Lung cancer is a prevalent malignancy and the leading cause of cancer-related deaths, posing a significant threat to human health. Despite advancements in treatment, the prognosis for lung cancer patients remains poor due to late diagnosis, cancer recurrence, and drug resistance. Epigenetic research, particularly in microRNAs, has introduced a new avenue for cancer prevention and treatment. MicroRNAs, including miR-137, play a vital role in tumor development by regulating various cellular processes. MiR-137 has garnered attention for its tumor-suppressive properties, with studies showing its potential in inhibiting cancer progression. In lung cancer, miR-137 is of particular interest, with numerous reports exploring its role and mechanisms. A comprehensive review is necessary to consolidate current evidence. This review highlights recent studies on miR-137 in lung cancer, covering cell proliferation, migration, apoptosis, drug resistance, and therapy, emphasizing its potential as a biomarker and therapeutic target for lung cancer treatment and prognosis.

This study aimed to determine the expression levels of the autophagy markers Beclin-1 and p62 in patients with diffuse large B-cell lymphoma (DLBCL) and explore the association between autophagy and disease prognosis. The expression of Beclin-1 and p62 was investigated in patients with DLBCL (n=60) and patients with reactive lymphoproliferative disease (RLD; n=20) using immunohistochemistry. The association between the clinical characteristics of patients with DLBCL and autophagy status was further analyzed. Beclin-1 levels were increased in patients with RLD compared to those with DLBCL, but the difference was not statistically significant (P>0.05). p62 levels in patients with DLBCL were significantly higher than those in patients with RLD (P<0.05). Beclin-1 expression was associated only with the Ann Arbor stage (P<0.05), whereas p62 expression was associated with the Ann Arbor stage, International Prognostic Index score, extranodal involvement, and Ki-67 index (P<0.05). Beclin-1 and p62 levels were not associated with short-term treatment efficacy in patients with DLBCL. Survival analysis showed that Beclin-1 expression had no significant effect on 2-year progression-free survival (PFS) or overall survival (OS) (P>0.05). However, high p62 expression in patients with DLBCL was associated with reduced 2-year PFS compared with that of patients with low p62 expression (P<0.05); the 2-year OS was not affected (P>0.05). Our results demonstrate that autophagic activity affects the prognosis of patients with DLBCL; the lower the autophagic activity, the shorter the PFS. Targeted p62 knockout may be a novel therapeutic strategy for the treatment of patients with DLBCL.

Colon cancer is a significant public health issue, and a deeper understanding of the molecular fundamentals [16] ehind is required to improve sensitivity and curability. This research explored the gene NDUFAF4 as a target of concern due to its link to a mitochondrial function and protein \"Relatively of liver tumorigenesis\", which remains unclear is attributable to its inclusion into the complex I (CI) pathway. The gene ontology analysis, in turn, showed that NDUFAF4 is a key player in several critical biological phases linked to mitochondrial function and energy metabolism. Furthermore, survival analysis displayed that there was a strong correlation between NDUFAF4 expression and the patients\' longevity suggesting that this factor may be important in colon cancer prognosis as well. The TCGA data proved that NDUFAF4 is elevated in colon cancer making the results of the analysis reported credible. All of the above justified the understanding of the role and importance of NDUFAF4 in treating each colon cancer patient as a molecular target. The findings help in understanding the colon cancer pathogenesis and suggest ways for developing more efficient diagnosis and treatment of the disease. SIGNIFICANCE: This research explored the gene NDUFAF4 as a target of concern due to its link to a mitochondrial function and protein \"Relatively of liver tumorigenesis\", which remains unclear is attributable to its inclusion into the complex I (CI) pathway. Using a comprehensive approach to Gene Ontology analysis, Protein-Protein Interaction network modelling, survival analysis, KEGG pathway analysis, and validation using TCGA data, we identified the activities of NDUFAF4 in colon cancer. The Gene Ontology analysis, in turn, showed that NDUFAF4 is a key player in several critical biological phases linked to mitochondrial function and energy metabolism. The construction of the PPI network illustrates the interactors of NDUFAF4, the functional association protein within the cellular regulatory networks. In addition, survival analysis indicated that there was a considerable relationship between the expression of NDUFAF4 and patient survival, indicating its potential role as a prognostic factor in colon cancer. KEGG pathway analysis suggested that NDUFAF4 plays a role in thermogenesis and mitochondrial biogenesis, biological processes that should be targeted due to their implication in cellular metabolism and cancer onset. The use of TCGA information confirmed the upregulation of NDUFAF4 in colon cancer, thus making the findings of the analysis reported dependable. Overall, our study provided necessary information on the role and significance of NDUFAF4, a potential molecular target in colon cancer cases. These present findings enhance our knowledge of the pathogenesis of colon cancer and open new opportunities for designing novel diagnostic and therapeutic approaches to improve patient outcomes.

