Zbp1 gene: a modulator of multiple aging hallmarks as potential therapeutic target for age-related diseases.

The Zbp1 gene has recently emerged as a potential therapeutic target for age-related diseases. Multiple studies have reported that Zbp1 plays a key role in regulating several aging hallmarks, including cellular senescence, chronic inflammation, DNA damage response, and mitochondrial dysfunction. Regarding cellular senescence, Zbp1 appears to regulate the onset and progression of senescence by controlling the expression of key markers such as p16INK4a and p21CIP1/WAF1. Similarly, evidence suggests that Zbp1 plays a role in regulating inflammation by promoting the production of pro-inflammatory cytokines, such as IL-6 and IL-1ß, through activation of the NLRP3 inflammasome. Furthermore, Zbp1 seems to be involved in the DNA damage response, coordinating the cellular response to DNA damage by regulating the expression of genes such as p53 and ATM. Additionally, Zbp1 appears to regulate mitochondrial function, which is crucial for energy production and cellular homeostasis. Given the involvement of Zbp1 in multiple aging hallmarks, targeting this gene represents a potential strategy to prevent or treat age-related diseases. For example, inhibiting Zbp1 activity could be a promising approach to reduce cellular senescence and chronic inflammation, two critical hallmarks of aging associated with various age-related diseases. Similarly, modulating Zbp1 expression or activity could also improve DNA damage response and mitochondrial function, thus delaying or preventing the development of age-related diseases. Overall, the Zbp1 gene appears to be a promising therapeutic target for age-related diseases. In the current review, we have discussed the molecular mechanisms underlying the involvement of Zbp1 in aging hallmarks and proposed to develop effective strategies to target this gene for therapeutic purposes.

Common factors among three types of cells aged in mice.

The greatest risk factor for the formation of numerous significant chronic disorders is aging. Understanding the core molecular underpinnings of aging can help to slow down the inevitable process. Systematic study of gene expression or DNA methylation data is possible at the transcriptomics and epigenetics levels. DNA methylation and gene expression are both affected by aging. Gene expression is an important element in the aging of Homo sapiens. In this work, we evaluated the expression of differentially expressed genes (DEGs), proteins, and transcription factors (TFs) in three different types of cells in mice: antibody-secreting cells, cardiac mesenchymal stromal cells, and skeletal muscle cells. The goal of this article is to uncover a common cause during aging among these cells in order to increase understanding about establishing complete techniques for preventing aging and improving people's quality of life. We conducted a comprehensive network-based investigation to establish which genes and proteins are shared by the three different types of aged cells. Our findings clearly indicated that aging induces gene dysregulation in immune, pharmacological, and apoptotic pathways. Furthermore, our research developed a list of hub genes with differential expression in aging responses that should be investigated further to discover viable anti-aging treatments.

Cell-cell communication in stem cells and cancer: Alone but in touch.

BACKGROUND: Cellular communication and signaling pathways are fundamental regulators of stem cell and cancer cell behaviors. This review explores the intricate interplay of these pathways in governing cellular behaviors, focusing on their implications for diseases, particularly cancer. OBJECTIVES: This comprehensive review aims to elucidate the significance of cellular signaling pathways in regulating the behavior of stem cells and cancer cells. It delves into the alterations in these pathways, their impact on cell fate, and their implications for developing diseases, notably cancer. The objective is to underscore the importance of understanding these signaling pathways for developing targeted therapeutic strategies. METHODS: The review critically analyzes existing literature and research findings concerning the roles of signaling pathways in stem cell behavior regulation, emphasizing their parallels and disparities in cancer cells. It synthesizes information on both direct and indirect modes of cell communication to delineate the complexity of signaling networks. RESULTS: Direct and indirect modes of cell communication intricately regulate the complex signaling pathways governing stem cell behaviors, influencing differentiation potential and tissue regeneration. Alterations in these pathways significantly impact stem cell fate, contributing to disease pathogenesis, including cancer. Understanding these signaling cascades offers insights into developing targeted therapies, particularly cancer treatment. CONCLUSION: Understanding the regulation of signaling pathways in stem cells and the specialized subset of cancer stem cells holds promise for innovative therapeutic approaches. By targeting aberrant signaling pathways, tailored interventions may improve treatment outcomes. This review underscores the critical role of signaling pathways in cellular behaviors, offering a pathway toward developing novel, more effective therapies for diverse diseases and disorders.

Unraveling molecular similarities between colorectal polyps and colorectal cancer: a systems biology approach.

BACKGROUND/AIMS: Colorectal cancer (CRC) and colorectal polyps are intimately linked, with polyps acting as precursors to CRC. Understanding the molecular mechanisms governing their development is crucial for advancing diagnosis and treatment. Employing a systems biology approach, we investigated the molecular similarities between polyp and CRC. METHODS: We analyzed gene expression profiles, protein-protein interactions, transcription factors, and gene ontology to identify common differentially expressed genes (DEGs) and unravel shared molecular pathways. RESULTS: Our analysis revealed 520 commonly dysregulated genes in polyps and CRC, serving as potential biomarkers and pivotal contributors to disease progression. Gene ontology analysis elucidated distinct biological processes associated with upregulated and downregulated DEGs in both conditions, highlighting common pathways, including signal transduction, cell adhesion, and positive regulation of cell proliferation. Moreover, protein-protein interaction networks shed light on subnetworks involved in rRNA processing, positive regulation of cell proliferation, mRNA splicing, and cell division. Transcription factor analysis identified major regulators and differentially expressed transcription factors in polyp and CRC. Notably, we identified common differentially expressed transcription factors, including ZNF217, NR3C1, KLF5, GATA6, and STAT3, with STAT3 and NR3C1 exhibiting increased expression. CONCLUSIONS: This comprehensive analysis enriches our understanding of the molecular mechanisms underlying polyp formation and CRC development, providing potential targets for further investigation and therapeutic intervention. Our findings contribute substantively to crafting personalized strategies for refining the diagnosis and treatment of polyps and CRC.

