A comprehensive review on Ellagic acid in breast cancer treatment: From cellular effects to molecular mechanisms of action.

Globally, breast cancer (BC) is the leading cause of cancer-related deaths in women. Hence, developing a therapeutic plan to overcome the disease is crucial. Numerous factors such as endogenous hormones and environmental factors may play a role in the pathophysiology of BC. Regarding the multi-modality treatment of BC, natural compounds like ellagic acid (EA) received has received increased interest in antitumor efficacy with lower adverse effects. Based on the results of this comprehensive review, EA has multiple effects on BC cells including (1) suppresses the growth of BC cells by arresting the cell cycle in the G0/G1 phase, (2) suppresses migration, invasion, and metastatic, (3) stimulates apoptosis in MCF-7 cells via TGF-ß/Smad3 signaling axis, (4) inhibits CDK6 that is important in cell cycle regulation, (5) binds to ACTN4 and induces its degradation via the ubiquitin-proteasome pathway, inducing decreased cell motility and invasion in BC cells, (6) inhibits the PI3K/AKT pathway, and (7) inhibits angiogenesis-associated activities including proliferation (reduces VEGFR-2 tyrosine kinase activity). In conclusion, EA exhibits anticancer activity through various molecular mechanisms that influence key cellular processes like apoptosis, cell cycle, angiogenesis, and metastasis in BC. However, further researches are essential to fully elucidate its molecular targets and implications for clinical applications.

The Anti-hypoxia Potentials of Trans-sodium Crocetinate in Hypoxiarelated Diseases: A Review.

Crocetin is a kind of apocarotenoid carboxylic acid extracted from saffron (Crocus sativus L.), which is effective in upregulating tissue oxygenation. However, crocetin is difficult to solubilize. It was shown that the trans isomer of crocetin is effective in improving oxygen diffusivity, while its cis isomer appears not to be. Hence, the isolated trans isomer of crocetin or trans-sodium crocetinate (TSC) can be used instead of crocetin. It is shown that TSC can upregulate hypoxic tissue oxygenation and be effective in treating some hypoxia-related diseases. Moreover, experimental and clinical studies have reported no adverse effects following TSC treatment, even at high doses. The current study will discuss the potential role of TSC in hemorrhagic shock, ischemia, brain tumor radiotherapy, and others.

In vitro BSA-binding, antimicrobial, and antitumor activity against human cancer cell lines of two lanthanide (III) complexes.

The investigation involved examining the binding of two lanthanide complexes, specifically those containing Holmium (Ho) and Dysprosium (Dy), with a ligand called 1, 10-phenanthroline (phen), and bovine serum albumin (BSA). The evaluation was carried out utilizing fluorescence measurements, Förster theory, and docking studies. The findings indicated that both the Ho-complex and Dy-complex possessed a significant ability to quench the emission of the protein. Furthermore, the primary mechanism of interaction was identified as a static process. The Kb values indicate a strong tendency of these complexes for binding with BSA. The Kb values show the strangely high affinity of BSA to complexes and the following order for binding affinity: Ho-complex > Dy-complex. The thermodynamic parameters were found to be negative, affirming that the main forces driving the interaction between BSA and the lanthanide complexes are van der Waals engagement and hydrogen bonds. Additionally, the investigation included the examination of competition site markers, and molecular docking proposed that the engagement sites of the Ho-complex and Dy-complex with BSA were predominantly located in site 3 (specifically, subdomain IB). Moreover, the Ho-complex and Dy-complex were specifically chosen for their potential anticancer and antimicrobial properties. Consequently, these complexes could present promising prospects as novel candidates for anti-tumor and antibacterial applications.

STAT3 Signaling Axis and Tamoxifen in Breast Cancer: A Promising Target for Treatment Resistance.

Signal transducers and activators of transcription 3 (STAT 3) have been proposed to be responsible for breast cancer development. Moreover, evidence depicted that upregulation of STAT3 is responsible for angiogenesis, metastasis, and chemo-resistance of breast cancer. Tamoxifen (TAM) resistance is a major concern in breast cancer management which is mediated by numerous signaling pathways such as STAT3. Therefore, STAT3 targeting inhibitors would be beneficial in breast cancer treatment. The information on the topic in this review was gathered from scientific databases such as PubMed, Scopus, Google Scholar, and ScienceDirect. The present review highlights STAT3 signaling axis discoveries and TAM targeting STAT3 in breast cancer. Based on the results of this study, we found that following prolonged TAM treatment, STAT3 showed overexpression and resulted in drug resistance. Moreover, it was concluded that STAT3 plays an important role in breast cancer stem cells, which correlated with TAM resistance.

