Targeting the autophagy-miRNA axis in prostate cancer: toward novel diagnostic and therapeutic strategies.

Since prostate cancer is one of the leading causes of cancer-related death, a better understanding of the molecular pathways guiding its development is imperative. A key factor in prostate cancer is autophagy, a cellular mechanism that affects both cell survival and death. Autophagy is essential in maintaining cellular homeostasis. Autophagy is a physiological mechanism wherein redundant or malfunctioning cellular constituents are broken down and recycled. It is essential for preserving cellular homeostasis and is implicated in several physiological and pathological conditions, including cancer. Autophagy has been linked to metastasis, tumor development, and treatment resistance in prostate cancer. The deregulation of miRNAs related to autophagy appears to be a crucial element in the etiology of prostate cancer. These miRNAs influence the destiny of cancer cells by finely regulating autophagic mechanisms. Numerous investigations have emphasized the dual function of specific miRNAs in prostate cancer, which alter autophagy-related pathways to function as either tumor suppressors or oncogenes. Notably, miRNAs have been linked to the control of autophagy and the proliferation, apoptosis, and migration of prostate cancer cells. To create customized therapy approaches, it is imperative to comprehend the dynamic interplay between autophagy and miRNAs in prostate cancer. The identification of key miRNAs provides potential diagnostic and prognostic markers. Unraveling the complex network of lncRNAs, like PCA3, also expands the repertoire of molecular targets for therapeutic interventions. This review explores the intricate interplay between autophagy and miRNAs in prostate cancer, focusing on their regulatory roles in cellular processes ranging from survival to programmed cell death.

LncRNAs in necroptosis: Deciphering their role in cancer pathogenesis and therapy.

Necroptosis, a controlled type of cell death that is different from apoptosis, has become a key figure in the aetiology of cancer and offers a possible target for treatment. A growing number of biological activities, including necroptosis, have been linked to long noncoding RNAs (lncRNAs), a varied family of RNA molecules with limited capacity to code for proteins. The complex interactions between LncRNAs and important molecular effectors of necroptosis, including mixed lineage kinase domain-like pseudokinase (MLKL) and receptor-interacting protein kinase 3 (RIPK3), will be investigated. We will explore the many methods that LncRNAs use to affect necroptosis, including protein-protein interactions, transcriptional control, and post-transcriptional modification. Additionally, the deregulation of certain LncRNAs in different forms of cancer will be discussed, highlighting their dual function in influencing necroptotic processes as tumour suppressors and oncogenes. The goal of this study is to thoroughly examine the complex role that LncRNAs play in controlling necroptotic pathways and how that regulation affects the onset and spread of cancer. In the necroptosis for cancer treatment, this review will also provide insight into the possible therapeutic uses of targeting LncRNAs. Techniques utilising LncRNA-based medicines show promise in controlling necroptotic pathways to prevent cancer from spreading and improve the effectiveness of treatment.

Noncoding RNAs as therapeutic targets in autophagy-related diabetic cardiomyopathy.

Diabetic cardiomyopathy, a multifaceted complication of diabetes mellitus, remains a major challenge in clinical management due to its intricate pathophysiology. Emerging evidence underscores the pivotal role of autophagy dysregulation in the progression of diabetic cardiomyopathy, providing a novel avenue for therapeutic intervention. Noncoding RNAs (ncRNAs), a diverse class of regulatory molecules, have recently emerged as promising candidates for targeted therapeutic strategies. The exploration of various classes of ncRNAs, including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs) reveal their intricate regulatory networks in modulating autophagy and influencing the pathophysiological processes associated with diabetic cardiomyopathy. The nuanced understanding of the molecular mechanisms underlying ncRNA-mediated autophagic regulation offers a rationale for the development of precise and effective therapeutic interventions. Harnessing the regulatory potential of ncRNAs presents a promising frontier for the development of targeted and personalized therapeutic strategies, aiming to ameliorate the burden of diabetic cardiomyopathy in affected individuals. As research in this field advances, the identification and validation of specific ncRNA targets hold immense potential for the translation of these findings into clinically viable interventions, ultimately improving outcomes for patients with diabetic cardiomyopathy. This review encapsulates the current understanding of the intricate interplay between autophagy and diabetic cardiomyopathy, with a focus on the potential of ncRNAs as therapeutic targets.

