Circular RNAs in the KRAS pathway: Emerging players in cancer progression.

Circular RNAs (circRNAs) have been recognized as key components in the intricate regulatory network of the KRAS pathway across various cancers. The KRAS pathway, a central signalling cascade crucial in tumorigenesis, has gained substantial emphasis as a possible therapeutic target. CircRNAs, a subgroup of non-coding RNAs known for their closed circular arrangement, play diverse roles in gene regulation, contributing to the intricate landscape of cancer biology. This review consolidates existing knowledge on circRNAs within the framework of the KRAS pathway, emphasizing their multifaceted functions in cancer progression. Notable circRNAs, such as Circ_GLG1 and circITGA7, have been identified as pivotal regulators in colorectal cancer (CRC), influencing KRAS expression and the Ras signaling pathway. Aside from their significance in gene regulation, circRNAs contribute to immune evasion, apoptosis, and drug tolerance within KRAS-driven cancers, adding complexity to the intricate interplay. While our comprehension of circRNAs in the KRAS pathway is evolving, challenges such as the diverse landscape of KRAS mutant tumors and the necessity for synergistic combination therapies persist. Integrating cutting-edge technologies, including deep learning-based prediction methods, holds the potential for unveiling disease-associated circRNAs and identifying novel therapeutic targets. Sustained research efforts are crucial to comprehensively unravel the molecular mechanisms governing the intricate interplay between circRNAs and the KRAS pathway, offering insights that could potentially revolutionize cancer diagnostics and treatment strategies.

Exploring the oncogenic and tumor-suppressive roles of Circ-ADAM9 in cancer.

Circular RNAs (circRNAs) constitute a recently identified category of closed continuous loop RNA transcripts, serving as a subset of competing endogenous RNAs (ceRNAs) with the capacity to modulate genes by acting as microRNA sponges. In the context of cancer growth, numerous investigations have explored the potential functions of circRNAs, revealing their diverse functions either as oncogenes, promoting cancer progression, or as tumor suppressors, mitigating disease development. Among these, circRNA ADAM9 (Circ-ADAM9) is now recognized as an important player in a variety of mechanisms, both physiological and pathological, especially in cancer. The aberrant expression of Circ-ADAM9 has been observed across multiple human malignancies, implying a significant involvement in tumorigenesis. This comprehensive review aims to synthesize recent findings elucidating the function of Circ-ADAM9 in many malignancies. Additionally, the review explores the possibility of Circ-ADAM9 as a valuable biomarker, offering insights into its prognostic, diagnostic, and therapeutic implications. By summarizing the latest discoveries in this field, the review contributes to our understanding of the multifaceted contribution of Circ-ADAM9 in tumor biology and its potential applications in clinical settings.

Kaempferol: Paving the path for advanced treatments in aging-related diseases.

Aging-related diseases (ARDs) are a major global health concern, and the development of effective therapies is urgently needed. Kaempferol, a flavonoid found in several plants, has emerged as a promising candidate for ameliorating ARDs. This comprehensive review examines Kaempferol's chemical properties, safety profile, and pharmacokinetics, and highlights its potential therapeutic utility against ARDs. Kaempferol's therapeutic potential is underpinned by its distinctive chemical structure, which confers antioxidative and anti-inflammatory properties. Kaempferol counteracts reactive oxygen species (ROS) and modulates crucial cellular pathways, thereby combating oxidative stress and inflammation, hallmarks of ARDs. Kaempferol's low toxicity and wide safety margins, as demonstrated by preclinical and clinical studies, further substantiate its therapeutic potential. Compelling evidence supports Kaempferol's substantial potential in addressing ARDs through several mechanisms, notably anti-inflammatory, antioxidant, and anti-apoptotic actions. Kaempferol exhibits a versatile neuroprotective effect by modulating various proinflammatory signaling pathways, including NF-kB, p38MAPK, AKT, and the ß-catenin cascade. Additionally, it hinders the formation and aggregation of beta-amyloid protein and regulates brain-derived neurotrophic factors. In terms of its anticancer potential, kaempferol acts through diverse pathways, inducing apoptosis, arresting the cell cycle at the G2/M phase, suppressing epithelial-mesenchymal transition (EMT)-related markers, and affecting the phosphoinositide 3-kinase/protein kinase B signaling pathways. Subsequent studies should focus on refining dosage regimens, exploring innovative delivery systems, and conducting comprehensive clinical trials to translate these findings into effective therapeutic applications.