The cross-talk between LncRNAs and JAK-STAT signaling pathway in cancer.

Long non-coding RNAs (lncRNAs) are non-coding RNAs that were transcribed from the human genome and have become important regulators in a number of cellular activities, mostly via controlling gene expression. A growing body of evidence shows that lncRNAs regulate various factors to impact various biological activities that are related to tumorigenesis, including the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway. lncRNAs influence the JAK-STAT signaling pathway either by directly targeting or via indirectly modulating other upstream or downstream pathways' components like members of the suppressor of cytokine signaling (SOCS) family, and other genes that regulate cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition. Furthermore, lncRNAs can act as downstream effectors of the JAK-STAT pathway and mediates tumorigenesis. The relationship between JAK-STAT signaling and lncRNAs differs among various types of cancers. Besides, lncRNAs, as biological molecules, have been shown to play a dual role in either tumorigenesis or tumor suppression in various cancers. In this review, we focus on the reciprocated regulation and functions of lncRNAs and the JAK-STAT signaling pathway in cancer, as well as narrate the latest research progress on this association. A deeper understanding of this correlation may simplify the recognition of potential targets for clinical therapeutics.

Functions, mechanisms, and clinical applications of lncRNA LINC00857 in cancer pathogenesis.

Emerging data indicated that long noncoding RNAs (lncRNAs) are crucial players in the biological processes via regulating epigenetics, transcription, and protein translation. A novel lncRNA, LINC00857, was indicated to upregulate in several types of cancer. In addition, LINC00857 was functionally related to the modulation of the cancer-linked behaviors, including invasion, migration, proliferation, epithelial-mesenchymal transition (EMT), cell cycle, and apoptosis. The importance of LINC00857 in cancer onset and development proposed that LINC00857 has major importance in the cancer progression and may be considered as a novel prognostic/diagnostic biomarker as well as a treatment target. Here, we retrospectively investigate the available progress in biomedical research investigating the functions of LINC00857 in cancer, focusing on finding the molecular mechanisms affecting various cancer-related behaviors and exploring its clinical applications.

Targeting Nrf2 signaling pathway by quercetin in the prevention and treatment of neurological disorders: An overview and update on new developments.

BACKGROUND: Neurological disorders (NLDs) are widely acknowledged as a significant public health concern worldwide. Stroke, Alzheimer's disease (AD), and traumatic brain injury (TBI) are three of these disorders that have sparked major study attention. Neurological dysfunction, protein buildup, oxidation and neuronal injury, and aberrant mitochondria are all prevalent neuropathological hallmarks of these disorders. The signaling cascade of nuclear factor erythroid 2 related factor 2 (Nrf2) shares all of them as a common target. Several studies have found that overexpression of Nrf2 is a promising treatment method in NLDs. Effective treatment of these disorders continues to be a universal concern regardless of various medicines. In order to treat a variety of neurological problems, organic remedies may provide an alternative treatment. It has been demonstrated that polyphenols like quercetin (Que) offer considerable capabilities for treating NLDs. One of Que's greatest key targets, Nrf2, has the capacity to control the production of a number of cytoprotective enzymes that exhibit neuroprotective, detoxifying, and antioxidative effects. Additionally, Que enhanced the expression of Nrf2 and inhibited alterations in the shape and death of neurons in the hippocampus. OBJECTIVE: In this review, we have focused on Que's medicinal prospects as a neuroprotective drug. METHODS: PubMed, Scopus, Science Direct, and Google Scholar were used to search articles for this study. RESULTS: The findings of this research demonstrate that (1) Que protected the blood-brain barrier via stimulating Nrf2 in animal stroke, which alleviated ischemic reperfusion and motor dysfunction. (2) By triggering the Nrf2 pathway, Que reduced the neuroinflammation and oxidative damage brought on by TBI in the cortex. (3) In an experimental model of AD, Que enhanced cognitive function by decreasing A1-4, antioxidant activity, and Nrf2 levels in the brain. CONCLUSION: We discuss recent research on Que-mediated Nrf2 expression in the management of several NLDs in this paper.

