https://jep.usb.ac.ir/ Journal of Epigenetics en daily 1 Wed, 01 Apr 2026 00:00:00 +0330 Wed, 01 Apr 2026 00:00:00 +0330 https://jep.usb.ac.ir/article_9586.html AbstractBackground: Alterations in cell–extracellular matrix (ECM) interactions are pivotal events that drive key hallmarks of breast cancer metastasis, including anchorage-independent growth, resistance to apoptosis, and enhanced cellular motility. Parvin alpha (Parva) and Parvin beta (Parvb), both localized at focal adhesions, are critical regulators of cell adhesion, migration, and cytoskeletal dynamics. This study aimed to investigate the potential role of Parvins in promoting the metastatic capacity of breast tumor cells.Methods: Primary (4T1T) and metastatic (4T1B and 4T1L) breast tumor cells were isolated from a murine model of metastatic breast cancer. Cell viability and migration were evaluated using MTT and wound-healing assays, respectively. Quantitative real-time PCR (RT-qPCR) was employed to analyze the expression levels of Parva and Parvb.Results: No significant differences in cell viability were observed between primary and metastatic tumor cells under both 2D and 3D culture conditions. In contrast, metastatic cells demonstrated substantially greater migratory capacity. Notably, RT-qPCR analysis revealed a significant upregulation of Parva and Parvb expression in metastatic tumor cells compared with their primary counterparts.Conclusion: Parvin α (Parva) and Parvin β (Parvb) are significantly upregulated in highly metastatic 4T1 breast tumor cells compared with their primary counterparts. This upregulation correlates with increased migratory capacity in vitro. These preliminary findings suggest a potential association of Parvins with metastatic properties; however, functional studies are required to establish causality and therapeutic relevance. https://jep.usb.ac.ir/article_9695.html Mitochondrial dysfunction and the resulting oxidative stress have been increasingly recognized as playing a significant role in the development and progression of polycystic ovary syndrome (PCOS), which is the most prevalent endocrine disorder affecting women during their reproductive years. This study was designed to explore the potential therapeutic effects of MitoQ10, a novel antioxidant specifically targeted to the mitochondria, on mitochondrial function and oxidative stress markers in a mouse model of PCOS.We focused on examining the expression levels of phosphorylated apoptosis signal-regulating kinase 1 (p-ASK1) and tumor necrosis factor receptor-associated factors 2 and 6 (TRAF2/6) in granulosa cells (GCs) obtained from a dehydroepiandrosterone (DHEA)-induced PCOS mouse model by Real-Time PCR and Western blot. Female BALB/c mice were randomly assigned to one of three experimental groups: a Control group, a PCOS group induced by DHEA, and a PCOS + MitoQ10 (500 μmol/L) group. All groups were treated for a duration of 21 days.The results of our study revealed that the expression levels of p-ASK1, TRAF2, and TRAF6 were significantly elevated in the PCOS group compared to the control group, indicating increased oxidative stress and inflammatory signaling in the PCOS model. Importantly, treatment with MitoQ10 resulted in a downregulation of these elevated expression levels (p ˂ 0.05), suggesting a mitigating effect of MitoQ10 on oxidative stress. However, it was noted that TRAF6 gene expression did not show a statistically significant difference between the MitoQ10-treated group and the PCOS group, indicating a potentially more complex regulatory mechanism for TRAF6.In conclusion, these preliminary findings provide evidence suggesting that MitoQ10, a readily available dietary supplement, holds promise as a potential effective adjunct in the treatment of PCOS. The observed beneficial effects warrant further investigation through properly designed clinical trials. https://jep.usb.ac.ir/article_9769.html Background: Colorectal cancer (CRC) remains a major cause of cancer deaths worldwide, emphasizing the need for new treatments. Although vitamin D is known to impact cell growth and apoptosis, its precise mechanisms in affecting CRC and regulating apoptosis-related genes are not fully understood. This study investigated the possible cytotoxicity of vitamin D on human colon adenocarcinoma HT-29 cells and examined changes in BAX and BCL-2 gene expression.Methods: HT29 cells were cultured and exposed to vitamin D at concentrations ranging from 50 to 3750 µg/ml for 24 hours, with untreated cells as controls. Cell viability was assessed using an MTT assay, followed by RNA extraction. The RNA was reverse-transcribed into cDNA, allowing quantitative measurement of BAX and BCL-2 transcripts through real-time PCR, with data normalized to GAPDH. Statistical