Incorporation of immunotherapies and nanomedicine to better normalize angiogenesis-based cancer treatment.

Neoadjuvant targeting of tumor angiogenesis has been developed and approved for the treatment of malignant tumors. However, vascular disruption leads to tumor hypoxia, which exacerbates the treatment process and causes drug resistance. In addition, successful delivery of therapeutic agents and efficacy of radiotherapy require normal vascular networks and sufficient oxygen, which complete tumor vasculopathy hinders their efficacy. In view of this controversy, an optimal dose of FDA-approved anti-angiogenic agents and combination with other therapies, such as immunotherapy and the use of nanocarrier-mediated targeted therapy, could improve therapeutic regimens, reduce the need for administration of high doses of chemotherapeutic agents and subsequently reduce side effects. Here, we review the mechanism of anti-angiogenic agents, highlight the challenges of existing therapies, and present how the combination of immunotherapies and nanomedicine could improve angiogenesis-based tumor treatment.

Electrochemical DNA-nano biosensor for the detection of Goserelin as anticancer drug using modified pencil graphite electrode.

Goserelin is an effective anticancer drug, but naturally causes several side effects. Hence the determination of this drug in biological samples, plays a key role in evaluating its effects and side effects. The current studies have concentrated on monitoring Goserelin using an easy and quick DNA biosensor for the first time. In this study, copper(II) oxide nanoparticles were created upon the surface of multiwalled carbon nanotubes (CuO/MWCNTs) as a conducting mediator. The modified pencil graphite electrode (ds-DNA/PA/CuO/MWCNTs/PGE) has been modified with the help of polyaniline (PA), ds-DNA, and CuO/MWCNTs nanocomposite. Additionally, the issue with the bio-electroanalytical guanine oxidation signal in relation to ds-DNA at the surface of PA/CuO/MWCNTs/PGE has been examined to determination Goserelin for the first time. It also, established a strong conductive condition to determination Goserelin in nanomolar concentration. Thus, Goserelin's determining, however, has a 0.21 nM detection limit and a 1.0 nM-110.0 µM linear dynamic range according to differential pulse voltammograms (DPV) of ds-DNA/PA/CuO/MWCNTs/PGE. Furthermore, the molecular docking investigation highlighted that Goserelin is able to bind ds-DNA preferentially and supported the findings of the experiments. The determining of Goserelin in real samples has been effectively accomplished in the last phase using ds-DNA/PA/CuO/MWCNTs/PGE.

LncRNA NEAT1 in the pathogenesis of liver-related diseases.

Nuclear paraspeckle assembly transcript 1 (NEAT1) is a long noncoding RNA (lncRNA) that is widely expressed in a variety of mammalian cell types. Altered expression levels of the lncRNA NEAT1 have been reported in liver-related disorders including cancer, fatty liver disease, liver fibrosis, viral hepatitis, and hepatic ischemia. lncRNA NEAT1 mostly acts as a competing endogenous RNA (ceRNA) to sponge various miRNAs (miRs) to regulate different functions. In regard to hepatic cancers, the elevated expression of NEAT1 has been reported to have a relation with the proliferation, migration, angiogenesis, apoptosis, as well as epithelial-mesenchymal transition (EMT) of cancer cells. Furthermore, NEAT1 upregulation has contributed to the pathogenesis of other liver diseases such as fibrosis. In this review, we summarize and discuss the molecular mechanisms by which NEAT1 contributes to liver-related disorders including acute liver failure, nonalcoholic fatty liver disease (NAFLD), liver fibrosis, and liver carcinoma, providing novel insights and introducing NEAT1 as a potential therapeutic target in these diseases.

A new vision of the efficacy of both CAR-NK and CAR-T cells in treating cancers and autoimmune diseases.

Chimeric Antigen Receptor (CAR) based therapies are becoming increasingly important in treating patients. CAR-T cells have been shown to be highly effective in the treatment of hematological malignancies. However, harmful therapeutic barriers have been identified, such as the potential for graft-versus-host disease (GVHD), neurotoxicity, and cytokine release syndrome (CRS). As a result, CAR NK-cell therapy is expected to be a new therapeutic option. NK cells act as cytotoxic lymphocytes, supporting the innate immune response against autoimmune diseases and cancer cells by precisely detecting and eliminating malignant cells. Genetic modification of these cells provides a dual approach to the treatment of AD and cancer. It can be used through both CAR-independent and CAR-dependent mechanisms. The use of CAR-based cell therapies has been successful in treating cancer patients, leading to further investigation of this innovative treatment for alternative diseases, including AD. The complementary roles of CAR T and CAR NK cells have stimulated exploration in this area. Our study examines the latest research on the therapeutic effectiveness of these cells in treating both cancer and ADs.

