The role of long non-coding RNA NORAD in digestive system tumors.

In recent years, it has been discovered that the expression of long non-coding RNAs is highly deregulated in several types of cancer and contributes to its progression and development. Recently, it has been described that in tumors of the digestive system, such as colorectal cancer, pancreatic cancer, and gastric cancer, DNA damage-activated lncRNA (NORAD) was frequently up-regulated. The purpose of this review is to elucidate the functions of NORAD in tumors of the digestive system, emphasizing its involvement in important cellular processes such as invasion, metastasis, proliferation, and apoptosis. NORAD acts as a ceRNA (competitive endogenous RNA) that sponges microRNAs and regulates the expression of target genes involved in tumorigenesis. Thus, the mechanisms underlying the effects of NORAD are complex and involve multiple signaling pathways. This review consolidates current knowledge on the role of NORAD in digestive cancers and highlights the need for further research to explore its potential as a therapeutic target. Understanding the intricate functions of NORAD could elucidate the way for innovative approaches to cancer treatment.

Biological functions and affected signaling pathways by Long Non-Coding RNAs in the immune system.

Recently, the various regulative functions of long non-coding RNAs (LncRNAs) have been well determined. Recently, the vital role of LncRNAs as gene regulators has been identified in the immune system, especially in the inflammatory response. All cells of the immune system are governed by a complex and ever-changing gene expression program that is regulated through both transcriptional and post-transcriptional processes. LncRNAs regulate gene expression within the cell nucleus by influencing transcription or through post-transcriptional processes that affect the splicing, stability, or translation of messenger RNAs (mRNAs). Recent studies in immunology have revealed substantial alterations in the expression of lncRNAs during the activation of the innate immune system as well as the development, differentiation, and activation of T cells. These lncRNAs regulate key aspects of immune function, including the manufacturing of inflammatory molecules, cellular distinction, and cell movement. They do this by modulating protein-protein interactions or through base pairing with RNA and DNA. Here we review the current understanding of the mechanism of action of lncRNAs as novel immune-related regulators and their impact on physiological and pathological processes related to the immune system, including autoimmune diseases. We also highlight the emerging pattern of gene expression control in important research areas at the intersection between immunology and lncRNA biology.

Molecular Mechanism of lncRNAs in Regulation of Breast Cancer Metastasis; a Comprehensive Review.

Although the number of breast cancer deaths has decreased, and there have been developments in targeted therapies and combination treatments for the management of metastatic illness, metastatic breast cancer is still the second most common cause of cancer-related deaths in U.S. women. Numerous phases and a vast number of proteins and signaling molecules are involved in the invasion-metastasis cascade. The tumor cells penetrate and enter the blood or lymphatic vessels, and travel to distant organs via the lymphatic or blood vessels. Tumor cells enter cell cycle arrest, adhere to capillary beds in the target organ, and then disseminate throughout the organ's parenchyma, proliferating and enhancing angiogenesis. Each of these processes is regulated by changes in the expression of different genes, in which lncRNAs play a role in this regulation. Transcripts that are longer than 200 nucleotides and do not translate into proteins are called RNAs. LncRNA molecules, whose function depends on their unique molecular structure, play significant roles in controlling the expression of genes at various epigenetic levels, transcription, and so on. LncRNAs have essential functions in regulating the expression of genes linked to cell development in healthy and pathological processes, specialization, programmed cell death, cell division, invasion, DNA damage, and spread to other parts of the body. A number of cancer types have been shown to exhibit aberrant expression of lncRNAs. In this review, we describe the general characteristics, potential molecular mechanisms and targeted therapy of lncRNAs and discuss the emerging functions of lncRNAs in breast cancer.

Non-coding RNAs in meningitis: Key regulators of immune response and inflammation.