The association of in-utero exposure to polycyclic aromatic hydrocarbons and umbilical liver enzymes.

BACKGROUND: The adverse health influences of polycyclic aromatic hydrocarbons (PAHs) exposures have been examined in several previous research. However, the evidence on the health influences of PAHs exposure during pregnancy and childhood is scarce, with no study on the infant's liver function. Therefore, in this study, the association of in-utero exposure to particulate matter-bound PAHs (PM-bound PAHs) on the umbilical liver enzymes was investigated. METHODS: A total of 450 mother-pair samples were assessed in this cross-sectional study in Sabzevar, Iran (2019-2021). The concentrations of PM-bound PAHs were estimated based on spatiotemporal models at residential addresses. The umbilical cord blood alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) were measured as indicators of infant's liver function. The association of PM-bound PAHs with umbilical liver enzymes was evaluated using multiple linear regression, controlled for relevant covariates. The quantile g-computation (g-comp) was used to investigate the combined impact of the 15 PAHs on liver function biomarkers. RESULTS: Higher levels of total 4-ring PAHs, Dibenzo[a,h]anthrancene, Anthracene, Pyrene, Benzo[a]anthracene, Phenanthrene, Fluorene, Acenaphthylene and Naphthalene were associated with higher umbilical ALP. An increase in total 5-ring PAHs, Benzo[g,h,i]perylene, Benzo[a]pyrene and Chrysene was associated with higher umbilical AST levels. Each 1 ng/m3 increase in exposure to Benzo[g,h,i]perylene was related with 182.21 U/L (95 % CI: 116.11, 248.31, P < 0.01) increase in umbilical GGT. PAHs mixture exposure was positively associated with higher umbilical AST and ALT, while no significant associations were noted for ALP and GGT. We observed a potentially stronger association for girls compared to boys based on umbilical ALT and AST. However, for GGT and ALP, these associations were stronger for boys compared to girls. CONCLUSION: Overall our findings suggested that exposure to PAHs during pregnancy had adverse effects on infant's liver function.

Metabolomic profiling of bacterial biofilm: trends, challenges, and an emerging antibiofilm target.

Biofilm-related infections substantially contribute to bacterial illnesses, with estimates indicating that at least 80% of such diseases are linked to biofilms. Biofilms exhibit unique metabolic patterns that set them apart from their planktonic counterparts, resulting in significant metabolic reprogramming during biofilm formation. Differential glycolytic enzymes suggest that central metabolic processes are markedly different in biofilms and planktonic cells. The glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is highly expressed in Staphylococcus aureus biofilm progenitors, indicating that changes in glycolysis activity play a role in biofilm development. Notably, an important consideration is a correlation between elevated cyclic di-guanylate monophosphate (c-di-GMP) activity and biofilm formation in various bacteria. C-di-GMP plays a critical role in maintaining the persistence of Pseudomonas aeruginosa biofilms by regulating alginate production, a significant biofilm matrix component. Furthermore, it has been demonstrated that S. aureus biofilm development is initiated by several tricarboxylic acid (TCA) intermediates in a FnbA-dependent manner. Finally, Glucose 6-phosphatase (G6P) boosts the phosphorylation of histidine-containing protein (HPr) by increasing the activity of HPr kinase, enhancing its interaction with CcpA, and resulting in biofilm development through polysaccharide intercellular adhesion (PIA) accumulation and icaADBC transcription. Therefore, studying the metabolic changes associated with biofilm development is crucial for understanding the complex mechanisms involved in biofilm formation and identifying potential targets for intervention. Accordingly, this review aims to provide a comprehensive overview of recent advances in metabolomic profiling of biofilms, including emerging trends, prevailing challenges, and the identification of potential targets for anti-biofilm strategies.

The Effects of Curcumin on Astrocytes in Common Neurodegenerative Conditions.