The mechanisms behind the dual role of long non-coding RNA (lncRNA) metastasis suppressor-1 in human tumors: Shedding light on the molecular mechanisms.

When the expression levels of metastasis suppressor-1 (MTSS1) were discovered to be downregulated in a metastatic cancer cell line in 2002, it was proposed that MTSS1 functioned as a suppressor of metastasis. The 755 amino acid long protein MTSS1 connects to actin and organizes the cytoskeleton. Its gene is located on human chromosome 8q24. The suppressor of metastasis in metastatic cancer was first found to be MTSS1. Subsequent reports revealed that MTSS1 is linked to the prevention of metastasis in a variety of cancer types, including hematopoietic cancers like diffuse large B cell lymphoma and esophageal, pancreatic, and stomach cancers. Remarkably, conflicting results have also been documented. For instance, it has been reported that MTSS1 expression levels are elevated in a subset of melanomas, hepatocellular carcinoma associated with hepatitis B, head and neck squamous cell carcinoma, and lung squamous cell carcinoma. This article provides an overview of the pathological effects of lncRNA MTSS1 dysregulation in cancer. In order to facilitate the development of MTSS1-based therapeutic targeting, we also shed light on the current understanding of MTS1.

A comprehensive review of lncRNA CRNDE in cancer progression and pathology, with a specific glance at the epithelial-mesenchymal transition (EMT) process.

It has been suggested that the long non-coding RNAs (lncRNAs), such as colorectal neoplasia differentially expressed (CRNDE), may contribute to the formation of human cancer. It is yet unknown, though, what therapeutic significance CRNDE expression has for different forms of cancer. CRNDE has recently been proposed as a possible diagnostic biomarker and prognostic pred for excellent specificity and sensitivity in cancer tissues and plasma. To provide the groundwork for potential future therapeutic uses of CRNDE, we briefly overview its biological action and related cancer-related pathways. Next, we mainly address the impact of CRNDE on the epithelial-mesenchymal transition (EMT). The epithelial-mesenchymal transition, or EMT, is an essential biological mechanism involved in the spread of cancer.

Getting to know ovarian cancer: Focusing on the effect of LncRNAs in this cancer and the effective signaling pathways.

This article undertakes a comprehensive investigation of ovarian cancer, examining the complex nature of this challenging disease. The main focus is on understanding the role of long non-coding RNAs (lncRNAs) in the context of ovarian cancer (OC), and their regulatory functions in disease progression. Through extensive research, the article identifies specific lncRNAs that play significant roles in the intricate molecular processes of OC. Furthermore, the study examines the signaling pathways involved in the development of OC, providing a detailed comprehension of the underlying molecular mechanisms. By connecting lncRNA dynamics with signaling pathways, this exploration not only advances our understanding of ovarian cancer but also reveals potential targets for therapeutic interventions. The findings open up opportunities for targeted treatments, highlighting the importance of personalized approaches in addressing this complex disease and driving progress in ovarian cancer research and treatment strategies.

COX 2-inhibitors; a thorough and updated survey into combinational therapies in cancers.

Cyclooxygenase (COX) enzymes are pivotal in inflammation and cancer development. COX-2, in particular, has been implicated in tumor growth, angiogenesis, and immune evasion. Recently, COX-2 inhibitors have arisen as potential therapeutic agents in cancer treatment. In addition, combining COX inhibitors with other treatment modalities has demonstrated the potential to improve therapeutic efficacy. This review aims to investigate the effects of COX inhibition, both alone and in combination with other methods, on signaling pathways and carcinogenesis in various cancers. In this study, a literature search of all major academic databases was conducted (PubMed, Scholar google), including the leading research on the mechanisms of COX-2, COX-2 inhibitors, monotherapy with COX-2 inhibitors, and combining COX-2-inhibitors with chemotherapeutic agents in tumors. The study encompasses preclinical and clinical evidence, highlighting the positive findings and the potential implications for clinical practice. According to preclinical studies, multiple signaling pathways implicated in tumor cell proliferation, survival, invasion, and metastasis can be suppressed by inhibiting COX. In addition, combining COX inhibitors with chemotherapy drugs, targeted therapies, immunotherapies, and miRNA-based approaches has enhanced anti-tumor activity. These results suggest that combination therapy has the potential to overcome resistance mechanisms and improve treatment outcomes. However, caution must be exercised when selecting and administering combination regimens. Not all combinations of COX-2 inhibitors with other drugs result in synergistic effects; some may even have unfavorable interactions. Therefore, personalized approaches that consider the specific characteristics of the cancer and the medications involved are crucial for optimizing therapeutic strategies. In conclusion, as monotherapy or combined with other methods, COX inhibition bears promise in modulating signaling pathways and inhibiting carcinogenesis in various cancers. Additional studies and well-designed clinical trials are required to completely elucidate the efficacy of COX inhibition and combination therapy in enhancing cancer treatment outcomes. This narrative review study provides a detailed summary of COX-2 monotherapy and combination targeted therapy in cancer treatment.