Over the last fifteen years, numerous studies have sought to decipher the role of lipoprotein-associated phospholipase A2 (Lp-PLA2) in vascular inflammation-related diseases, notably atherosclerosis. Despite the disappointing results of clinical trials using the Lp-PLA2 inhibitor darapladib, new pathophysiological, epidemiological and genetic data have enabled the development of new inhibitors. Recent studies also show that Lp-PLA2 is involved in vascular inflammation-related diseases other than atherosclerosis (ischemic stroke, Alzheimer\'s disease and vascular dementia, diabetes, cancers…), and inhibition of Lp-PLA2 could have beneficial therapeutic in these diseases. This review aims to present new data on Lp-PLA2 and to evaluate its current interest as a biomarker but also as a therapeutic target.

BACKGROUND: Focal segmental glomerulosclerosis (FSGS), a histologic pattern of injury in the glomerulus, is one of the leading glomerular causes of end-stage renal disease (ESRD) worldwide. Despite extensive research, the underlying biological alterations causing FSGS remain poorly understood. Studying variations in gene expression profiles offers a promising approach to gaining a comprehensive understanding of FSGS molecular pathogenicity and identifying key elements as potential therapeutic targets. This work is a meta-analysis of gene expression profiles from glomerular samples of FSGS patients. The main aims of this study are to establish a consensus list of differentially expressed genes in FSGS, validate these findings, understand the disease\'s pathogenicity, and identify novel therapeutic targets.
METHODS: After a thorough search in the GEO database and subsequent quality control assessments, seven gene expression datasets were selected for the meta-analysis: GSE47183 (GPL14663), GSE47183 (GPL11670), GSE99340, GSE108109, GSE121233, GSE129973, and GSE104948. The random effect size method was applied to identify differentially expressed genes (meta-DEGs), which were then used to construct a regulatory network (STRING, MiRTarBase, and TRRUST) and perform various pathway enrichment analyses. The expression levels of several meta-DEGs, specifically ADAMTS1, PF4, EGR1, and EGF, known as angiogenesis regulators, were analyzed using quantitative reverse transcription polymerase chain reaction (RT-qPCR).
RESULTS: The identified 2,898 meta-DEGs, including 665 downregulated and 669 upregulated genes, were subjected to various analyses. A co-regulatory network comprising 2,859 DEGs, 2,688 microRNAs (miRNAs), and 374 transcription factors (TFs) was constructed, and the top molecules in the network were identified based on degree centrality. Part of the pathway enrichment analysis revealed significant disruption in the angiogenesis regulatory pathways in the FSGS kidney. The RT-qPCR results confirmed an imbalance in angiogenesis pathways by demonstrating the differential expression levels of ADAMTS1 and EGR1, two key angiogenesis regulators, in the FSGS condition.
CONCLUSIONS: In addition to presenting a consensus list of differentially expressed genes in FSGS, this meta-analysis identified significant distortions in angiogenesis-related pathways and factors in the FSGS kidney. Targeting these factors may offer a viable strategy to impede the progression of FSGS.

UNASSIGNED: Psoriatic arthritis (PsA) is a debilitating chronic condition characterized by inflammation of the joints, bones, enthesis, and skin. The pivotal role of interleukin-23 (IL-23) in the pathogenesis of PsA has become increasingly evident. This proinflammatory cytokine is markedly elevated in patients with PsA, suggesting its potential as a therapeutic target. Consequently, IL-23 inhibitors have emerged as promising first-line biologic treatments for PsA.
UNASSIGNED: This review delves into the immunopathogenic mechanisms of IL-23 at the cellular and molecular levels in PsA. Furthermore, it provides the recent efficacy and safety profiles of IL-23 inhibitors. We conducted a literature search in PubMed for the following terms: \'IL-23 and psoriatic arthritis,\' \'Ustekinumab,\' \'Guselkumab,\' \'Risankizumab,\' and \'Tildrakizumab.\' In addition, we retrieved clinical trials involving IL-23 inhibitors registered in ClinicalTrials.gov, EudraCT, and ICTRP.
UNASSIGNED: Despite the promising outcomes observed with IL-23 inhibitors, several challenges persist. The long-term effects of these agents require further investigation through prospective studies, and their limited accessibility worldwide necessitates urgent attention. Additionally, ongoing research is warranted to explore other potential drug targets within the IL-23/IL-23 R axis. The development of reliable biomarkers could greatly enhance early detection, tailored management strategies, and personalized treatment approaches for patients with PsA.