Non-coding RNAs (ncRNAs) contain circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), and micro-ribonucleic acids (miRNAs). These RNAs receive good functionality in modulation of gene expressions & cellular roles. Recent research is shedding light on their pivotal roles in the pathophysiology of inflammatory meningitis, such as viral, fungal, or bacterial infections. This review addresses the intricate roles of non-coding RNAs (ncRNAs) that transcribe code-independent mRNA and other biological elements that control inflammation and immunological events extant during meningitis. ncRNAs, acting on a myriad of immune cell development, cytokine production, pathogen recognition, and so forth, finely orchestrate the host's immune response. Although lncRNAs and circRNAs are associated with gene networks regulating immune responses, miRNAs can precisely modulate the expression of pro- and anti-inflammatory cytokines. Moreover, ncRNAs have unique expression patterns in disease states and are stable in bio-fluids; therefore, they can serve as specific molecular biomarkers for meningitis concerning the diagnosis and prognosis. It might also be helpful to target ncRNAs as a therapeutic strategy to impact immune regulation and inflammation. Here, we review the current knowledge of how ncRNAs function in meningitis and discuss adopted approaches and perspectives and their implications for therapeutic strategies.

Prognostic cellular senescence-related lncRNAs patterns to predict clinical outcome and immune response in colon cancer.

Background: Cellular senescence (CS) is believed to be a major factor in the evolution of cancer. However, CS-related lncRNAs (CSRLs) involved in colon cancer regulation are not fully understood. Our goal was to create a novel CSRLs prognostic model for predicting prognosis and immunotherapy and exploring its potential molecular function in colon cancer. Methods: The mRNA sequencing data and relevant clinical information of GDC TCGA Colon Cancer (TCGA-COAD) were obtained from UCSC Xena platform, and CS-associated genes was acquired from the CellAge website. Pearson correlation analysis was used to identify CSRLs. Then we used Kaplan-Meier survival curve analysis and univariate Cox analysis to acquire prognostic CSRL. Next, we created a CSRLs prognostic model using LASSO and multivariate Cox analysis, and evaluated its prognostic power by Kaplan-Meier and ROC curve analysis. Besides, we explored the difference in tumor microenvironment, somatic mutation, immunotherapy, and drug sensitivity between high-risk and low-risk groups. Finally, we verified the functions of MYOSLID in cell experiments. Results: Three CSRLs (AC025165.1, LINC02257 and MYOSLID) were identified as prognostic CSRLs. The prognostic model exhibited a powerful predictive ability for overall survival and clinicopathological features in colon cancer. Moreover, there was a significant difference in the proportion of immune cells and the expression of immunosuppressive point biomarkers between the different groups. The high-risk group benefited from the chemotherapy drugs, such as Teniposide and Mitoxantrone. Finally, cell proliferation and CS were suppressed after MYOSLID knockdown. Conclusion: CSRLs are promising biomarkers to forecast survival and therapeutic responses in colon cancer patients. Furthermore, MYOSLID, one of 3-CSRLs in the prognostic model, could dramatically regulate the proliferation and CS of colon cancer.

Pyroptosis in lung cancer: The emerging role of non-coding RNAs.

Lung cancer remains an intractable malignancy worldwide, prompting novel therapeutic modalities. Pyroptosis, a lethal form of programmed cell death featured by inflammation, has been involved in cancer progression and treatment response. Simultaneously, non-coding RNA has been shown to have important roles in coordinating pattern formation and oncogenic pathways, including long non-coding RNA (lncRNAs), microRNA (miRNAs), circular RNA (circRNAs), and small interfering RNA (siRNAs). Recent studies have revealed that ncRNAs can promote or inhibit pyroptosis by interacting with key molecular players such as NLRP3, GSDMD, and various transcription factors. This dual role of ncRNAs offers a unique therapeutic potential to manipulate pyroptosis pathways, providing opportunities for innovative cancer treatments. In this review, we integrate current research findings to propose novel strategies for leveraging ncRNA-mediated pyroptosis as a therapeutic intervention in lung cancer. We explore the potential of ncRNAs as biomarkers for predicting patient response to treatment and as targets for overcoming resistance to conventional therapies.

Integrating Bioinformatics and Experimental Validation to Identify Mitochondrial Permeability Transition-Driven Necrosis-Related lncRNAs that can Serve as Prognostic Biomarkers and Therapeutic Targets in Endometrial Carcinoma.