analysis of cell viability was performed using one-way ANOVA and Dunnett's post-hoc tests, while differences in gene expression were examined with t-tests.Results: Vitamin D decreased HT-29 cell viability in a dose-dependent and nonlinear way (p < 0.0001), with the highest inhibition seen at concentrations between 250-500 µg/ml. However, there was no significant difference in BAX expression (p = 0.1431) or BCL-2 expression (p = 0.5943). Conclusions: These data indicate that Vitamin D can cause cytotoxicity in HT-29 cells without altering the transcriptional targets BAX/BCL-2, and may also induce cell death through other pathways such as inhibited proliferation. Overall, this suggests that Vitamin D has potential association as a complementary therapy for CRC and warrants further mechanistic research, including studies with in vivo CRC models. https://jep.usb.ac.ir/article_9779.html The diamondback moth, Plutella xylostella, is notorious for rapid evolution of resistance, often implicating cytochrome P450–mediated detoxification in control failures. This study evaluated whether geographically distinct Iranian populations exhibit consistent or divergent transcriptional responses of two candidate P450 genes following exposure to two widely used insecticide classes. We compared three field populations after exposure to acetamiprid (neonicotinoid) and cypermethrin (pyrethroid) and quantified time-dependent transcript changes in CYP321E1 and CYP9G2 at 48 h and 72 h, complemented by phylogenetic placement of both loci to contextualize sequence relatedness. CYP321E1 showed pronounced and sustained induction in the Arak population under both insecticides (≈22–68-fold after acetamiprid and ≈50–59-fold after cypermethrin across 48–72 h), whereas Karaj displayed intermediate induction with marked attenuation at 72 h under cypermethrin, and Qazvin exhibited a stronger response to acetamiprid than to cypermethrin with declining expression at 72 h. CYP9G2 responses were heterogeneous: Qazvin showed robust induction across insecticides and time points, Arak exhibited a transient increase primarily under cypermethrin at 48 h with minimal late response, and Karaj showed its clearest induction at 72 h under cypermethrin. Phylogenetic reconstructions supported clearer near-neighbor placements but weakly resolved deeper relationships, consistent with rapid P450 diversification. Collectively, these findings indicate population-specific detoxification transcriptional architectures and nominate CYP321E1/CYP9G2 as region-sensitive candidate markers to prioritize for functional validation and resistance monitoring. https://jep.usb.ac.ir/article_9812.html Insects increasingly experience climatic extremes as coupled stressors rather than isolated challenges, with high temperatures frequently co-occurring with low humidity to create compound heat–desiccation events. These hot–dry episodes threaten survival by simultaneously destabilizing proteostasis, elevating oxidative stress, and accelerating water loss, thereby compressing thermal safety margins and amplifying failure risk during and after exposure. This study synthesizes current evidence that insect stress transcriptomes are organized into coordinated gene-expression modules—rather than scattered, independent responses—and that the timing, magnitude, and integration of these modules can predict resilience, collapse, and recovery capacity. This study emphasizes a conserved “core” program centered on molecular chaperones (including HSP families), redox buffering, and damage-control pathways, which is repeatedly recruited under both heat and severe dehydration. Layered onto this core are stressor- and lineage-specific modules that govern water balance and osmotic stability, including cuticular barrier remodeling, transport and excretory regulation, osmolyte metabolism (notably trehalose pathways in extreme tolerance), and protective proteins. It further examines regulatory architectures that tune these modules—stress-activated signaling networks, transcription factors, and epigenetic or chromatin-linked mechanisms that may shape acclimation and short-term stress “memory,” while noting that strong evidence for durable, generalizable epigenetic memory remains uneven across insect taxa. Finally, it highlights emerging priorities for the field: field-realistic thermal–humidity trajectories, life-stage- and tissue-resolved sampling, multi-omics integration, and causal perturbation pipelines that move from signatures to mechanisms. Together, a modular framework clarifies why similar transcriptional activation can yield divergent outcomes across species and populations and provides a practical basis for biomarker discovery, conservation physiology, and climate-aware pest management.