Long non-coding RNAs (lncRNAs) have been identified as important participants in several biological functions, particularly their complex interactions with the KRAS pathway, which provide insights into the significant roles lncRNAs play in cancer development. The KRAS pathway, a central signaling cascade crucial for cell proliferation, survival, and differentiation, stands out as a key therapeutic target due to its aberrant activation in many human cancers. Recent investigations have unveiled a myriad of lncRNAs, such as H19, ANRIL, and MEG3, intricately modulating the KRAS pathway, influencing both its activation and repression through various mechanisms, including epigenetic modifications, transcriptional regulation, and post-transcriptional control. These lncRNAs function as fine-tuners, delicately orchestrating the balance required for normal cellular function. Their dysregulation has been linked to the development and progression of multiple malignancies, including lung, pancreatic, and colorectal carcinomas, which frequently harbor KRAS mutations. This scrutiny delves into the functional diversity of specific lncRNAs within the KRAS pathway, elucidating their molecular mechanisms and downstream effects on cancer phenotypes. Additionally, it underscores the diagnostic and prognostic potential of these lncRNAs as indicators for cancer detection and assessment. The complex regulatory network that lncRNAs construct within the context of the KRAS pathway offers important insights for the creation of focused therapeutic approaches, opening new possibilities for precision medicine in oncology. However, challenges such as the dual roles of lncRNAs in different cancer types and the difficulty in therapeutically targeting these molecules highlight the ongoing debates and need for further research. As ongoing studies unveil the complexities of lncRNA-mediated KRAS pathway modulation, the potential for innovative cancer interventions becomes increasingly promising.

The compilation of ligand and structure-based molecular modeling methods has become an important practice in virtual screening applied to drug discovery. This systematic review addresses and ranks various virtual screening strategies to drive the selection of the optimal method for studies that have as their starting point a multi-ligand investigation and investigation based on the protein structure of a therapeutic target. This study shows examples of applications and an evaluation based on the objective and problematic of a series of virtual screening studies present in the ScienceDirect® database. The results showed that the molecular docking technique is widely used in scientific production, indicating that approaches that use protein structure as a starting point are the most promising strategy for drug discovery that relies on virtual screening-based research.

This editorial discusses a recently published paper in the World Journal of Gastroenterology. Our research focuses on p53\'s regulatory mechanism for controlling ferroptosis, as well as the intricate connection between ferroptosis and liver diseases. Ferroptosis is a specific form of programmed cell death that is de-pendent on iron and displays unique features in terms of morphology, biology, and genetics, distinguishing it from other forms of cell death. Ferroptosis can affect the liver, which is a crucial organ responsible for iron storage and meta-bolism. Mounting evidence indicates a robust correlation between ferroptosis and the advancement of liver disorders. P53 has a dual effect on ferroptosis through various distinct signaling pathways. However, additional investigations are required to clarify the regulatory function of p53 metabolic targets in this complex association with ferroptosis. In the future, researchers should clarify the mechanisms by which ferroptosis and other forms of programmed cell death contribute to the progression of liver diseases. Identifying and controlling important regulatory factors associated with ferroptosis present a promising therapeutic strategy for liver disorders.

Progranulin (PGRN), a multifunctional growth factor-like protein expressed by a variety of cell types, serves an important function in the physiologic and pathologic processes of fibrotic diseases, including wound healing and the inflammatory response. PGRN was discovered to inhibit pro-inflammation effect by competing with tumor necrosis factor-alpha (TNF-α) binding to TNF receptors. Notably, excessive tissue repair in the development of inflammation causes tissue fibrosis. Previous investigations have indicated the significance of PGRN in regulating inflammatory responses. Recently, multiple studies have shown that PGRN was linked to fibrogenesis, and was considered to monitor the formation of fibrosis in multiple organs, including liver, cardiovascular, lung and skin. This paper is a comprehensive review summarizing our current knowledge of PGRN, from its discovery to the role in fibrosis. This is followed by an in-depth look at the characteristics of PGRN, consisting of its structure, basic function and intracellular signaling. Finally, we will discuss the potential of PGRN in the diagnosis and treatment of fibrosis.