Progress in Biophysics & Molecular Biology最新文献

Gastric cancer (GC), particularly in East Asia, is among the most prevalent cancers with high mortality rates. According to recent epidemiological data, patients with GC account for over a quarter of all cancer incidences and approximately one third of cancer-related deaths in East Asia. Liver metastasis (LM) is not only a common form of GC distant metastasis but also poses a major challenge to the prognosis and treatment of patients with advanced GC. Increasing evidence has shown that the gut-liver axis plays a pivotal role in maintaining the stomach-liver-gut homeostasis. Exosomes are small secreted vesicles enriched with specific proteins, lipids, and nucleic acids. These vesicles exhibit significant activities in signal transmission to adjacent or distant cells in the gut-liver axis, as well as in remodeling the tumor microenvironment. Some research have pointed out that exosomes promote LM of various cancers. However, there still lack of complete and systematic review on how exosomes affect GC-LM. In this article, we present a comprehensive description to explore the role of GC-derived exosomes in the occurrence and development of metastatic hepatocellular carcinoma (HCC).

Vinculin, a crucial adhesion plaque protein, plays a significant role in cell morphology and tissue development. Dysregulation of focal adhesion proteins has been linked to numerous diseases, including cardiovascular conditions, gastrointestinal disorders, and cancer. Recent studies increasingly highlight vinculin's involvement in the progression of these diseases; however, a comprehensive review remains lacking. Therefore, an in-depth and timely review is essential to consolidate the latest findings on vinculin's role in disease mechanisms. This study aims to examine how vinculin coordinates a complex network of signaling pathways across various pathological contexts.

One of the most important goals of contemporary biology is to understand the principles of the molecular order underlying the complex dynamic architecture of cells. Here, we present an overview of the main driving forces involved in the cellular molecular complexity and in the emergent functional dynamic structures, spanning from the most basic molecular organization levels to the complex emergent integrative systemic behaviors. First, we address the molecular information processing which is essential in many complex fundamental mechanisms such as the epigenetic memory, alternative splicing, regulation of transcriptional system, and the adequate self-regulatory adaptation to the extracellular environment. Next, we approach the biochemical self-organization, which is central to understand the emergency of metabolic rhythms, circadian oscillations, and spatial traveling waves. Such a complex behavior is also fundamental to understand the temporal compartmentalization of the cellular metabolism and the dynamic regulation of many physiological activities. Numerous examples of biochemical self-organization are considered here, which show that practically all the main physiological processes in the cell exhibit this type of dynamic molecular organization. Finally, we focus on the biochemical self-assembly which, at a primary level of organization, is a basic but important mechanism for the order in the cell allowing biomolecules in a disorganized state to form complex aggregates necessary for a plethora of essential structures and physiological functions. In total, more than 500 references have been compiled in this review. Due to these main sources of order, systemic functional structures emerge in the cell, driving the metabolic functionality towards the biological complexity.

Gastric cancer (GC) remains a significant global health burden due to its high aggressiveness, early metastasis, and poor prognosis. Despite advances in chemotherapy and targeted therapies, drug resistance remains a major obstacle to improving patient outcomes. Integrins, a family of transmembrane receptors, play a pivotal role in mediating tumor growth, invasion, and drug resistance by interacting with the tumor microenvironment (TME) and regulating signaling pathways such as Wnt/β-catenin, FAK, and MAPK. This review highlights the critical functions of various integrin subunits (e.g., α5, αv, β1, β3, β6) in promoting GC progression and their involvement in chemoresistance mechanisms. Additionally, integrins modulate immune cell infiltration and stromal cell interactions within the TME, further complicating GC treatment. Emerging evidence suggests that targeting integrins, either through inhibitors or integrin-specific therapeutic strategies, holds potential in overcoming drug resistance and improving clinical outcomes. This review underscores the need for further exploration of integrins as therapeutic targets in GC and suggests promising avenues for integrin-based therapies in personalized medicine.

Ovarian cancer is one of the most prevalent gynaecological malignancies. The rapid development of single-cell RNA sequencing (scRNA-seq) has allowed scientists to use this technique to study ovarian cancer development, heterogeneity, and tumour environment. Although multiple original research articles have reported the use of scRNA-seq in understanding ovarian cancer and how therapy resistance occurs, there is a lack of a comprehensive review that could summarize the findings from multiple studies. Therefore, this review aimed to fill this gap by comparing and summarizing the results from different studies that have used scRNA-seq in understanding ovarian cancer development, heterogeneity, tumour microenvironment, and treatment resistance. This review will begin with an overview of scRNA-seq workflow, followed by a discussion of various applications of scRNA-seq in studying ovarian cancer. Next, the limitations and future directions of scRNA-seq in ovarian cancer research will be presented.