Neurodegenerative diseases are age-related, multifactorial, and complicated conditions that affect the nervous system. In most cases, these diseases may begin with an accumulation of misfolded proteins rather than decay before they develop clinical symptoms. The progression of these diseases can be influenced by a number of internal and external factors, including oxidative damage, neuro-inflammation, and the accumulation of misfolded amyloid proteins. Astrocytes, with the highest abundance among the cells of the mammalian central nervous system, perform several important activities, such as maintaining brain homeostasis and playing a role in the neurodegenerative condition onset and progress. Therefore, these cells have been considered to be potential targets for managing neurodegeneration. Curcumin, with multiple special properties, has been effectively prescribed to manage various diseases. It has hepato-protective, anti-carcinogenic, cardio-protective, thrombo-suppressive, anti-inflammatory, chemo-therapeutic, anti-arthritic, chemo-preventive, and anti-oxidant activities. In the current review, the effects of curcumin on astrocytes in common neurodegenerative conditions, such as Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer's disease, and Parkinson's disease, are discussed. Hence, it can be concluded that astrocytes play a critical role in neurodegenerative diseases, and curcumin is able to directly modulate astrocyte activity in neurodegenerative diseases.

Malignant function of nuclear factor-kappaB axis in prostate cancer: Molecular interactions and regulation by non-coding RNAs.

Prostate carcinoma is a malignant situation that arises from genomic alterations in the prostate, leading to changes in tumorigenesis. The NF-κB pathway modulates various biological mechanisms, including inflammation and immune responses. Dysregulation of NF-κB promotes carcinogenesis, including increased proliferation, invasion, and therapy resistance. As an incurable disease globally, prostate cancer is a significant health concern, and research into genetic mutations and NF-κB function has the efficacy to facilitate the introduction of novel therapies. NF-κB upregulation is observed during prostate cancer progression, resulting in increased cell cycle progression and proliferation rates. Additionally, NF-κB endorses resistance to cell death and enhances the capacity for metastasis, particularly bone metastasis. Overexpression of NF-κB triggers chemoresistance and radio-resistance, and inhibition of NF-κB by anti-tumor compounds can reduce cancer progression. Interestingly, non-coding RNA transcripts can regulate NF-κB level and its nuclear transfer, offering a potential avenue for modulating prostate cancer progression.

Associated health risk assessment due to exposure to BTEX compounds in fuel station workers.

OBJECTIVES: The purpose of this review study was to assess the risk of exposure to BTEX compounds in gas station workers and operators. CONTENT: The main components of BTEX compounds are Benzene, Toluene, Ethyl benzene and Xylene. Petroleum, coal large quantities in crude oil and its products are the most important sources of BTEX compounds. These compounds have both high solubility (found in surface and underground waters) and evaporate quickly. Gas stations are one of the most important sources of emission of these compounds in communities. Workers who work in these places have a lot of exposure to these compounds. Exposure to these dangerous compounds can cause many problems for workers. This study was a narrative review article. According to different databases: PubMed, Web of Science, Springer, Cochran and Science Direct, 451 articles were retrieved. 55 full-text articles entered into the analysis process. Finally, 32 articles were selected in this study. The search was restricted to English-language papers published between 1 February 1995 and 13 August 2022. The results of our study showed that the carcinogenic risk (ILCR) for gas station workers in Bangkok (1.82 ∗ 10-4 - 2.50 ∗ 10-4), Shiraz (6.49∗10-7 - 1.27 ∗ 10-5), Brazil (1.82 ∗ 10-4), Ardabil (390∗10-6 ± 1884 ∗ 10-6) and Johannesburg (3.78 ∗ 10-4) was high. The non-cancer risk for oil industry workers of Dilijan (Iran) who were exposed to toluene was also reported in the range of 10-6∗176. The health of gas station workers is affected by exposure to BTEX and gasoline vapor emissions. According to the result this study, BTEX compounds cause genotoxic changes, chromosomal and genetic abnormalities. SUMMARY AND OUTLOOK: Genotoxicity at high levels in gas station workers can cause cancerous and non-cancerous risks. Improving the production process of diesel fuel and gasoline in refineries, using periodical examinations of workers and operators at gas and fuel stations, using Euro 4 and 5 fuels, and replacing worn out cars can play an important role in reducing the emission of BTEX compounds and thus reducing health risks and carcinogenic.

Overview of the role and action mechanism of microRNA-128 in viral infections.