Osteomyelitis and non-coding RNAS: A new dimension in disease understanding.

Osteomyelitis, a debilitating bone infection, presents considerable clinical challenges due to its intricate etiology and limited treatment options. Despite strides in surgical and chemotherapeutic interventions, the treatment landscape for osteomyelitis remains unsatisfactory. Recent attention has focused on the role of non-coding RNAs (ncRNAs) in the pathogenesis and progression of osteomyelitis. This review consolidates current knowledge on the involvement of distinct classes of ncRNAs, including microRNAs, long ncRNAs, and circular RNAs, in the context of osteomyelitis. Emerging evidence from various studies underscores the potential of ncRNAs in orchestrating gene expression and influencing the differentiation of osteoblasts and osteoclasts, pivotal processes in bone formation. The review initiates by elucidating the regulatory functions of ncRNAs in fundamental cellular processes such as inflammation, immune response, and bone remodeling, pivotal in osteomyelitis pathology. It delves into the intricate network of interactions between ncRNAs and their target genes, illuminating how dysregulation contributes to the establishment and persistence of osteomyelitic infections. Understanding their regulatory roles may pave the way for targeted diagnostic tools and innovative therapeutic interventions, promising a paradigm shift in the clinical approach to this challenging condition. Additionally, we delve into the promising therapeutic applications of these molecules, envisioning novel diagnostic and treatment approaches to enhance the management of this challenging bone infection.

Unraveling NEAT1's complex role in lung cancer biology: a comprehensive review.

This review delves into the pivotal role of the long non-coding RNA NEAT1 in cancer biology, particularly in lung cancer (LC). It emphasizes NEAT1's unique subcellular localization and active involvement in gene regulation and chromatin remodeling. The review highlights NEAT1's impact on LC development and progression, including cell processes such as proliferation, migration, invasion, and resistance to therapy, positioning it as a potential diagnostic marker and therapeutic target. The complex web of NEAT1's regulatory interactions with proteins and microRNAs is explored, alongside challenges in targeting it therapeutically. The review concludes optimistically, suggesting future avenues for research and personalized LC therapies, shedding light on NEAT1's crucial role in LC. See also the Graphical abstract(Fig. 1).

Unlocking the secrets: Volatile Organic Compounds (VOCs) and their devastating effects on lung cancer.

Lung cancer (LCs) is still a serious health problem globally, with many incidences attributed to environmental triggers such as Volatile Organic Compounds (VOCs). VOCs are a broad class of compounds that can be released via various sources, including industrial operations, automobile emissions, and indoor air pollution. VOC exposure has been linked to an elevated risk of lung cancer via multiple routes. These chemicals can be chemically converted into hazardous intermediate molecules, resulting in DNA damage and genetic alterations. VOCs can also cause oxidative stress, inflammation, and a breakdown in the cellular protective antioxidant framework, all of which contribute to the growth of lung cancer. Moreover, VOCs have been reported to alter critical biological reactions such as cell growth, apoptosis, and angiogenesis, leading to tumor development and metastasis. Epidemiological investigations have found a link between certain VOCs and a higher probability of LCs. Benzene, formaldehyde, and polycyclic aromatic hydrocarbons (PAHs) are some of the most well-researched VOCs, with comprehensive data confirming their cancer-causing potential. Nevertheless, the possible health concerns linked with many more VOCs and their combined use remain unknown, necessitating further research. Identifying the toxicological consequences of VOCs in LCs is critical for establishing focused preventative tactics and therapeutic strategies. Better legislation and monitoring mechanisms can limit VOC contamination in occupational and environmental contexts, possibly reducing the prevalence of LCs. Developing VOC exposure indicators and analyzing their associations with genetic susceptibility characteristics may also aid in early identification and targeted therapies.

Dietary, addictive and habitual factors, and risk of colorectal cancer.

