Ecology of freshwater harmful euglenophytes: A review.

A diverse array of aquatic ecosystems are inhabited by the euglenophytes, a group of autotrophic and eukaryotic organisms. In inland waterbodies, the red bloom is caused by a rapid development or accumulation of euglenophytes. Recent studies have designated euglenophytes as bioindicator of organic pollution. The ecology of euglenophytes is influenced by the changes in the intensity of sunlight, temperature, nutrient cycles, and seasons. Most of the species of euglenophytes grow prolifically with the increase of water temperature. Nitrogen and phosphorus are often thought to be the main nutrients that influence the cellular growth of toxic euglenophytes. A high concentration of nutrients is required for the euglenophytes to grow and to form bloom. Heavy bloom of euglenophytes in the summer season is the characteristic of eutrophic ponds. Inland waterbodies in many countries suffer from euglenophyte blooms, which shade submerged vegetation, deplete the dissolved oxygen and disrupt the aquatic food webs. Dense bloom of euglenophytes clog the gills of fishes, cause breathing difficulties and in extreme cases results mortality. Red blooms of the deadly toxin producing Euglena sanguinea negatively affect the water quality resulting massive mortality of fishes. Consequently, aquaculture systems and fisheries are facing a serious threat from the predicted outbreak of toxic red blooms of euglenophytes worldwide. To ensure sustainability in the fisheries and aquaculture industry, it is essential to analyze the ecology of euglenophytes. Again, interesting research on euglenophycin, a Euglena-derived natural product, has shown that it can be utilized as a potential anti-cancer drug. This paper comes up with a thorough review of the latest research in this area, revealing new insights and solutions that can help mitigate the negative impact of the freshwater harmful euglenophytes. By implementing considerable management strategies, the health of the valuable aquatic ecosystems and the future of the aquaculture and fisheries can also be secured.

Promising Role of Alkaloids in the Prevention and Treatment of Thyroid Cancer and Autoimmune Thyroid Disease: A Comprehensive Review of the Current Evidence.

Thyroid cancer (TC) and thyroid autoimmune disorders (AITD) are among the most common diseases in the general population, with higher incidence in women. Chronic inflammation and autoimmunity play a pivotal role in carcinogenesis. Some studies, indeed, have pointed out the presence of AITD as a risk factor for TC, although this issue remains controversial. Prevention of autoimmune disease and cancer is the ultimate goal for clinicians and scientists, but it is not always feasible. Thus, new treatments, that overcome the current barriers to prevention and treatment of TC and AITD are needed. Alkaloids are secondary plant metabolites endowed with several biological activities including anticancer and immunomodulatory properties. In this perspective, alkaloids may represent a promising source of prophylactic and therapeutic agents for TC and AITD. This review encompasses the current published literature on alkaloids effects on TC and AITD, with a specific focus on the pathways involved in TC and AITD development and progression.

Design, synthesis, and biological evaluation of novel 2,3-Di-O-Aryl/Alkyl sulfonate derivatives of l-ascorbic acid: Efficient access to novel anticancer agents via in vitro screening, tubulin polymerization inhibition, molecular docking study and ADME predictions.

A series of novel l-ascorbic acid derivatives bearing aryl and alkyl sulfonate substituents were synthesized and characterized. In vitro anticancer evaluation against MCF-7 (breast) and A-549 (lung) cancer cell lines revealed potent activity for most of the compounds, with 2b being equipotent to the standard drug colchicine against MCF-7 (IC50 = 0.04 µM). Notably, compound 2b displayed 89-fold selectivity for MCF-7 breast cancer over MCF-10A normal breast cells. Derivatives with two sulfonate groups (2a-g, 3a-g) exhibited superior potency over those with one sulfonate (4a-c,5g, 6b). Compounds 2b and 2c potently inhibited tubulin polymerization in A-549 cancer cells (73.12 % and 62.09 % inhibition, respectively), substantiating their anticancer potential through microtubule disruption. Molecular docking studies showed higher binding scores and affinities for these compounds at the colchicine-binding site of α, ß-tubulin compared to colchicine itself. In-silico ADMET predictions indicated favourable drug-like properties, with 2b exhibiting the highest binding affinity. These sulfonate derivatives of l-ascorbic acid represents promising lead scaffolds for anticancer drug development.