Recently in vivo and in vitro studies have provided evidence establishing the significance of microRNAs (miRNAs) in both physiological and pathological conditions. In this regard, the role of miRNA-128 (miR-128) in health and diseases has been found, and its critical regulatory role in the context of some viral diseases has been recently identified. For instance, it has been found that miR-128 can serve as an antiviral mediator and significantly limit the replication and dissemination of human immunodeficiency virus type 1 (HIV-1). Besides, it has been noted that poliovirus receptor-related 4 (PVRL4) is post-transcriptionally regulated by miR-128, representing possible miRNA targets that can modulate measles virus infection. Of note, the downregulation of seminal exosomes eca-miR-128 is associated with the long-term persistence of Equine arteritis virus (EAV) in the reproductive tract, and this particular miRNA is a putative regulator of chemokine ligand 16 (C-X-C motif) as determined by target prediction analysis. In this review, the latest information on the role and action mechanism of miR-128 in viral infections will be summarized and discussed in detail.

Cardiac Injury Following Chemo/Radiation Therapy: An Updated Review on Mechanisms and Therapeutic Approaches.

Cardiovascular disorders are among the critical side effects of cancer therapy. Damage to the function and normal structure of the heart can cause serious threats to patients that are being treated for cancer. Cardiovascular complications may be induced by various types of chemotherapy drugs and also radiation therapy. The severity of cardiovascular toxicity depends on several factors, such as types of drugs, tumor location for radiotherapy, the presence of cardiac disease history, the dose of drugs or ionizing radiation, etc. Radiotherapy and chemotherapy can cause heart diseases through various mechanisms, such as oxidative stress, inflammation, cell death, fibrosis, endothelial to mesenchymal transition (EndMT), etc. Chronic inflammation following damage to a huge number of cells can trigger more accumulation of inflammatory cells and chronic release of reactive oxygen species (ROS) and nitric oxide (NO). Oxidative stress can induce more cell death and cardiac remodeling through damage to vessels and valvular and disruption of the normal structure of the extracellular matrix. These changes may lead to cardiomyopathy, myocarditis, pericarditis, and vascular disorders that may lead to heart attack and death. This review provides basic information on cellular and molecular mechanisms of different types of cardiovascular disorders following cancer therapy by radiation or chemotherapy. We also recommend some adjuvants and targets to reduce the risk of heart toxicity by radiation/chemotherapy.

The emerging crosstalk between atherosclerosis-related microRNAs and Bermuda triangle of foam cells: Cholesterol influx, trafficking, and efflux.

In atherosclerosis, the gradual buildup of lipid particles into the sub-endothelium of damaged arteries leads to numerous lipid alterations. The absorption of these modified lipids by monocyte-derived macrophages in the arterial wall leads to cholesterol accumulation and increases the likelihood of foam cell formation and fatty streak, which is an early characteristic of atherosclerosis. Foam cell formation is related to an imbalance in cholesterol influx, trafficking, and efflux. The formation of foam cells is heavily regulated by various mechanisms, among them, the role of epigenetic factors like microRNA alteration in the formation of foam cells has been well studied. Recent studies have focused on the potential interplay between microRNAs and foam cell formation in the pathogenesis of atherosclerosis; nevertheless, there is significant space to progress in this attractive field. This review has focused to examine the underlying processes of foam cell formation and microRNA crosstalk to provide a deep insight into therapeutic implications in atherosclerosis.

Recent Advancements in Metallic Drug-Eluting Implants.

Over the past decade, metallic drug-eluting implants have gained significance in orthopedic and dental applications for controlled drug release, specifically for preventing infection associated with implants. Recent studies showed that metallic implants loaded with drugs were substituted for conventional bare metal implants to achieve sustained and controlled drug release, resulting in a desired local therapeutic concentration. A number of secondary features can be provided by the incorporated active molecules, including the promotion of osteoconduction and angiogenesis, the inhibition of bacterial invasion, and the modulation of host body reaction. This paper reviews recent trends in the development of the metallic drug-eluting implants with various drug delivery systems in the past three years. There are various types of drug-eluting implants that have been developed to meet this purpose, depending on the drug or agents that have been loaded on them. These include anti-inflammatory drugs, antibiotics agents, growth factors, and anti-resorptive drugs.

Unraveling the role of natural killer cells in leishmaniasis.

