Journal of Epigenetics
Volume:4 Issue: 2, Autumn 2023

Cervical cancer is one of the most common cancers in women and is the third leading cause of cancer-related mortality. Metabolic dysregulation is a common hallmark of cancer. Reactive-oxygen-species(ROS) are oxygen metabolism byproducts that are impacted by metabolic instability. ROS can trigger cellular apoptosis as a safety switch by controlling the intrinsic mitochondrial apoptosis pathway. MSRB3(methionine sulfoxide reductase B3) can inhibit ROS-mediated-apoptosis in cervical cancer cells,promoting tumorigenesis and metastasis. In this article,the effect of miR-331-3p,and miR-338-3p on reducing gene expression is investigated.The unfavorable proteins in cervical cancer tissues were selected and obtained using the Human-Protein-Atlas(HPA) database. OncoDB was used to find differentially-expressed-genes(DEGs) linked with the cancer stage. STRING database was used to predict functional interactions of human proteins with specific genes. The upstream transcription factor, Gene Ontology analysis, and potential mechanism of MSRB3 and its interacting proteins were all investigated using Enrichr. HPA identified 223 genes linked with poor prognosis in cervical cancer patients. OncoDB was used to identify the top 1,000 DEGs related to cervical cancer patients' clinical stages. MSRB3 expression was shown to be correlated with cervical cancer patient survival and clinical stage. A tight relationship between MSRB3 expression and ROS was discovered by Reactome.According to STRING, MSRB3 interacts with two additional genes (TXN(Thioredoxin) and FXN(Frataxin)). According to GO analysis, these genes were engaged in protein-repair pathways and had oxidoreductase-activity. We discovered that MSRB3 expression is associated with poor prognosis in cervical cancer patients. Using the miRWalk database,we predicted that the miR-331-3p, miR-338-3p, and hsa-let-7b-3p have the potential to be involved in regulating MSRB3 Also, due to the TRRUST analysis, HSF2 is an upstream transcription factor of MSRB3, TXN, and FXN can be knocked down in order to suppress MSRB3 with two additional genes. Thus, treatment strategies that target MSRB3 expression may prone cervical cancer cells to apoptosis.

Epigenetic modifications are heritable changes in gene expression that do not involve changes to the core DNA sequence. These modifications can be passed down across generations. It has been proven that epigenetic alterations have a significant influence on the regulation of a plant's response to environmental stress. This article provides an overview of the various defense mechanisms that plants use when confronted with unfavorable environmental conditions. These defense mechanisms include alterations in the patterns of DNA methylation, modifications to histones, and gene silence that is mediated by tiny RNA molecules. This discussion will focus on the current state of our understanding of the hereditary and ecological factors that influence epigenetic modifications in flora and the possible consequences these factors have for an organism's response to stress. In addition, this discussion highlights the challenges and opportunities associated with investigating epigenetic alterations in flora. These include the need for advanced precision methodologies to identify epigenetic modifications and the possibility of utilizing epigenetic diversity in breeding programs. The current investigation provides a comprehensive review of the significance of epigenetics in the context of plant adaptation to environmental stress. This examination highlights the value of this field of study in the context of addressing challenges pertaining to worldwide food security.

The positive and protective effects of regular exercise on the learning and memory impairments induced by sleep deprivation (SD) have been demonstrated in previous studies, and recently, it was found that miR-191-5p by targeting BDNF as an essential factor in cognitive function causes memory and learning impairments in sleep deprivation conditions. This study aims to investigate the effects of regular treadmill exercise on the expression of miR-191-5p in sleep-deprived rats. Ovariectomized (OVX) rats are more vulnerable to the effects of sleep deprivation than intact rats. In this study, we performed our experiments on OVX female rats. MiRNAs are vital regulators of many biological functions, mainly brain functions such as learning and memory. The effect of 72 hours of sleep deprivation and four weeks of treadmill exercise on the expression of miR-191-5p and BDNF was investigated. Seventy-two hours of sleep deprivation was performed using the multiple platform method, and the exercise protocol was four weeks of regular treadmill exercise. Expression of miR-191-5p and BDNF was done using the Real-time PCR method. Sleep deprivation down-regulated the level of miR-191-5p and BDNF, all of which were ameliorated by four weeks of treadmill exercise. Despite increased BDNF expression in exercised rats, miR-191-5p did not show significant changes. The mechanism of the possible effect of exercise on the expression of BDNF was independent of its effect on the expression of miR-191-5p.