BACKGROUND: In Pakistan, the incidence of colorectal cancer (CRC) has sharply increased in recent years. Although several studies have reported global risk factors for CRC, no study has been conducted in Khyber Pakhtunkhwa (KPK), Pakistan, to investigate the risk factors associated with the increased CRC burden in this population. OBJECTIVES: Therefore, we conducted a clinical survey using a case-control study design to explore the risk factors associatd with CRC. METHODS: In the present study, one control was enrolled for each case. Both cases and controls were asked to complete a questionnaire to gather data. We analyzed all data using SPSS. RESULTS: Our study found that certain dietary factors, such as consuming fast food (OR: 3.0; P = 0.0001) and reusing ghee (OR: 2.45; P = 0.0001) and oil (OR: 4.30; P = 0.0001), increase the risk of CRC. Additionally, use of tobacco products like smoking cigarettes (OR: 1.91; P = 0.0001) and using snuff (OR: 3.72; P = 0.0001) significantly increases the risk of CRC. Certain habitual factors, including binge eating (OR: 2.42; P = 0.0001) and spending excessive time watching TV (OR: 1.98; P = 0.0001), also increase the odds of developing CRC. However, our study also identified some protective factors against CRC, such as consuming vegetables (OR: .41; P = 0.0001), developing healthy eating habits (OR: .61; P = 0.0001), and maintaining regular sleeping patterns (OR: .45; P = 0.0001). CONCLUSION: Given these findings, targeted health education is necessary to prevent the increase in CRC in this area. We also recommend developing and enforcing appropriate control guidelines for cancer risk factors to curb the incidence of CRC.

Immunopathology of herpes simplex virus-associated neuroinflammation: Unveiling the mysteries.

The immunopathology of herpes simplex virus (HSV)-associated neuroinflammation is a captivating and intricate field of study within the scientific community. HSV, renowned for its latent infection capability, gives rise to a spectrum of neurological expressions, ranging from mild symptoms to severe encephalitis. The enigmatic interplay between the virus and the host's immune responses profoundly shapes the outcome of these infections. This review delves into the multifaceted immune reactions triggered by HSV within neural tissues, intricately encompassing the interplay between innate and adaptive immunity. Furthermore, this analysis delves into the delicate equilibrium between immune defence and the potential for immunopathology-induced neural damage. It meticulously dissects the roles of diverse immune cells, cytokines, and chemokines, unravelling the intricacies of neuroinflammation modulation and its subsequent effects. By exploring HSV's immune manipulation and exploitation mechanisms, this review endeavours to unveil the enigmas surrounding the immunopathology of HSV-associated neuroinflammation. This comprehensive understanding enhances our grasp of viral pathogenesis and holds promise for pioneering therapeutic strategies designed to mitigate the neurological ramifications of HSV infections.

Development and Validation of Reverse-Phase High-Performance Liquid Chromatography Method for Simultaneous Estimation of Doxorubicin and Clotrimazole.

A reverse-phase high-performance liquid chromatographic (RP-HPLC) method was developed to analyze the simultaneous estimation of doxorubicin and clotrimazole. The method was achieved by Nucleodur C18 column with dimension 250 × 4.6 mm (5 µm) using gradient elution. The mobile phase contained 0.2% formic acid (pH 3.2) and acetonitrile. The flow rate was kept at 1.0 mL/min and detection and quantitation of both drugs (doxorubicin and clotrimazole) were achieved using a photodiode array detector at 276 nm, which was the isosbestic point for both drugs. The proposed method was validated according to the current International Council for Harmonization of Technical Requirements of Pharmaceuticals for Human Use guidelines for specificity, linearity, accuracy, precision, and robustness. The developed method showed a linear response (R2 > 0.999), and was accurate (recoveries 97%-103%), precise (resolution ≤1.0%), sensitive, and specific. Thus, the developed RP-HPLC method for the simultaneous estimation of both drugs was successfully validated and can be utilized for the estimation of these drugs in the formulations being developed.

From carcinogenesis to therapeutic avenues: lncRNAs and mTOR crosstalk in lung cancer.