Artificial intelligence in cancer diagnosis: Opportunities and challenges.

Since cancer is one of the world's top causes of death, early diagnosis is critical to improving patient outcomes. Artificial intelligence (AI) has become a viable technique for cancer diagnosis by using machine learning algorithms to examine large volumes of data for accurate and efficient diagnosis. AI has the potential to alter the way cancer is detected fundamentally. Still, it has several disadvantages, such as requiring a large amount of data, technological limitations, and ethical concerns. This overview looks at the possibilities and restrictions of AI in cancer detection, as well as current applications and possible future developments. We can better understand how to use AI to improve patient outcomes and reduce cancer mortality rates by looking at its potential for cancer detection.

Novel and potential therapy options for a range of cancer diseases: Using Flavonoid.

Cancer is a complex group of diseases characterized by the uncontrolled growth and spread of abnormal cells in the body. These abnormal cells can form tumors or invade nearby tissues and organs, leading to a range of health problems. There are many different types of cancer, which can be categorized based on the location of the primary tumor, the type of cell involved, and the stage of the disease. Some common types of cancer include breast cancer, lung cancer, colon cancer, prostate cancer, and skin cancer. Nanoparticles are very small particles, typically ranging in size from 1 to 100 nanometers, that have unique physical and chemical properties. These properties make them attractive for use in a variety of applications, including cancer treatment. Flavonoids, which are natural compounds found in fruits, vegetables, and other plant-based foods, have been extensively studied for their potential role in cancer prevention and treatment. Flavonoids have been shown to possess a wide range of biological activities, including antioxidant, anti-inflammatory, anti-cancer, and anti-metastatic effects.

LncRNA-miRNA interaction is involved in colorectal cancer pathogenesis by modulating diverse signaling pathways.

LncRNAs function as molecular sponges for miRNAs to control their availability for targeting mRNA molecules. This procedure indirectly regulates the expression of cancer-related genes. Some lncRNAs also directly interact with miRNAs, leading to their degradation or sequestration, which can negatively impact gene expression. miRNAs, on the other hand, play a critical role in controlling the expression of genes, including oncogenes and tumor suppressor genes. Multiple types of cancer have been linked to the onset and progression of miRNA dysregulation. Even though there is a lot of potential for treating CRC by targeting the LncRNA-miRNA axis, several challenges remain to be overcome. The specificity of the targeting approach, delivery methods, resistance, safety, and cost-effectiveness are critical research areas that must be addressed to advance this field and improve treatment outcomes for people with CRC.

A comprehension of signaling pathways and drug resistance; an insight into the correlation between microRNAs and cancer.

Despite the development of numerous therapies, cancer remains an incurable disease due to various factors, including drug resistance produced by cancer cells. MicroRNAs (miRNAs) regulate different target genes involved in biological and pathological processes, including cancer, through post-transcriptional mechanisms. The development of drug resistance in cancer treatment is a significant barrier because it decreases drug uptake, cellular transport, and changes in proteins involved in cell proliferation, survival, and apoptotic pathways. Numerous studies have found a connection between miRNAs and the development of drug resistance in cancer cells. This paper provides a broad overview of how miRNAs regulate signaling pathways and influence treatment resistance in different cancers.

Involving stemness factors to improve CAR T-cell-based cancer immunotherapy.

Treatment with chimeric antigen receptor (CAR) T cells indicated remarkable clinical responses with liquid cancers such as hematological malignancies; however, their therapeutic efficacy faced with many challenges in solid tumors due to severe toxicities, antigen evasion, restricted and limited tumor tissue trafficking and infiltration, and, more importantly, immunosuppressive tumor microenvironment (TME) factors that impair the CAR T-cell function adds support survival of cancer stem cells (CSCs), responsible for tumor recurrence and resistance to current cancer therapies. Therefore, in-depth identification of TME and development of more potent CAR platform targeting CSCs may overcome the raised challenges, as presented in this review. We also discuss recent stemness-based innovations in CAR T-cell production and engineering to improve their efficacy in vivo, and finally, we propose solutions and strategies such as oncolytic virus-based therapy and combination therapy to revive the function of CAR T-cell therapy, especially in TME of solid tumors in future.