Intellectual disability (ID) consists of a broad range of disorders characterized by low general intellectual functioning (IQ below 70). ID etiologic causes are heterogeneous, ranging from environmental to chromosomal and monogenic conditions. Although many autosomal genes responsible for ID are expected, but only a small number of these have been identified and up to now most progress has been made in the area of X-linked translocation ID; but many autosomal chromosome genes play a crucial role in the development of a central nervous system. Any change which lead to lose or reduce the function or change the expression of them; high or low, even have a damaging effect on the functional protein might lead to different phenotype like developmental delay, growth retardation or intellectual disabilities.

In this paper, we discuss the importance of balanced chromosomal translocations in the etiologic cause of newborn intellectual disabilities. Balanced translocation is the result of breaking off two chromosomes and reattached in a way that the sections of two chromosomes have switched places. These rearrangements are found as de novo events in 1/2,000 live births and give rise to some congenital anomalies which is the product of submicroscopic deletions, duplications, inversion or disruption, activation, or inactivation of a gene or different genes located at or near the breakpoints in the basepair level. These apparently balanced translocations due to positional effect lead to occur abnormal phenotype. In conclusion, Cryptic genomic imbalances cause mentality are very rare condition but new technologies like NGS long-read genome sequencing could detect rapid breakpoint effects on live birth healthy and discover a new way for prenatal diagnosis.

Colorectal cancer is a common cancer in both men and women. Colorectal cancer is the third widely diagnosed cancer in the world. The emergence of nanotechnology led the researchers to introduce novel nano-products for cancer diagnosis and treatment. Treating colon cancer has difficulties associated with the inefficiency of adjuvant chemotherapy and the development of metastatic disease. In this work, CoFe2O4@Ag nanocomposite was synthesized using the Spirulina platensis extract and characterized by FT-IR (Fourier-transform infrared spectroscopy), XRD (X-Ray diffraction), SEM (Scanning electron microscopy), TEM (Transmission electron microscopy), DLS (Dynamic light scattering), Zeta potential, and EDS-mapping analyses. Then, the effect of the nanocomposite on the survival, apoptosis, and expression of the BAX and Bcl-2 genes in colon cancer cells was investigated. The spherical nanocomposite particles were synthesized properly with a size range of 20-40 nm, the zeta potential of -42 mV, and hydrodynamic size of 250 nm. The 50% inhibitory concentration (IC50) of the nanocomposite for normal and colon cancer cells was measured 256 and 65 µg/mL, respectively, indicating the higher susceptibility of cancer cells. Further, treating colon cancer cells with the nanocomposite significantly increased the frequency of apoptotic cells from 4.47 to 65.6%. In addition, the BAX and Bcl-2 genes were up-regulated by 2.7 and 1.25 folds, respectively. According to the results, the CoFe2O4@Ag could considerably inhibit colon cancer cells through the activation of the pro-apoptotic signaling pathways.

Multiple endocrine neoplasia type 1 (MEN1) is a hereditary condition manifesting as an autosomal dominant genetic pattern. This genetic anomaly is marked by the formation of tumors in diverse endocrine glands, leading to a complex array of clinical manifestations. The correlation between colorectal cancer (CRC) and MEN1 mutations remains unknown. This study aimed to report an Iranian female CRC patient with a MEN1 genetic mutation.

A 37-year-old female presented to a physician complaining of rectal lesions, tubular adenoma, and rectal adenocarcinoma, suggesting moderately differentiated colorectal adenocarcinoma symptoms. HLA typing was tested for her. Finally, whole exome sequencing (WES) was performed using the patient's DNA. Based on a standard pipeline, the variant was identified and interpreted.

The findings demonstrated a known heterozygous missense mutation in the exon 2 of the MEN1 gene, g.64577373T-G, c.209A>C, p.Asp70Ala in the patients which has a variant uncertain significant (VUS) pathogenicity. She also had no celiac disease (HLA-DQ2/DQ8 genotypes are negative).

The correlation between the identified genotype and the anatomical phenotype of the patient suggested that the identified variant can lead to colorectal abnormalities in the patient, contributing to the distinctive features of MEN1 disease. Understanding the underlying genetic mechanisms is important for diagnosing and treating this condition.