationship between

and

. Western blot was employed to determine expressions of VGLL4 and epithelial-mesenchymal transition (EMT) markers on protein levels. Immuno-histochemistry (IHC) method was adopted to assess VGLL4 protein expression in NSCLC tissues.

expression was down-regulated in NSCLC tissues and cells, and

suppressed multiplication, migration, invasion and EMT of NSCLC cells.

expression was upregulated in NSCLC tissues and cells, and

worked as a target of

. VGLL4 was down-regulated in NSCLC tissues and cells, and knockdown of VGLL4 accelerated multiplication, migration, invasion and EMT of NSCLC cells.

enhanced VGLL4 expression by competitively binding with

.

axis regulated NSCLC progression.

Circ_0006427/miR-346/VGLL4 axis regulated NSCLC progression.

It was in the early 20

century when the quest for

spermatogenesis started. In vitro spermatogenesis is critical for male cancer patients undergoing gonadotoxic treatment. Dynamic culture system creates

-like conditions. In this study, it was intended to evaluate the progression of spermatogenesis after testicular tissue culture in mini-perfusion bioreactor.

In this experimental study, 12 six-day postpartum neonatal mouse testes were removed and fragmented, placed on an agarose gel in parallel to bioreactor culture, and incubated for 8 weeks. Histological, molecular and immunohistochemical evaluations were carried out after 8 weeks.

Histological analysis suggested successful maintenance of spermatogenesis in tissues grown in the bioreactor but not on agarose gel, possibly because the central region did not receive sufficient oxygen and nutrients, which led to necrotic or degenerative changes. Molecular analysis indicated that

and

were expressed and that their expression did not differ signif supports induction of spermatogenesis for generation of haploid cells. WH-4-023 ic50 Further studies will be needed to address the fertility of the sperm generated in the bioreactor system..

Growing evidences have exposed the important roles of long noncoding RNAs (lncRNAs) in the triple negative breast cancer (TNBC) inhibition. The function of glucuronidase beta pseudogene 11 (

) in the TNBC occurrence remains obscure. To detect the function of

in TNBC progression and explore its downstream molecular mechanism.

In this experimental study, using quantitative reverse transcription real-time polymerase chain reaction (RT-qPCR), we measured the

expression in the TNBC cell lines. Gain-of-function assays, including colony formation, flow cytometry, and western blot were used to identify the probable effects of

overexpression on the malignant behaviors of TNBC cell lines. Moreover, mechanism assays, including RNA immunoprecipitation (RIP), RNA pull down and luciferase reporter assays were taken to measure the possible mechanism of

in the TNBC cell lines.

expressed at a low RNA level in the TNBC cell lines. Overexpression of GUSBP11 RNA expression inhibited the proliferation, migration, epithelial-to-mesenchymal transition (EMT) and stemness while elevated the apoptosis of the TNBC cell lines.

positively regulated the expression of sphingolipid transporter 2 (

) via acting as a competing endogenous RNA (ceRNA) of

, thereby suppressing the development of TNBC cell lines.

impedes TNBC progression via modulating the miR-579-3p/SPNS2 axis.

GUSBP11 impedes TNBC progression via modulating the miR-579-3p/SPNS2 axis.

Decellularized greater omentum (GOM) is a good extracellular matrix (ECM) source for regenerative medicine applications. The aim of the current study was to compare the efficiency of three protocols for sheep GOM decellularization based on sufficient DNA depletion and ECM content retention for tissue engineering application.

In this experimental study, in the first protocol, low concentrations of sodium dodecyl sulfate (SDS 1%), hexane, acetone, ethylenediaminetetraacetic acid (EDTA), and ethanol were used. In the second one, a high concentration of SDS (4%) and ethanol, and in the last one sodium lauryl ether sulfate (SLES 1%) were used to decellularize the GOM. To evaluate the quality of scaffold prepared with various protocols, histochemical staining, DNA, and glycosaminoglycan (GAGs) quantification, scanning electron microscopy (SEM), Raman confocal microscopy, Bradford assay, and ELISA were performed.