Inflammatory diseases: Function of LncRNAs in their emergence and the role of mesenchymal stem cell secretome in their treatment.

One of the best treatments for inflammatory diseases such as COVID-19, respiratory diseases and brain diseases is treatment with stem cells. Here we investigate the effect of stem cell therapy in the treatment of brain diseases.Preclinical studies have shown promising results, including improved functional recovery and tissue repair in animal models of neurodegenerative diseases, strokes,and traumatic brain injuries. However,ethical implications, safety concerns, and regulatory frameworks necessitate thorough evaluation before transitioning to clinical applications. Additionally, the complex nature of the brain and its intricate cellular environment present unique obstacles that must be overcome to ensure the successful integration and functionality of genetically engineered MSCs. The careful navigation of this path will determine whether the application of genetically engineered MSCs in brain tissue regeneration ultimately lives up to the hype surrounding it.

Experimental and theoretical investigations of Erbium complex: DNA/BSA interaction, anticancer and antibacterial studies.

To assess the biological potential of an Er complex that contains a 2,2'-bipyridine ligand, various techniques such as multispectral and molecular modeling procedures were utilized to examine its DNA-binding ability, BSA binding affinity, antimicrobial effects, and anticancer properties. By analyzing fluorescent information and employing the vant' Hoff equation, important parameters such as the innate docking coefficient (Kb), Stern-Volmer coefficient (KSV), and thermodynamic properties including modifications in liberated energy (ΔG°), enthalpy (∆H°), and entropy (∆S°) were determined. The trial findings suggest that the compound can bind to DNA, primarily through groove binding. Additionally, the engagement between the Er compound and the protein BSA was examined using emission spectroscopy technique, revealing a powerful binding affinity between the compound and BSA. The Er complex binds to BSA primarily via hydrogen links and van der Waals forces, as indicated by the adverse values of ΔH° and ∆S°. Through a static quenching process, the complex significantly reduces the intrinsic fluorescence of BSA. Molecular binding calculations and rivalrous binding trials confirm that this compound dock to hydrophobic remains found in site III of BSA. Additionally, the Er complex demonstrates promising results in terms of its anticancer and antimicrobial activities based on screening tests.

LncRNA PVT1: as a therapeutic target for breast cancer.

A significant number of women are identified with breast cancer (BC) every year, making it among the most prevalent malignancies and one of the leading causes of mortality globally. Despite significant progress in understanding BC pathogenesis and treatment options, there is still a need to identify new therapeutic targets and develop more effective treatments. LncRNAs have been discovered as biomarkers and a promising target for various cancers, including BC. PVT1 is a particular one of these lncRNAs, and research has indicated that it has a significant impact on the appearance and progression of BC.PVT1 is an attractive therapeutic target for BC due to its role in promoting cancer cell growth, metastasis and invasion. In addition to its potential as a treatment strategy, PVT1 may also have diagnostic value in BC. In this article, we will discuss targeting PVT1 as a treatment strategy for BC.

Hyperbaric oxygen therapy and coenzyme Q10 synergistically attenuates damage progression in spinal cord injury in a rat model.

BACKGROUND: Identifying effective spinal cord injury (SCI) treatments remains a major challenge, and current approaches are still unable to effectively improve its. Currently, we investigated the combined effects of hyperbaric oxygen (HBO) along with coenzyme Q10 (CoQ10) in the recovery of SCI in rats. MATERIAL AND METHODS: Ninety female mature Sprague-Dawley rats were allocated into five equal groups, including; sham group, SCI group, HBO group (underwent SCI and received HBO), CoQ10 group (underwent SCI and received CoQ10), and HBO+CoQ10 group (underwent SCI and received HBO plus CoQ10). Tissue samples at the lesion site were obtained for evaluation of stereological, immunohistochemical, biochemical, molecular. Also, functional tests were performed to evaluate of behavioral properties. RESULTS: We found that a significant increase in stereological parameters, biochemical factors (GSH, SOD and CAT), IL-10 gene expression and behavioral functions (BBB and EMG Latency) in the treatment groups, especially HBO+CoQ10 group, compared to SCI group. In addition, MDA levels, the density of apoptotic cells, as well as expression of inflammatory genes (TNF-α and IL-1ß) were considerably reduced in the treatment groups, especially HBO+CoQ10 group, compared to SCI group. CONCLUSION: We conclude that co-administration of HBO and HBO+CoQ10 has a synergistic neuroprotective effects in animals undergoing SCI.