Inhibition of cancer cells by Quinoline-Based compounds: A review with mechanistic insights.

This article includes a thorough examination of the inhibitory potential of quinoline-based drugs on cancer cells, as well as an explanation of their modes of action. Quinoline derivatives, due to their various chemical structures and biological activity, have emerged as interesting candidates in the search for new anticancer drugs. The review paper delves into the numerous effects of quinoline-based chemicals in cancer progression, including apoptosis induction, cell cycle modification, and interference with tumor-growth signaling pathways. Mechanistic insights on quinoline derivative interactions with biological targets enlightens their therapeutic potential. However, obstacles such as poor bioavailability, possible off-target effects, and resistance mechanisms make it difficult to get these molecules from benchside to bedside. Addressing these difficulties might be critical for realizing the full therapeutic potential of quinoline-based drugs in cancer treatment.

Discovery of a SHP2 Degrader with In Vivo Anti-Tumor Activity.

Src homology 2 domain-containing phosphatase 2 (SHP2) is an attractive target for cancer therapy due to its multifaceted roles in both tumor and immune cells. Herein, we designed and synthesized a novel series of proteolysis targeting chimeras (PROTACs) using a SHP2 allosteric inhibitor as warhead, with the goal of achieving SHP2 degradation both inside the cell and in vivo. Among these molecules, compound P9 induces efficient degradation of SHP2 (DC50 = 35.2 ± 1.5 nM) in a concentration- and time-dependent manner. Mechanistic investigation illustrates that the P9-mediated SHP2 degradation requires the recruitment of the E3 ligase and is ubiquitination- and proteasome-dependent. P9 shows improved anti-tumor activity in a number of cancer cell lines over its parent allosteric inhibitor. Importantly, administration of P9 leads to a nearly complete tumor regression in a xenograft mouse model, as a result of robust SHP2 depletion and suppression of phospho-ERK1/2 in the tumor. Hence, P9 represents the first SHP2 PROTAC molecule with excellent in vivo efficacy. It is anticipated that P9 could serve not only as a new chemical tool to interrogate SHP2 biology but also as a starting point for the development of novel therapeutics targeting SHP2.

Piperlongumine Induces Apoptosis and Cytoprotective Autophagy via the MAPK Signaling Pathway in Human Oral Cancer Cells.

Oral cancer is a malignant tumor that primarily affects areas such as the lips, tongue, buccal mucosa, salivary gland, and gingiva and has a very high malignancy. Piperlongumine (PL), isolated from long pepper (Piper longum L.), is a natural alkaloid with pharmacological effects, such as anti-inflammatory and anti-atherosclerotic effects. The effect and mechanism of PL in oral cancer cell lines has not been explored. Therefore, this study aimed to investigate the mechanism of anticancer effects of PL in the human oral cancer cell lines MC-3 and HSC-4 in vitro. This study demonstrated that PL inhibits cell proliferation by inducing apoptosis and autophagy in human oral cancer cell lines, which was confirmed by the levels of apoptosis- and autophagy-related proteins through Western blotting. Moreover, the pharmacological blockade of autophagy activation by hydroxychloroquine (HCQ), an autophagy inhibitor, significantly improved PL-induced apoptosis in MC-3 cells, suggesting a cytoprotective effect. In addition, activation of the mitogen-activated protein kinase (MAPK) signaling pathway contributed to PL-induced apoptosis. Collectively, the study suggested that combining an autophagy inhibitor with PL treatment can exert effective anticancer properties in oral cancer cells by inducing apoptosis and cytoprotective autophagy via the JNK-mediated MAPK pathway.