A comparison of DNA content showed that SDS-based protocols omitted DNA more efficiently than the SLESbased protocol. Histochemical staining showed that all protocols preserved the neutral carbohydrates, collagen, and elastic fibers; however, the SLES-based protocol removed the lipid droplets better than the SDS-based protocols. Although SEM images showed that all protocols preserved the ECM architecture, Raman microscopy, GAGs quantification, total protein, and vascular endothelial growth factor (VEGF) assessments revealed that SDS 1% preserved ECM more efficiently than the others.

The SDS 1% can be considered a superior protocol for decellularizing GOM in tissue engineering applications.

The SDS 1% can be considered a superior protocol for decellularizing GOM in tissue engineering applications.

Epigenetic alterations, including any change in DNA methylation pattern, could be the missing link of understanding radiation-induced genomic instability. Dapper, Dishevelled-associated antagonist of β-catenin homolog 2 (

) is a tumor suppressor gene regulating Wnt/β-catenin. In hepatocellular carcinoma (HCC),

is hypermethylated, while methylation status of its promoter regulates the corresponding expression. Radionuclides have been used to reduce proliferation and induce apoptosis in cancerous cells. Epigenetic impact of radionuclides as therapeutic agents for treatment of HCC is still unknown. The aim of this study was to evaluate epigenetic impact of 188Rhenium perrhenate (

ReO

) on HCC cells.

In this in vitro experimental study, HepG2 and Huh7 cells were treated with 188ReO4, receiving 55 and 73 Mega Becquerel (MBq) exposures, respectively. For cell viability measurement, live/dead staining was carried out 18, 24, and 48 hours post-exposure. mRNA expression level of

and

genes were quantifiTreatment with 188ReO4 reduced viability of HepG2 and Huh7 cells. Although DACT2 expression was increased after 188ReO4 exposure in HepG2 cells, methylation pattern of its promoter remained unchanged. This study assessed impacts of the 188ReO4 β-irradiation on expression and induction of DACT2 epigenetic aberrations as well as the correlation of this agent with viability of cells.

Cordycepin, also known as 3'-deoxyadenosine, is the main bioactive ingredient of

and possesses various pharmacological effects. This study was performed to investigate the role of cordycepin in regulating the biological behaviors of colon cancer cells and the potential mechanism behind it.

In this experimental study, after treatment of colon cancer cells with different concentrations of cordycepin, inhibition of proliferation was detected by the 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Colon cancer cell migration and invasion abilities were analyzed by wound healing and Transwell assays. Flow cytometry was performed to detect cell apoptosis. A lung metastasis model in nude mice was utilized to examine the effect of cordycepin on the metastasis of colon cancer cells in

. Western blot was used to quantify GSK3β, β-catenin and cyclin D1 expression levels.

Cordycepin inhibited colon cancer cell proliferation, migration and invasion, induced apoptosis

, and inhibited lung metastasis of colon cancer cells

. GSK-3β inhibitor (CHIR99021) treatment abolished the effects of cordycepin on cell viability, migration, invasion and apoptosis. Additionally, cordycepin promoted the expressions of GSK3β, and inhibited β-catenin and cyclin D1 in colon cancer cells, while co-treatment with CHIR99021 reversed the above effects.

Cordycepin suppresses the malignant phenotypes of colon cancer through the GSK3β/β-catenin/cyclin D1 signaling pathway.

Cordycepin suppresses the malignant phenotypes of colon cancer through the GSK3β/β-catenin/cyclin D1 signaling pathway.

The induction of immunity against cancer stem cells (CSCs) can boost the efficiency of cancer vaccines. Heat shock proteins (HSPs) are required for the successful activation of anti-tumor immune responses. Glycoprotein 96 (gp96) is a well-known HSP that promotes the cross-presentation of tumor antigens. The aim of the present study was to optimize the temperature for induction of gp96 in grade 3 breast cancer spheres.

In the experimental study, CSCs were enriched from breast tumor tissue samples and cultured in DMEM-F12 with epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), B27, and bovine serum albumin (BSA) for 22 days. The expression level of CD24 and CD44 as CSC markers was measured by flow cytometry in secondary mammospheres, and the expression of

, and

genes in CSCs was also analyzed using the real-time polymerase chain reaction (PCR). To find the optimal temperature regulation of gp96, the mammosphere was incubated at different temperatures for 1 hour, and gp96 expression was measured using the western blotting assay.