Identification of common factors among fibrosarcoma, rhabdomyosarcoma, and osteosarcoma by network analysis.

Sarcoma cancers are uncommon malignant tumors, and there are many subgroups, including fibrosarcoma (FS), which mainly affects middle-aged and older adults in deep soft tissues. Rhabdomyosarcoma (RMS), on the other hand, is the most common soft-tissue sarcoma in children and is located in the head and neck area. Osteosarcomas (OS) is the predominant form of primary bone cancer among young adults, primarily resulting from sporadically random mutations. This frequently results in the dissemination of cancer cells to the lungs, commonly known as metastasis. Mesodermal cells are the origin of sarcoma cancers. In this study, a rather radical approach has been applied. Instead of comparing homogenous cancer types, we focus on three main subtypes of sarcoma: fibrosarcoma, rhabdomyosarcoma, and osteosarcoma, and compare their gene expression with normal cell groups to identify the differentially expressed genes (DEGs). Next, by applying protein-protein interaction (PPI) network analysis, we determine the hub genes and crucial factors, such as transcription factors (TFs), affected by these types of cancer. Our findings indicate a modification in a range of pathways associated with cell cycle, extracellular matrix, and DNA repair in these three malignancies. Results showed that fibrosarcoma (FS), rhabdomyosarcoma (RMS), and osteosarcoma (OS) had 653, 1270, and 2823 differentially expressed genes (DEGs), respectively. Interestingly, there were 24 DEGs common to all three types. Network analysis showed that the fibrosarcoma network had two sub-networks identified in FS that contributed to the catabolic process of collagen via the G-protein coupled receptor signaling pathway. The rhabdomyosarcoma network included nine sub-networks associated with cell division, extracellular matrix organization, mRNA splicing via spliceosome, and others. The osteosarcoma network has 13 sub-networks, including mRNA splicing, sister chromatid cohesion, DNA repair, etc. In conclusion, the common DEGs identified in this study have been shown to play significant and multiple roles in various other cancers based on the literature review, indicating their significance.

The Epigenetic Regulation of Quiescent in Stem Cells.

This review article discusses the epigenetic regulation of quiescent stem cells. Quiescent stem cells are a rare population of stem cells that remain in a state of cell cycle arrest until activated to proliferate and differentiate. The molecular signature of quiescent stem cells is characterized by unique epigenetic modifications, including histone modifications and deoxyribonucleic acid (DNA) methylation. These modifications play critical roles in regulating stem cell behavior, including maintenance of quiescence, proliferation, and differentiation. The article specifically focuses on the role of histone modifications and DNA methylation in quiescent stem cells, and how these modifications can be dynamically regulated by environmental cues. The future perspectives of quiescent stem cell research are also discussed, including their potential for tissue repair and regeneration, their role in aging and age-related diseases, and their implications for cancer research. Overall, this review provides a comprehensive overview of the epigenetic regulation of quiescent stem cells and highlights the potential of this research for the development of new therapies in regenerative medicine, aging research, and cancer biology.

Machine learning and deep learning techniques for breast cancer diagnosis and classification: a comprehensive review of medical imaging studies.

BACKGROUND: Breast cancer is a major public health concern, and early diagnosis and classification are critical for effective treatment. Machine learning and deep learning techniques have shown great promise in the classification and diagnosis of breast cancer. PURPOSE: In this review, we examine studies that have used these techniques for breast cancer classification and diagnosis, focusing on five groups of medical images: mammography, ultrasound, MRI, histology, and thermography. We discuss the use of five popular machine learning techniques, including Nearest Neighbor, SVM, Naive Bayesian Network, DT, and ANN, as well as deep learning architectures and convolutional neural networks. CONCLUSION: Our review finds that machine learning and deep learning techniques have achieved high accuracy rates in breast cancer classification and diagnosis across various medical imaging modalities. Furthermore, these techniques have the potential to improve clinical decision-making and ultimately lead to better patient outcomes.

Cancer stem cells as therapeutic targets of pancreatic cancer.

The discovery of stem cells and their potential abilities in self-renewal and differentiation has opened a new horizon in medicine. Scientists have found a small population of stem cells in some types of cancers with the same functions as normal stem cells. There are two models for tumor progression: clonal (stochastic) and cancer stem cell (CSCs) models. According to the first model, all transformed cells in the tumor have carcinogenic potential and are able to proliferate and produce the same cells. The latter model, which has received more attention recently, considers the role of CSCs in drug resistance and tumor metastasis. Following the model, researchers have found that targeting CSCs may be a promising way in cancer therapy. This review describes CSC characteristics in general, while also focusing on CSC properties in the context of pancreatic cancer.