Xanthohumol hinders invasion and cell cycle progression in cancer cells through targeting MMP2, MMP9, FAK and P53 genes in three-dimensional breast and lung cancer cells culture.

BACKGROUND: Despite recent advances in the treatment of lung and breast cancer, the mortality with these two types of cancer is high. Xanthohumol (XN) is known as a bioactive compound that shows an anticancer effect on cancer cells. Here, we intended to investigate the anticancer effects of XN on the breast and lung cancer cell lines, using the three-dimensional (3D) cell culture. METHODS: XN was isolated from Humulus lupulus using Preparative-Thin Layer Chromatography (P-TLC) method and its authenticity was documented through Fourier Transform Infrared spectroscopy (FT-IR) and Hydrogen Nuclear Magnetic Resonance (H-NMR) methods. The spheroids of the breast (MCF-7) and lung (A549) cancer cell lines were prepared by the Hanging Drop (HD) method. Subsequently, the IC50s of XN were determined using the MTT assay in 2D and 3D cultures. Apoptosis was evaluated by Annexin V/PI flow cytometry and NFκB1/2, BAX, BCL2, and SURVIVIN expressions. Cell cycle progression was determined by P21, and P53 expressions as well as PI flow cytometry assays. Multidrug resistance was investigated through examining the expression of MDR1 and ABCG2. The invasion was examined by MMP2, MMP9, and FAK expression and F-actin labeling with Phalloidin-iFluor. RESULTS: While the IC50s for the XN treatment were 1.9 µM and 4.74 µM in 2D cultures, these values were 12.37 µM and 31.17 µM in 3D cultures of MCF-7 and A549 cells, respectively. XN induced apoptosis in MCF-7 and A549 cell lines. Furthermore, XN treatment reduced cell cycle progression, multidrug resistance, and invasion at the molecular and/or cellular levels. CONCLUSIONS: According to our results of XN treatment in 3D conditions, this bioactive compound can be introduced as an adjuvant anti-cancer agent for breast and lung cancer.

Hydroquinidine demonstrates remarkable antineoplastic effects on non-small cell lung cancer cells.

BACKGROUND: Despite recent progress in drug development, lung cancer remains a complex disease that poses a major public health issue worldwide, and new therapeutic strategies are urgently needed because of the failure of standard treatments. Ion channels play a critical role in various cellular processes that regulate cell proliferation, differentiation, and cell death. OBJECTIVES: The potential of ion channel modulators as tumor growth suppressors has been highlighted in recent studies. Therefore, we hypothesized that hydroquinidine (HQ), a previously understudied potassium channel modulator, might have anticarcinogenic activity against A549 cells. METHODS: The anticancer potential of HQ was investigated using various well-established in vitro assays. RESULTS: HQ significantly decreased colony formation and tumorigenicity and exhibited a significant anti-migratory effect in A549 cells. Our results demonstrated that HQ significantly inhibited the growth of cancer cells by decreasing the proliferation rate while increasing cell death. The altered gene expression profile in response to treatment with HQ was consistent with the observed cellular effects. Incubation of cells with HQ resulted in the downregulation of genes involved in cell division and survival, while genes promoting cell cycle arrest and apoptosis were upregulated. CONCLUSION: Our findings suggest that HQ has the potential to limit lung cancer growth as a novel potent anticarcinogenic agent. However, more investigations are needed to gain further insight into the mechanism of action of HQ and to evaluate its efficacy in in-vivo models.

Cancer outpatients during the COVID-19 pandemic: what Oncoral has to teach us about medical drug use and the perception of telemedicine.