Pyroptosis-related non-coding RNAs emerging players in atherosclerosis pathology.

Globally, atherosclerosis a persistent inflammatory condition of the artery walls continues to be the primary cause of cardiovascular illness and death. The ncRNAs are important regulators of important signalling pathways that affect pyroptosis and the inflammatory environment in atherosclerotic plaques. Comprehending the complex interaction between pyroptosis and non-coding RNAs (ncRNAs) offers fresh perspectives on putative therapeutic targets for ameliorating cardiovascular problems linked to atherosclerosis. The discovery of particular non-coding RNA signatures linked to the advancement of atherosclerosis could lead to the creation of novel biomarkers for risk assessment and customised treatment approaches. A thorough investigation of the regulatory networks regulated by these non-coding RNAs has been made possible by the combination of cutting-edge molecular methods and bioinformatics tools. Studying pyroptosis-related ncRNAs in detail appears to be a promising way to advance our understanding of disease pathophysiology and develop focused therapeutic methods as we work to unravel the complex molecular tapestry of atherosclerosis. This review explores the emerging significance of non-coding RNAs (ncRNAs) in the regulation of pyroptosis and their consequential impact on atherosclerosis pathology.

The dual role of MiR-210 in the aetiology of cancer: A focus on hypoxia-inducible factor signalling.

Tumorigenesis exemplifies the complex process of neoplasm origination, which is characterised by somatic genetic alterations and abnormal cellular growth. This multidimensional phenomenon transforms previously dormant cells into malignant equivalents, resulting in uncontrollable proliferation and clonal expansion. Various elements, including random mutations, harmful environmental substances, and genetic predispositions, influence tumorigenesis's aetiology. MicroRNAs (miRNAs) are now recognised as crucial determinants of gene expression and key players in several biological methods, including oncogenesis. A well-known hypoxia-inducible miRNA is MiR-210, which is of particular interest because of its complicated role in the aetiology of cancer and a variation of physiological and pathological situations. MiR-210 significantly impacts cancer by controlling the hypoxia-inducible factor (HIF) signalling pathway. By supporting angiogenesis, metabolic reprogramming, and cellular survival in hypoxic microenvironments, HIF signalling orchestrates adaptive responses, accelerating the unstoppable development of tumorous growth. Targeting several components of this cascade, including HIF-1, HIF-3, and FIH-1, MiR-210 plays a vital role in modifying HIF signalling and carefully controlling the HIF-mediated response and cellular fates in hypoxic environments. To understand the complexities of this relationship, careful investigation is required at the intersection of MiR-210 and HIF signalling. Understanding this relationship is crucial for uncovering the mechanisms underlying cancer aetiology and developing cutting-edge therapeutic approaches. The current review emphasises MiR-210's significance as a vital regulator of the HIF signalling cascade, with substantial implications spanning a range of tumor pathogenesis.

Non-coding RNAs (ncRNAs) and multidrug resistance in glioblastoma: Therapeutic challenges and opportunities.