Endometrial carcinoma (EC) is a common malignant tumor in women with high mortality and relapse rates. Mitochondrial permeability transition (MPT)-driven necrosis is a novel form of programmed cell death. The MPT-driven necrosis related lncRNAs (MRLs) involved in EC development remain unclear. We aimed to predict the outcomes of patients with EC by constructing a novel prognostic model based on MRLs and explore potential molecular functions. A risk prognostic model was developed utilizing multi-Cox regression in conjunction with the Least Absolute Shrinkage and Selection Operator (LASSO) regression algorithm, which was based on MRLs. The predictive efficacy of the model was evaluated through receiver operating characteristic (ROC) curve analysis, as well as nomogram and concordance index (C-index) assessments. Patients were categorized into high- and low-risk groups based on their median risk scores. Notably, the high-risk group exhibited significantly poorer overall survival (OS) outcomes. Gene ontology (GO) and Gene set enrichment analysis (GSEA) demonstrated that Hedgehog and cell cycle pathways were enriched in the high-risk group. Tumor Immune Dysfunction and Exclusion (TIDE) displayed that patients in the high-risk group showed a high likelihood of immune evasion and less effective immunotherapy. A significant disparity in immune function was also observed between two groups. Based on the nine-MRLs, drug sensitivity analysis identified several anticancer drugs with potential efficacy in prognosis. Meanwhile, the results demonstrated that OGFRP1 plays a carcinogenic role by affecting mitochondrial membrane permeability in EC. Therefore, the risk model constructed by nine MRLs could be used to predict the clinical outcomes and therapeutic responses in patients with EC effectively.

Targeting non-coding RNAs as a promising biomarker in peritoneal metastasis: Background, mechanism, and therapeutic approach.

Peritoneal metastasis (PM) pathophysiology is complex and not fully understood. PM, originating from gastrointestinal (GI) cancer, is a condition that significantly worsens patient prognosis due to its complex nature and limited treatment options. The non-coding RNAs (ncRNAs) have been shown to play pivotal roles in cancer biology, influencing tumorigenesis, progression, metastasis, and therapeutic resistance. Increasing evidence has demonstrated the regulatory functions of different classes of ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in PM. Identifying biomarkers for early detection of PM is a crucial step towards improving patient outcomes, and how ncRNA profiles correlate with survival rates, response to therapy, and recurrence risks have raised much attention in recent years. Additionally, exploring innovative therapeutic approaches utilizing ncRNAs, such as targeted therapy and gene silencing, may offer new horizons in treating this dire condition. Recent advances in systemic treatments and the development of novel loco-regional therapies have opened doors to multimodal treatment approaches. Radical surgeries combined with hyperthermic intraperitoneal chemotherapy (HIPEC) have shown promising results, leading to extended patient survival. Current research is focused on the molecular characterization of PM, which is crucial for early detection and developing future therapeutic strategies. By summarizing the latest findings, this study underscores the transformative potential of ncRNAs in enhancing the diagnosis, prognosis, and treatment of PM in GI cancer, paving the way for more personalized and effective clinical strategies.

Systematic profiling and analysis of growth and development responsive DE-lncRNAs in cluster bean (Cyamopsis tetragonoloba).

Long non-coding RNAs (lncRNAs) play crucial role in regulating genes involved in various processes including growth & development, flowering, and stress response in plants. The study aims to identify and characterize tissue-specific, growth & development and floral responsive differentially expressed lncRNAs (DE-lncRNAs) in cluster bean from a high-throughput RNA sequencing data. We have identified 3309 DE-lncRNAs, with an average length of 818 bp. Merely, around 4 % of DE-lncRNAs across the tissues were found to be conserved as rate of evolution of lncRNAs is high. Among the identified DE-lncRNAs, 204 were common in leaf vs. shoot, leaf vs. flower and flower vs. shoot. A total of 60 DE-lncRNAs targeted 10 protein-coding genes involved in flower development and initiation processes. We investigated 179 tissue-specific DE-lncRNAs based on tissue specificity index. Three DE-lncRNAs: Cb_lnc_0820, Cb_lnc_0430, Cb_lnc_0260 and their target genes show their involvement in floral development and stress mechanisms, which were validated by Quantitative real-time PCR (qRT-PCR). The identified DE-lncRNAs were expressed higher in flower bud than in leaf and similar expression pattern was observed in both RNA-seq data and qRT-PCR analyses. Notably, 362 DE-lncRNAs were predicted as eTM-lncRNAs with the participation of 84 miRNAs. Whereas 46 DE-lncRNAs were predicted to possess the internal ribosomal entry sites (IRES) and can encode for small peptides. The regulatory networks established between DE-lncRNAs, mRNAs and miRNAs have provided an insight into their association with plant growth & development, flowering, and stress mechanisms. Comprehensively, the characterization of DE-lncRNAs in various tissues of cluster bean shed a light on interactions among lncRNAs, miRNAs and mRNAs and help understand their involvement in growth & development and floral initiation processes. The information retrieved from the analyses was shared in the public domain in the form of a database: Cb-DElncRNAdb, and made available at http://backlin.cabgrid.res.in/Cb-DElncRNA/index.php, which may be useful for the scientific community engaged cluster bean research.