Long non-coding RNAs (lncRNAs) have been demonstrated to have a crucial function in the modulation of the activity of genes, impacting a variety of homeostatic processes involving growth, survival, movement, and genomic consistency. Certain lncRNAs' aberrant expression has been linked to carcinogenesis, tumor growth, and therapeutic resistance. They are beneficial for the management of malignancies since they can function as cancer-causing or cancer-suppressing genes and behave as screening or prognosis indicators. The modulation of the tumor microenvironment, metabolic modification, and spread have all been linked to lncRNAs in lung cancer. Recent research has indicated that lncRNAs may interact with various mTOR signalling systems to control expression in lung cancer. Furthermore, the route can affect how lncRNAs are expressed. Emphasizing the function of lncRNAs as crucial participants in the mTOR pathway, the current review intends to examine the interactions between the mTOR cascade and the advancement of lung cancer. The article will shed light on the roles and processes of a few lncRNAs associated with the development of lung cancer, as well as their therapeutic prospects.

Exploring the role of lncrna neat1 knockdown in regulating apoptosis across multiple cancer types: A review.

Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators of gene expression, contributing significantly to a diverse range of cellular processes, including apoptosis. One such lncRNA is NEAT1, which is elevated in several types of cancer and aid in cancer growth. However, recent studies have also demonstrated that the knockdown of NEAT1 can inhibit cancer cells proliferation, movement, and infiltration while enhancing apoptosis. This article explores the function of lncRNA NEAT1 knockdown in regulating apoptosis across multiple cancer types. We explore the existing understanding of NEAT1's involvement in the progression of malignant conditions, including its structure and functions. Additionally, we investigate the molecular mechanisms by which NEAT1 modulates the cell cycle, cellular proliferation, apoptosis, movement, and infiltration in diverse cancer types, including acute myeloid leukemia, breast cancer, cervical cancer, colorectal cancer, esophageal squamous cell carcinoma, glioma, non-small cell lung cancer, ovarian cancer, prostate cancer, and retinoblastoma. Furthermore, we review the recent studies investigating the therapeutic potential of NEAT1 knockdown in cancer treatment. Targeting the lncRNA NEAT1 presents a promising therapeutic approach for treating cancer. It has shown the ability to suppress cancer cell proliferation, migration, and invasion while promoting apoptosis in various cancer types.

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.

Probing the links: Long non-coding RNAs and NF-κB signalling in atherosclerosis.

Atherosclerosis is a chronic inflammatory disease that involves the accumulation of lipids and immune cells in the arterial wall. NF-kB signaling is a key regulator of inflammation and is known to play a critical role in atherosclerosis. Recent studies have shown that lncRNAs can regulate NF-kB and contribute to the development and progression of atherosclerosis. Preliminary findings reveal significant alterations in the expression of specific lncRNAs in atherosclerotic lesions compared to healthy arterial tissue. Experimental evidence suggests that these dysregulated lncRNAs can influence the NF-kB pathway. By unravelling the crosstalk between lncRNAs and NF-kB signaling, this review aims to enhance our understanding of the molecular mechanisms underlying atherosclerosis. Identifying novel therapeutic targets and diagnostic markers may lead to developing interventions and management strategies for this prevalent cardiovascular disease. This review summarizes the current knowledge on the role of lncRNAs in NF-kB signaling in atherosclerosis and highlights their potential as therapeutic targets for this disease.

Long non-coding RNAs in lung cancer: Unraveling the molecular modulators of MAPK signaling.

Lung cancer (LC) continues to pose a significant global medical burden, necessitating a comprehensive understanding of its molecular foundations to establish effective treatment strategies. The mitogen-activated protein kinase (MAPK) signaling system has been scientifically associated with LC growth; however, the intricate regulatory mechanisms governing this system remain unknown. Long non-coding RNAs (lncRNAs) are emerging as crucial regulators of diverse cellular activities, including cancer growth. LncRNAs have been implicated in LC, which can function as oncogenes or tumor suppressors, and their dysregulation has been linked to cancer cell death, metastasis, spread, and proliferation. Due to their involvement in critical pathophysiological processes, lncRNAs are gaining attention as potential candidates for anti-cancer treatments. This article aims to elucidate the regulatory role of lncRNAs in MAPK signaling in LC. We provide a comprehensive review of the key components of the MAPK pathway and their relevance in LC, focusing on aberrant signaling processes associated with disease progression. By examining recent research and experimental findings, this article examines the molecular mechanisms through which lncRNAs influence MAPK signaling in lung cancer, ultimately contributing to tumor development.