NK cells are known as frontline responders that are efficient in combating several maladies as well as leishmaniasis caused by Leishmania spp. As such they are being investigated to be used for adoptive transfer therapy and vaccine. In spite of the lack of antigen-specific receptors at their surface, NK cells can selectively recognize pathogens, accomplished by the activation of the receptors on the NK cell surface and also as the result of their effector functions. Activation of NK cells can occur through interaction between TLR-2 expressed on NK cells and. LPG of Leishmania parasites. In addition, NK cell activation can occur by cytokines (e.g., IFN-γ and IL-12) that also lead to producing cytokines and chemokines and lysis of target cells. This review summarizes several evidences that support NK cells activation for controlling leishmaniasis and the potentially lucrative roles of NK cells during leishmaniasis. Furthermore, we discuss strategies of Leishmania parasites in inhibiting NK cell functions. Leishmania LPG can utilizes TLR2 to evade host-immune responses. Also, Leishmania GP63 can directly binds to NK cells and modulates NK cell phenotype. Finally, this review analyzes the potentialities to harness NK cells effectiveness in therapy regimens and vaccinations.

Dietary Thymol Improved Growth, Body Composition, Digestive Enzyme Activities, Hematology, Immunity, Antioxidant Defense, and Resistance to Streptococcus iniae in the Rainbow Trout (Oncorhynchus mykiss).

In this study, thymol (TYM) at dietary levels of 0, 1, 1.5, 2, and 2.5 g/kg diet was used to evaluate its effects on growth, digestive performance, immunity, and resistances to the infection induced by Streptococcus iniae in the rainbow trout, Oncorhynchus mykiss. A number of 450 fish (35.8 ± 4.4 g; Mean ± SD) were distributed to 15 tanks (30 fish/tank) in three replicates and fed TYM for 60 days. After feeding period, Fish fed 1.5-2.5 g TYM showed better growth, higher digestive enzyme activity, and body protein content compared to other diets (P < 0.05). Regression analysis indicated a polynomial relationship between growth parameters and dietary TYM levels. Based upon the varied growth parameters, the optimum dietary TYM level was 1.89% for FCR. TYM at dietary levels of 1.5-2.5 g significantly enhanced liver antioxidant enzyme activity [superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT)], immune components in blood [alternative complement activity (C3), total immunoglobulin (Ig), lysozyme activity, bactericidal activity, and total protein], and in mucus [alkaline phosphatase (ALP), protease activity, lysozyme activity, bactericidal activity, and total protein] compared to other diets (P < 0.05). TYM at dietary levels of 2-2.5 g significantly decreased malondialdehyde (MDA) levels compared to other experimental groups (P < 0.05). In addition, use of TYM at dietary levels of 1.5-2.5 g upregulated the expression of the immune-related genes (C3, Lyz, and Ig) (P < 0.05). In contrast, the expression of inflammatory genes, tumor necrosis factor (TNF-α) and Interleukin-8 (IL-8) significantly were downregulated in response to 2-2.5 g TYM (P < 0.05). The hematology of the fish also altered in response to dietary TYM, where the values of corpuscular hemoglobin concentration (MCHC), hemoglobin (Hb), red blood cell (RBC), hematocrit (Hct), and white blood cell (WBC) significantly increased in fish fed 2-2.5 g TYM compared to other diets (P < 0.05). In addition, MCV significantly decreased in response to 2-2.5 g TYM (P < 0.05). After challenge with Streptococcus iniae, the survival rate was significantly higher in fish fed 2-2.5 g TYM compared to other diets (P < 0.05). The results of the present study concluded that TYM in the diet of rainbow trout can improve the fish growth and immunity and increase the resistance of the fish to Streptococcus iniae infection. The results of this study recommend an optimized dietary level of 2-2.5 g TYM for the fish.

Development of the DNA-based voltammetric biosensor for detection of vincristine as anticancer drug.

In the article presented herein, a deoxyribonucleic acid (DNA) biosensor is introduced for Vincristine determination in pharmaceutical preparations based on the modification of screen printed electrode (SPE) with double-stranded DNA (ds-DNA), polypyrrole (PP), peony-like CuO:Tb3+ nanostructure (P-L CuO:Tb3+ NS). The developed sensor indicated a wide linear response to Vincristine concentration ranged from 1.0 nM to 400.0 µM with a limit of detection as low as .21 nM. The intercalation of Vincristine with DNA guanine led to the response. The optimized parameters for the biosensor performance were ds-DNA/Vincristine interaction time, DNA concentration and type of buffer solution. The docking investigation confirm the minor groove interaction between guanine base at surface of or ds-DNA/PP/P-L CuO:Tb3+ NS/SPE and Vincristine. The proposed sensor could successfully determine Vincristine in Vincristine injections and biological fluids, with acceptable obtains.