Induction of Invasive Basal Phenotype in Triple-Negative Breast Cancers by Long Noncoding RNA BORG.

BACKGROUND/OBJECTIVES: Long noncoding RNAs (lncRNAs) are known to play key roles in breast cancers; however, detailed mechanistic studies of lncRNA function have not been conducted in large cohorts of breast cancer tumors, nor has inter-donor and inter-subtype variability been taken into consideration for these analyses. Here we provide the first identification and annotation of the human BORG lncRNA gene. METHODS/RESULTS: Using multiple tumor cohorts of human breast cancers, we show that while BORG expression is strongly induced in breast tumors as compared to normal breast tissues, the extent of BORG induction varies widely between breast cancer subtypes and even between different tumors within the same subtype. Elevated levels of BORG in breast tumors are associated with the acquisition of core cancer aggression pathways, including those associated with basal tumor and pluripotency phenotypes and with epithelial-mesenchymal transition (EMT) programs. While a subset of BORG-associated pathways was present in high BORG-expressing tumors across all breast cancer subtypes, many were specific to tumors categorized as triple-negative breast cancers. Finally, we show that genes induced by heterologous expression of BORG in murine models of TNBC both in vitro and in vivo strongly overlap with those associated with high BORG expression levels in human TNBC tumors. CONCLUSION: Our findings implicate human BORG as a novel driver of the highly aggressive basal TNBC tumor phenotype.

Molecular insights into the hedgehog signaling pathway correlated non-coding RNAs in acute lymphoblastic leukemia, a bioinformatics study.

BACKGROUND: Acute lymphoblastic leukemia (ALL) is a common hematologic cancer with unique incidence and prognosis patterns in people of all ages. Recent molecular biology advances have illuminated ALL's complex molecular pathways, notably the Hedgehog (Hh) signaling system and non-coding RNAs (ncRNAs). This work aimed to unravel the molecular complexities of the link between Hh signaling and ALL by concentrating on long non-coding RNAs (lncRNAs) and their interactions with significant Hh pathway genes. METHODS: To analyze differentially expressed lncRNAs and genes in ALL, microarray data from the Gene Expression Omnibus (GEO) was reanalyzed using a systems biology approach. Hh signaling pathway-related genes were identified and their relationship with differentially expressed long non-coding RNAs (DElncRNAs) was analyzed using Pearson's correlation analysis. A regulatory network was built by identifying miRNAs that target Hh signaling pathway-related mRNAs. RESULTS: 193 DEGs and 226 DElncRNAs were found between ALL and normal bone marrow samples. Notably, DEGs associated with the Hh signaling pathway were correlated to 26 DElncRNAs. Later studies showed interesting links between DElncRNAs and biological processes and pathways, including drug resistance, immune system control, and carcinogenic characteristics. DEGs associated with the Hh signaling pathway have miRNAs in common with miRNAs already known to be involved in ALL, including miR-155-5p, and miR-211, highlighting the complexity of the regulatory landscape in this disease. CONCLUSION: The complex connections between Hh signaling, lncRNAs, and miRNAs in ALL have been unveiled in this study, indicating that DElncRNAs linked to Hh signaling pathway genes could potentially serve as therapeutic targets and diagnostic biomarkers for ALL.

To Elucidate the Effective Role of Small Molecule Regulated lncRNAs in the Tumour Microenvironment in Immunotherapy.