From nature to therapy: Luteolin's potential as an immune system modulator in inflammatory disorders.

Inflammation is an essential immune response that helps fight infections and heal tissues. However, chronic inflammation has been linked to several diseases, including cancer, autoimmune disorders, cardiovascular diseases, and neurological disorders. This has increased interest in finding natural substances that can modulate the immune system inflammatory signaling pathways to prevent or treat these diseases. Luteolin is a flavonoid found in many fruits, vegetables, and herbs. It has been shown to have anti-inflammatory effects by altering signaling pathways in immune cells. This review article discusses the current research on luteolin's role as a natural immune system modulator of inflammatory signaling mechanisms, such as its effects on nuclear factor-kappa B, mitogen-activated protein kinases, Janus kinase/signal transducer and activator of transcription, and inflammasome signaling processes. The safety profile of luteolin and its potential therapeutic uses in conditions linked to inflammation are also discussed. Overall, the data point to Luteolin's intriguing potential as a natural regulator of immune system inflammatory signaling processes. More research is needed to fully understand its mechanisms of action and possible therapeutic applications.

The Burden of Cardiovascular Diseases Due to COVID-19 Pandemic.

The coronavirus disease 2019 (COVID-19) is an infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that produces respiratory symptoms and has serious consequences for people's cardiovascular systems (CVS). It is a severe issue and a major task not only for health care experts but also for governments to contain this pandemic. SARS-CoV-2 is the seventh member of the human coronavirus family to be implicated in this zoonotic outbreak. COVID-19's CV interactions are comparable to those of SARS-CoV, Middle East respiratory syndrome (MERS-CoV), and influenza. Those who have COVID-19 and underlying cardiovascular diseases (CVDs) are at a higher risk of serious illness and mortality, and disease has been linked to several direct and indirect CV consequences. COVID-19 causes CVDs such as arrhythmias, cardiac arrest, cardiogenic shock, myocarditis, stress-cardiomyopathy, and acute myocardial damage (AMD) as a consequence of acute coronary syndrome. The provision of CV care may expose health care professionals to risk as they become hosts or vectors of viral transmission. It binds to the angiotensin-converting enzyme receptor, causing constitutional and pulmonary signs in the beginning, and then as the infection advances, it affects other organs such as the gastrointestinal tract, CVS, neurological system, and so on. COVID-19 mortality is increased by underlying CVDs comorbidities.

Nanotechnology based advanced therapeutic strategies for targeting interleukins in chronic respiratory diseases.

Both communicable and non-communicable chronic respiratory conditions have accorded for suffering of millions of people of all ages and stated to be leading cause of death, morbidity, economic and social pressures, and disability-adjusted life-years (DALYs) worldwide. These illnesses impair patient's health and negatively impacts families and society, particularly in low and middle-income countries. Chronic respiratory diseases (CRDs) affect different organs of respiratory system, involving airways, parenchyma, and pulmonary vasculature. As the number of respiratory diseases are exponentially escalating but still the stakeholders are not paying attention towards its serious complications. Currently, the treatment being used primarily focusses only on alleviating symptoms of these illness rather delivering the therapeutic agent at target site for optimal care and/or prevention. Lately, extensive research is being conducted on airways and systemic inflammation, oxidative stress, airway, or parenchymal rehabilitation. From which macrophages, neutrophils, and T cells, as well as structural cells as fibroblasts, epithelial, endothelial, and smooth muscle cells have been found to be active participants that are involved in these chronic respiratory diseases. The pathogenesis of all these chronic respiratory diseases gets caused differently via mediators and proteins, including cytokines, chemokines, growth factors and oxidants. Presently, the target of prescription therapies is to reduce the inflammation of airways and relieve the airway contraction. In all studies, cytokines have been found to play an imperative role in fostering chronic airway inflammation and remodelling. Owing to the limitations of conventional treatments, the current review aims to summarize the current knowledge about the chronic respiratory disease and discuss further about the various conventional methods that can be used for treating this ailment. Additionally, it also highlights and discusses about the advanced drug delivery system that are being used for targeting the interleukins for the treatment of CRDs.