PURPOSE: The COVID-19 pandemic has disrupted healthcare access and telemedicine has been widely deployed. The aim of this study is to assess the impact of this health crisis on treatment consumption and telemedicine development in outpatients treated by oral anti-cancer agents and followed by the Oncoral hospital/community multidisciplinary program where continuity care is maintained by a pharmacist/nurse pair. METHODS: A prospective monocentric study was conducted among cancer patients who received Oncoral telephone follow-up during the 1st lockdown in France using a 56-item questionnaire which covered sociodemographic data, patient medication management, and telehealth. RESULTS: 178 patients received Oncoral follow-up during the 1st lockdown and 67.4% responded to the questionnaire. During lockdown, 9.2% of patients took medication or CAM for fatigue, 6.7% for mood alteration, 10.8% for sleep disorder, 11.7% for stress and anxiety, and 12.5% to get more energy. Homeopathy consumption was triggered by the pandemic. Habits about getting drugs from the pharmacy changed significantly (p < 0.001), while other treatment habits did not. 83% of patients were satisfied by the telephone follow-up established, 69% would be in favor of repeating this in case of a new epidemic wave. Those most in favor of using telemedicine seemed to be the youngest (p < 0.001), with several dependent children (p < 0.007), high school degree or higher education (p = 0.023), and in work (p < 0.001). CONCLUSION: Health system reorganization enables to limit the impact of the crisis on patients' drug use in oncology care. Telemedicine is a promising public health tool.

In vitro anti-carcinogenic effect of andarine as a selective androgen receptor modulator on MIA-PaCa-2 cells by decreased proliferation and cell-cycle arrest at G0/G1 phase.

Pancreatic cancer (PC) continues to be devastating due to its highly malignant nature and poor prognosis. The limited benefits of the chemotherapeutic drugs and increasing resistance pose a critical challenge to overcome and warrant investigations for new therapeutic agents. Several preclinical and clinical studies have suggested a possible role of the androgen receptor (AR) signaling pathway in PC development and progression. Nevertheless, the studies are limited and inconclusive in explaining the molecular link between AR signaling and PC. Selective androgen receptor modulators (SARMs) are small molecule drugs with high affinity for the androgen receptor. SARMs elicit selective anabolic activities while abrogating undesired androgenic side effects. There is no study focusing on the utility of SARMs as inhibitors of PC. Here, we report the first study evaluating the possible anti-carcinogenic influences of andarine, a member of the SARMs, on PC. The data we presented here has illustrated that andarine repressed PC cell growth and proliferation via cell cycle arrest at G0/G1 phase. Gene expression analysis revealed that it downregulates CDKN1A expression level accordingly. Furthermore, we established that the anti-carcinogenic activity of andarine is not mediated by the PI3K/AKT/mTOR signaling pathway, a crucial regulator of cell survival. Our findings suggest that andarine might be considered as a prospective drug for PC.

Biogenic green metal nano systems as efficient anti-cancer agents.

Metal/metal oxide nano systems (M-NSs) of tunable and manipulative properties are emerging suitable for cancer management via immunity development, early-stage diagnosis, nanotherapeutics, and targeted drug delivery systems. However, noticeable toxicity, off-targeted actions, lacking biocompatibility, and being expensive limit their acceptability. Moreover, involving high energy (top-down routes) and hazardous chemicals (bottom-up chemical routes) is altering human cycle. To manage such challenges, biomass (plants, microbes, animals) and green chemistry-based M-NSs due to scalability, affordability, are cellular, tissue, and organ acceptability are emerging as desired biogenic M-NSs for cancer management with enhanced features. The state-of-art and perspective of green metal/metal oxide nano systems (GM-NSs) as an efficient anti-cancer agent including, imaging, immunity building elements, site-specific drug delivery, and therapeutics developments are highlighted in this review critically. It is expected that this report will serve as guideline for design and develop high-performance GM-NSs for establishing them as next-generation anti-cancer agent capable to manage cancer in personalized manner.

Design, Synthesis and Biological Evaluation of Multi-Target Anti-Cancer Agent PYR26.