The tumour microenvironment is a complex ecosystem comprising tumour cells, and cancer stem cells, and support cells that facilitate cancer growth and escape from treatment. Cancer immunotherapy focuses on immunological pathways such as PD-1/PD-L1 and CTLA-4 to target cancer stem cells via immune cells. Small molecules, immune checkpoint inhibitors, are employed to impede tumour growth by targeting cellular mediators in the cell cycle and tumour microenvironment. Long non-coding RNAs (lncRNAs) affect the growth, development, motility, and differentiation of cancer cells by regulating gene expression and are therefore considered important biomarkers. Small molecules demonstrate their effects on gene expression and behaviour of cancer cells by inducing lncRNAs. This relationship between lncRNAs and small molecules is of great importance in terms of their impact on cancer and the tumour microenvironment. The evaluation of this communication in clinical trials is of critical importance for the development of therapeutic strategies. This review provides a detailed description of the role of lncRNAs and small molecules in the tumour microenvironment and their relationship with cancer stem cells. Thus, the potential of controlling lncRNAs and using anti-cancer small molecules in TME to improve the efficacy of cancer therapy was evaluated.

A multispecies study reveals the diversity and potential regulatory role of long noncoding RNAs in cucurbits.

Plant long noncoding RNAs (lncRNAs) exhibit features such as tissue-specific expression, spatiotemporal regulation, and stress responsiveness. Although diverse studies support the regulatory role of lncRNAs in model plants, our knowledge about lncRNAs in crops is limited. We employ a custom pipeline on a dataset of over 1000 RNA-seq samples across nine representative species of the family Cucurbitaceae to predict 91 209 nonredundant lncRNAs. The lncRNAs were characterized according to three confidence levels and classified by their genomic context into intergenic, natural antisense, intronic, and sense-overlapping. Compared with protein-coding genes, lncRNAs were, on average, expressed at low levels and displayed significantly higher specificity when considering tissue, developmental stages, and stress responsiveness. The evolutionary analysis indicates higher positional conservation than sequence conservation, probably linked to the conserved modular motifs within syntenic lncRNAs. Moreover, a positive correlation between the expression of intergenic/natural antisense lncRNAs and their closest/parental gene was observed. For those intergenic, the correlation decreases with the distance to the neighboring gene, supporting that their potential cis-regulatory effect is within a short-range. Furthermore, the analysis of developmental studies showed that a conserved NAT-lncRNA family is differentially expressed in a coordinated way with their cognate sense protein-coding genes. These genes code for proteins associated with phloem development, thus providing insights about the potential involvement of some of the identified lncRNAs in a developmental process. We expect that this extensive inventory will constitute a valuable resource for further research lines focused on elucidating the regulatory mechanisms mediated by lncRNAs in cucurbits.

Integrated Long Noncoding RNA and Messenger RNA Expression Analysis Identifies Molecules Specifically Associated With Resiliency and Susceptibility to Depression and Antidepressant Response.

Background: Depression involves maladaptive processes impairing an individual's ability to interface with the environment appropriately. Long noncoding RNAs (lncRNAs) are gaining traction for their role in higher-order brain functioning. Recently, we reported that lncRNA coexpression modules may underlie abnormal responses to stress in rats showing depression-like behavior. The current study explored the global expression regulation of lncRNAs and messenger RNAs (mRNAs) in the hippocampus of rats showing susceptibility (learned helplessness [LH]) or resiliency (non-LH) to depression and fluoxetine response to LH (LH+FLX). Methods: Multiple comparison analysis was performed with an analysis of variance via the aov and summary function in the R platform to identify the differential expression of mRNAs and lncRNAs among LH, non-LH, tested control, and LH+FLX groups. Weighted gene coexpression network analysis was used to identify distinctive modules and pathways associated with each phenotype. A machine learning analysis was conducted to screen the critical target genes. Based on the combined analysis, the regulatory effects of lncRNAs on mRNA expression were explored. Results: Multiple comparison analyses revealed differentially expressed mRNAs and lncRNAs with each phenotype. Integrated bioinformatics analysis identified novel transcripts, specific modules, and regulatory pairs of mRNA-lncRNA in each phenotype. In addition, the machine learning approach predicted lncRNA-regulated Spp2 and Olr25 genes in developing LH behavior, whereas joint analysis of mRNA-lncRNA pairs identified Mboat7, Lmod1, I l 18, and Rfx5 genes in depression-like behavior and Adam6 and Tpra1 in antidepressant response. Conclusions: The study shows a novel role for lncRNAs in the development of specific depression phenotypes and in identifying newer targets for therapeutic development.