Non-coding RNAs (ncRNAs) have been recognized as pivotal regulators of transcriptional and post-transcriptional gene modulation, exerting a profound influence on a diverse array of biological and pathological cascades, including the intricate mechanisms underlying tumorigenesis and the acquisition of drug resistance in neoplastic cells. Glioblastoma (GBM), recognized as the foremost and most aggressive neoplasm originating in the brain, is distinguished by its formidable resistance to the cytotoxic effects of chemotherapeutic agents and ionizing radiation. Recent years have witnessed an escalating interest in comprehending the involvement of ncRNAs, particularly lncRNAs, in GBM chemoresistance. LncRNAs, a subclass of ncRNAs, have been demonstrated as dynamic modulators of gene expression at the epigenetic, transcriptional, and post-transcriptional levels. Disruption in the regulation of lncRNAs has been observed across various human malignancies, including GBM, and has been linked with developing multidrug resistance (MDR) against standard chemotherapeutic agents. The potential of targeting specific ncRNAs or their downstream effectors to surmount chemoresistance is also critically evaluated, specifically focusing on ongoing preclinical and clinical investigations exploring ncRNA-based therapeutic strategies for glioblastoma. Nonetheless, targeting lncRNAs for therapeutic objectives presents hurdles, including overcoming the blood-brain barrier and the brief lifespan of oligonucleotide RNA molecules. Understanding the complex relationship between ncRNAs and the chemoresistance characteristic in glioblastoma provides valuable insights into the fundamental molecular mechanisms. It opens the path for the progression of innovative and effective therapeutic approaches to counter the therapeutic challenges posed by this aggressive brain tumor. This comprehensive review highlights the complex functions of diverse ncRNAs, including miRNAs, circRNAs, and lncRNAs, in mediating glioblastoma's chemoresistance.

The complex role of MEG3: An emerging long non-coding RNA in breast cancer.

MEG3, a significant long non-coding RNA (lncRNA), substantially functions in diverse biological processes, particularly breast cancer (BC) development. Within the imprinting DLK-MEG3 region on human chromosomal region 14q32.3, MEG3 spans 35 kb and encompasses ten exons. It exerts regulatory effects through intricate interactions with miRNAs, proteins, and epigenetic modifications. MEG3's multifaceted function in BC is evident in gene expression modulation, osteogenic tissue differentiation, and involvement in bone-related conditions. Its role as a tumor suppressor is highlighted by its influence on miR-182 and miRNA-29 expression in BC. Additionally, MEG3 is implicated in acute myocardial infarction and endothelial cell function, emphasising cell-specific regulatory mechanisms. MEG3's impact on gene activity encompasses transcriptional and post-translational adjustments, including DNA methylation, histone modifications, and interactions with transcription factors. MEG3 dysregulation is linked to unfavourable outcomes and drug resistance. Notably, higher MEG3 expression is associated with enhanced survival in BC patients. Overcoming challenges such as unravelling context-specific interactions, understanding epigenetic control, and translating findings into clinical applications is imperative. Prospective endeavours involve elucidating underlying mechanisms, exploring epigenetic alterations, and advancing MEG3-based diagnostic and therapeutic approaches. A comprehensive investigation into broader signaling networks and rigorous clinical trials are pivotal. Rigorous validation through functional and molecular analyses will shed light on MEG3's intricate contribution to BC progression.

Broccoli: A Multi-Faceted Vegetable for Health: An In-Depth Review of Its Nutritional Attributes, Antimicrobial Abilities, and Anti-inflammatory Properties.

Broccoli, Brassica oleracea var. italica, has recently gained considerable attention due to its remarkable nutritional composition and numerous health benefits. In this review, the nutritional aspects of broccoli are examined, highlighting its rich nutrient content and essential bioactive compounds. The cruciferous vegetable broccoli is a rich source of several important nutrients, including fiber, vitamins (A, C, and K), minerals (calcium, potassium, and iron), and antioxidants. It has also been shown to contain bioactive compounds such as glucosinolates, sulforaphane, and indole-3-carbinol, all of which have been shown to have significant health-promoting effects. These chemicals are known to have potent antioxidant, anti-inflammatory, and anticancer effects. This review article aims to comprehensively examine the diverse spectrum of nutrients contained in broccoli and explore its medicinal potential to promote human health.

Synthesis, Crystal Structure, Antibacterial and In Vitro Anticancer Activity of Novel Macroacyclic Schiff Bases and Their Cu (II) Complexes Derived from S-Methyl and S-Benzyl Dithiocarbazate.