The objective of this systematic review and meta-analysis was to assess the carcinogenic effects of extremely low frequency magnetic fields (ELF-MF) by analyzing animal and comet assay studies. We have performed a global meta-analysis on all the animal studies on the relation between ELF-MF and cancer incidence and separate meta-analyses on the incidence of cancer, leukemia, lymphoma, breast cancer, brain cancer and DNA damage assessed with the comet assay. Of the 5145 references identified, 71 studies have been included in our systematic review and 22 studies in our meta-analyses. Our global meta-analysis indicated that ELF-MF exposure had no significant impact on the incidence of cancers in rodents (19 studies, OR = 1.10; 95% CI 0.91-1.32). However, our separate meta-analyses showed that ELF-MF increased the odds of developing leukemia in mice (4 studies, OR = 4.45; 95% CI 1.90-10.38) but not in rats. Our systematic review also suggests that ELF-MF can damage DNA in certain cell types like brain cells. Nevertheless, a meta-analysis on three comet assay studies indicated that ELF-MF did not increase DNA damage in neuroblastoma cells (SMD = -0.08; 95% CI -0.18-0.01). Overall, our results suggest that exposure to ELF-MF does not represent a major hazard for mammals and the carcinogenic effects of these magnetic fields could be limited to leukemia.

The intersection of electromagnetic radiation and neuronal communication, focusing on the potential role of biophoton emission in brain function and neurodegenerative diseases is an emerging research area. Traditionally, it is believed that neurons encode and communicate information via electrochemical impulses, generating electromagnetic fields detectable by EEG and MEG. Recent discoveries indicate that neurons may also emit biophotons, suggesting an additional communication channel alongside the regular synaptic interactions. This dual signaling system is analyzed for its potential in synchronizing neuronal activity and improving information transfer, with implications for brain-like computing systems. The clinical relevance is explored through the lens of neurodegenerative diseases and intrinsically disordered proteins, where oxidative stress may alter biophoton emission, offering clues for pathological conditions, such as Alzheimer's and Parkinson's diseases. The potential therapeutic use of Low-Level Laser Therapy (LLLT) is also examined for its ability to modulate biophoton activity and mitigate oxidative stress, presenting new opportunities for treatment. Here, we invite further exploration into the intricate roles the electromagnetic phenomena play in brain function, potentially leading to breakthroughs in computational neuroscience and medical therapies for neurodegenerative diseases.

The Cohesion Theory of the ascent of water in trees is a quiet triumph of modern science. Besides hydrodynamics, the physics of transpiration involves capillarity, evaporation and osmosis - phenomena which all have a history of considerable theoretical confusion. The aim of this paper is to supplement existing accounts of this physics in the plant science literature.

N⁶-methyladenosine (m⁶A) modification is the most common epitranscriptomic modification in eukaryotic RNA and has garnered extensive attention in the context of breast cancer research. The m⁶A modification significantly impacts tumorigenesis and tumor progression by regulating RNA stability, splicing, translation, and degradation. In this review we summarize recent advances in understanding the roles of m⁶A modification in the mechanisms underlying angiogenesis and vasculogenic mimicry in breast cancer. We review how m⁶A modification and associated transcripts influence relevant factors by affecting key factors and signaling pathways, highlighting the interactions among m⁶A "writers," "erasers," and "readers," and their overall impact on tumor angiogenesis and vasculogenic mimicry, as well as potential new therapeutic targets.

Glioblastoma (GBM) is a very deadly type of brain tumor with a poor prognosis and a short survival rate. Recent advancements in understanding GBM's molecular and genetic characteristics have led to the development of various therapeutic and diagnostic strategies. Key elements such as microRNAs, lncRNAs, exosomes, angiogenesis, and chromatin modifications are highlighted, alongside significant epigenetic alterations that impact therapy and diagnosis. Despite these advancements, molecular classifications have not improved patient outcomes due to intratumoral diversity complicating targeted therapies. In this article, it is tried to emphasize the potential of investigating the epigenetic landscape of GBM, particularly identifying patients with diffuse hypermethylation at gene promoters associated with better outcomes. Integrating epigenetic and genetic data has enhanced the identification of glioma subtypes with high diagnostic precision. The reversibility of epigenetic changes offers promising therapeutic prospects, as recent insights into the "epigenetic orchestra" suggest new avenues for innovative treatment modalities for this challenging cancer. In this review article, we focus on the roles of translational elements and their alterations in the context of GBM diagnosis and therapy.