We explored transcriptional signatures and regulatory patterns of mRNA and lncRNA in the rat hippocampus of a learned helplessness animal model, including stress-induced depression susceptibility and resilience and changes after antidepressant fluoxetine treatment to learned helpless rats. With the help of integrated bioinformatics analysis, we identified novel transcripts, specific modules, and mRNA-lncRNA regulatory pairs in each phenotype. This study built the foundation for the identification of specific drug targets for depression susceptibility and resilience.

Role of homeobox genes in cancer: immune system interactions, long non-coding RNAs, and tumor progression.

The intricate interplay between Homeobox genes, long non-coding RNAs (lncRNAs), and the development of malignancies represents a rapidly expanding area of research. Specific discernible lncRNAs have been discovered to adeptly regulate HOX gene expression in the context of cancer, providing fresh insights into the molecular mechanisms that govern cancer development and progression. An in-depth comprehension of these intricate associations may pave the way for innovative therapeutic strategies in cancer treatment. The HOX gene family is garnering increasing attention due to its involvement in immune system regulation, interaction with long non-coding RNAs, and tumor progression. Although initially recognized for its crucial role in embryonic development, this comprehensive exploration of the world of HOX genes contributes to our understanding of their diverse functions, potentially leading to immunology, developmental biology, and cancer research discoveries. Thus, the primary objective of this review is to delve into these aspects of HOX gene biology in greater detail, shedding light on their complex functions and potential therapeutic applications.

GLIDR-mediated regulation of tumor malignancy and cisplatin resistance in non-small cell lung cancer via the miR-342-5p/PPARGC1A axis.

BACKGROUND: Lung cancer, particularly non-small cell lung cancer (NSCLC), remains a significant cause of cancer-related mortality, with drug resistance posing a substantial obstacle to effective therapy. LncRNAs have emerged as pivotal regulators of NSCLC progression, suggesting potential targets for cancer diagnosis and treatment. Therefore, identifying new lncRNAs as therapeutic targets and comprehending their underlying regulatory mechanisms are crucial for treating NSCLC. MATERIALS AND METHODS: RNA-sequencing data from 149 lung adenocarcinoma (LUAD) patients, including 130 responders and 19 nonresponders to primary treatment, were analyzed to identify the most effective lncRNAs. The effects and regulatory pathways of the selected lncRNAs on NSCLC and cisplatin resistance were investigated. RESULTS: Glioblastoma-downregulated RNA (GLIDR) was the most effective lncRNA in nonresponsive NSCLC patients undergoing primary treatment, and it was highly expressed in NSCLC patients and those with cisplatin-resistant NSCLC. Reducing GLIDR expression enhanced cisplatin sensitivity in resistant NSCLC and decreased the malignant characteristics of NSCLC. Moreover, bioinformatic analysis and luciferase assays revealed that microRNA-342-5p (miR-342-5p) directly targets GLIDR. MiR-342-5p overexpression inhibited NSCLC cell proliferation, migration, and invasion, whereas miR-342-5p inhibition promoted NSCLC malignancy, which was rescued by suppressing GLIDR. Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PPARGC1A) was identified as a downstream target of miR-342-5p. PPARGC1A inhibition increased cisplatin sensitivity in resistant NSCLC. Moreover, PPARGC1A inhibition suppresses NSCLC malignancy, whereas PPARGC1A overexpression promoted it. Furthermore, GLIDR overexpression was found to counteract the inhibitory effects of miR-342-5p on PPARGC1A, and increased PPARGC1A expression reversed the inhibition of NSCLC malignancies caused by decreased GLIDR. CONCLUSIONS: GLIDR is a prognostic marker for cisplatin treatment in NSCLC and a therapeutic target in cisplatin-resistant NSCLC. GLIDR promotes NSCLC progression by sponging miR-342-5p to regulate PPARGC1A expression and regulates cisplatin resistance through the miR-342-5p/PPARGC1A axis, underscoring its potential as a therapeutic target in cisplatin-resistant NSCLC.

Deciphering the code: the pivotal role of lncRNAs in advancing TNBC therapy.