A series of novel macroacyclic Schiff base ligands and their Cu (II) complexes were synthesised via reacting dicarbonyls of varying chain lengths with S-methyl dithiocarbazate (SMDTC) and S-benzyl dithiocarbazate (SBDTC) followed by coordination with Cu (II) ions. X-ray crystal structures were obtained for compound 4, an SBDTC-diacetyl analogue, and Cu7, an SMDTC-hexanedione Cu (II) complex. Anticancer evaluation of the compounds showed that Cu1, an SMDTC-glyoxal complex, demonstrated the highest cytotoxic activity against MCF-7 and MDA-MB-231 breast cancer cells with IC50 values of 1.7 µM and 1.4 µM, respectively. There was no clear pattern observed between the effect of chain length and cytotoxic activity; however, SMDTC-derived analogues were more active than SBDTC-derived analogues against MDA-MB-231 cells. The antibacterial assay showed that K. rhizophila was the most susceptible bacteria to the compounds, followed by S. aureus. Compound 4 and the SMDTC-derived analogues 3, 5, Cu7 and Cu9 possessed the highest antibacterial activity. These active analogues were further assessed, whereby 3 possessed the highest antibacterial activity with an MIC of <24.4 µg/mL against K. rhizophila and S. aureus. Further antibacterial studies showed that at least compounds 4 and 5 were bactericidal. Thus, Cu1 and 3 were the most promising anticancer and antibacterial agents, respectively.

Formulation and Evaluation of Amikacin Sulfate Loaded Dextran Nanoparticles against Human Pathogenic Bacteria.

Amikacin sulfate-loaded dextran sulfate sodium nanoparticles were formulated, lyophilized (LADNP), and then analyzed. The LADNP had a -20.9 ± 8.35 mV zeta potential, PDI of 0.256, and % PDI of 67.7. The zeta average nano size of LADNP was 317.9 z. d.nm, while the dimension of an individual particle was 259.3 ± 73.52 nm, and nanoparticle conductivity in colloidal solution was 2.36 mS/cm. LADNP has distinct endothermic peaks at temperatures at 165.77 °C, according to differential scanning calorimetry (DSC). The thermogravimetric analysis (TGA) showed the weight loss of LADNP, which was observed as 95% at 210.78 °C. XRD investigation on LADNP exhibited distinct peaks at 2θ as 9.6°, 10.4°, 11.4°, 18.9°, 20.3°, 24.4°, 28.2°, 33.2°, 38.9°, and 40.4° confirming crystalline structure. The amikacin release kinetics from LADNP revealed zero order kinetics with a linear release showed zero order kinetics with 37% of drug release in 7 h and had an R2 value of 0.99. The antibacterial effect of LADNP showed broad-spectrum activity against tested human pathogenic bacteria. The preset study demonstrated that LADNP is a promising antibacterial agent.

Spectral Analysis and Antiulcer Potential of Lactuca sativa through the Amelioration of Proinflammatory Cytokines and Apoptosis Markers.

The objective of this study was to characterize the bioactive ingredients and antiulcer effects of Lactuca sativa leaves. Several bioactive chemicals were found in the cold methanolic extract of Lactuca sativa leaves after gas chromatography-mass spectrometry (GC-MS) research: 9,12-octadecadienoic acid (Z,Z)-, cyclononasiloxane, octadecamethyl-, n-hexadecanoic acid, Hexadecanoic acid, 2-hydroxy-1-(hydroxymethyl)ethyl, octadecanoic acid, 2-hydroxy-1-(hydroxymethyl)ethyl ester, 9-octadecenamide, (Z)-, hexadecanoic acid, stigmasterol, benzothiazole, ethyl iso-allocholate, and octacosane. Distinct fingerprint regions in GCMS indicated the existence of bioactive compounds. The leaf powder of Lactuca sativa (LPL) demonstrated substantial antiulcer properties at 400 mg/kg, which was almost equivalent to the standard drug at 20 mg/kg. The cytokine network was efficiently regulated by reducing the production of proinflammatory cytokines such as IL-1ß, IL-6, and TNF-α. The levels of caspase-3 and caspase-9 were also considerably lowered at p < 0.05 significant level.