Triple-negative breast cancer (TNBC) represents the most formidable subtype of breast cancer, characterized by a notable dearth in targeted therapeutic options. Deciphering the underlying molecular mechanisms of TNBC is pivotal for improving patient outcomes. Recent scientific advancements have spotlighted long non-coding RNAs (lncRNAs) as key players in the genesis, progression, and metastasis of cancers. This review delineates the significant influence of lncRNAs on the advancement, detection, and neoadjuvant chemotherapy efficacy in TNBC, detailing the diverse expression patterns of aberrant lncRNAs. The paper explores the specific mechanisms by which lncRNAs regulate gene expression in both the nucleus and cytoplasm, with a special focus on their involvement in TNBC's post-transcriptional landscape. Thorough investigations into TNBC-associated lncRNAs not only forge new avenues for early diagnosis and potent treatment strategies but also highlight these molecules as promising therapeutic targets, heralding an era of personalized and precision medicine in TNBC management.

LncRNA HIF1A-AS2 promotes triple-negative breast cancer progression and paclitaxel resistance via MRPS23 protein.

Dysregulation of lncRNAs is a critical factor in the migration and invasion of tumors. Here our study reveals that lncRNA HIF1A-AS2 is highly expressed in breast cancer tissues and various TNBC cell lines. Moreover, we present compelling evidence supporting the role of HIF1A-AS2 in promoting TNBC cell proliferation, metastasis, invasion, and resistance to paclitaxel treatment. Additionally, our transcriptome sequencing analysis identifies MRPS23 as a potential downstream target protein regulated by HIF1A-AS2 and knockdown of HIF1A-AS2 leads to decreased expression of MRPS23 in TNBC cells. Moreover, MRPS23 exhibits similar effects on enhancing cell proliferation, metastasis, invasion, and paclitaxel resistance in TNBC cells. Furthermore, downregulating HIF1A-AS2 suppresses the enhanced functionality observed in TNBC cells due to upregulated MRPS23 expression. These findings suggest that modulation of MRPS23 protein expression by HIF1A-AS2 may influence cellular processes and paclitaxel sensitivity in TNBC cells.

Epithelial­derived head and neck squamous tumourigenesis (Review).

Head and neck squamous cell carcinomas (HNSCCs), a heterogeneous group of cancers that arise from the mucosal epithelia cells in the head and neck areas, present great challenges in diagnosis, treatment and prognosis due to their complex aetiology and various clinical manifestations. Several factors, including smoking, alcohol consumption, oncogenic genes, growth factors, Epstein­Barr virus and human papillomavirus infections can contribute to HNSCC development. The unpredictable tumour microenvironment adds to the complexity of managing HNSCC. Despite significant advances in therapies, the prediction of outcome after treatment for patients with HNSCC remains poor, and the 5­year overall survival rate is low due to late diagnosis. Early detection greatly increases the chances of successful treatment. The present review aimed to bring together the latest findings related to the molecular mechanisms of HNSCC carcinogenesis and progression. Comprehensive genomic, transcriptomic, metabolomic, microbiome and proteomic analyses allow researchers to identify important biological markers such as genetic alterations, gene expression signatures and protein markers that drive HNSCC tumours. These biomarkers associated with the stages of initiation, progression and metastasis of cancer are useful in the management of patients with cancer in order to improve their life expectancy and quality of life.

Long journey on the role of long non-coding RNA (lncRNA) in acute kidney injury (AKI).

Acute kidney injury (AKI) has a high rate of morbidity, death, and medical expenses, making it a worldwide public health problem. There are still few viable treatment plans for AKI despite medical advancements. A subclass of non-coding RNAs with over 200 nucleotides in length, long non-coding RNAs (lncRNAs) have a wide range of biological roles. Lately, lncRNAs have become important mediators of AKI and prospective biomarkers. However, current studies show that, via constructing the lncRNA/microRNA/target gene regulatory axis, abnormal expression of lncRNAs has been connected to significant pathogenic processes associated with AKI, such as the inflammatory response, cell proliferation, and apoptosis. In order to compete with mRNAs for binding to the same miRNAs and affect the expression of transcripts targeted by miRNAs, lncRNAs may function as competing endogenous RNAs (ceRNAs). The most widely used approach for researching the biological roles of lncRNAs is the construction of ceRNA regulation networks. Our goal in this article is to deliver an updated review of lncRNAs in AKI and to provide more knowledge on their possible applications as therapeutic targets and AKI biomarkers.