This study investigates the synthesis of a new compound, PYR26, and the multi-target mechanism of PYR26 inhibiting the proliferation of HepG2 human hepatocellular carcinoma cells. PYR26 significantly inhibits the growth of HepG2 cells (p < 0.0001) and this inhibition has a concentration effect. There was no significant change in ROS release from HepG2 cells after PYR26 treatment. The mRNA expressions of CDK4, c-Met and Bak genes in HepG2 cells were significantly inhibited (p < 0.05), while mRNA expression of pro-apoptotic factors such as caspase-3 and Cyt c was significantly increased (p < 0.01). The expression of PI3K, CDK4 and pERK proteins decreased. The expression level of caspase-3 protein was increased. PI3K is a kind of intracellular phosphatidylinositol kinase. PI3K signaling pathway is involved in signal transduction of a variety of growth factors, cytokines and extracellular matrix and plays an important role in preventing cell apoptosis, promoting cell survival and influencing cell glucose metabolism. CDK4 is a catalytic subunit of the protein kinase complex and is important for G1 phase progression of the cell cycle. PERK refers to phosphorylated activated ERK, which is translocated from cytoplasm to the nucleus after activation, and then participates in various biological reactions such as cell proliferation and differentiation, cell morphology maintenance, cytoskeleton construction, cell apoptosis and cell canceration. Compared with the model group and the positive control group, the tumor volume of the nude mice in the low-concentration PYR26 group, the medium-concentration group and the high-concentration group was smaller, and the organ volume was smaller than that in the model group and the positive control group. The tumor inhibition rates of low-concentration group PYR26, medium-concentration group and high-concentration group reached 50.46%, 80.66% and 74.59%, respectively. The results showed that PYR26 inhibited the proliferation of HepG2 cells and induced apoptosis of HepG2 cells by down-regulating c-Met, CDK4 and Bak, up-regulating the mRNA expression of caspase-3 and Cyt c genes, down-regulating PI3K, pERK and CDK4 proteins and up-regulating the protein level of caspase-3. In a certain range, with the increase in PYR26 concentration, the tumor growth was slower and the tumor volume was smaller. Preliminary results showed that PYR26 also had an inhibitory effect on the tumors of Hepa1-6 tumor-bearing mice. These results suggest that PYR26 has an inhibitory effect on the growth of liver cancer cells, therefore it has potential to be developed into a new anti-liver cancer drug.

Identification of CYP3A4 inhibitors as potential anti-cancer agents using pharmacoinformatics approach.

Biguanide derivatives exhibit a wide variety of therapeutic applications, including anti-cancer effects. Metformin is an effective anti-cancer agent against breast cancer, lung cancer, and prostate cancer. In the crystal structure (PDB ID: 5G5J), it was found that metformin is found in the active site of CYP3A4, and the associated anti-cancer effect was explored. Taking clues from this work, pharmacoinformatics research has been carried out on a series of known and virtual biguanide, guanylthiourea (GTU), and nitreone derivatives. This exercise led to the identification of more than 100 species that exhibit greater binding affinity toward CYP3A4 in comparison to that of metformin. Selected six molecules were subjected to molecular dynamics simulations, and the results are presented in this work.

[Education Aimed at Patient Safety Management of Chemotherapy Conducted at University Education Sites].

The School Education Law was revised in 2006, and the university pharmacy education system and the national pharmacist examination system were changed. In line with the advancement of medical technology and the division of labor, 16 years have passed since the length of undergraduate pharmacy education was extended from 4 to 6 years in order to foster highly qualified pharmacists. During this period, the curriculum for practical training has been revised, and lectures and exercises focused on clinical education have been incorporated to foster pharmacists who can be useful in the medical field. In the area of cancer drug therapy, the university provides students with opportunities to learn about the basic mechanisms of action and side effects of anticancer drugs, but there is little coverage of clinical guidelines and pharmacological management of the latest therapies, such as cancer immunotherapy. Prior to my arrival at Hoshi University, I was involved in clinical work and clinical research at an oncology hospital for 13 years. Since my arrival, I have been exploring the gap between oncology pharmacotherapy and pharmacy education, and have been working to fill it. We have incorporated new curricula, such as exercises in formulation suggestions, lectures to deepen understanding of guidelines and supportive care, and information on the latest cancer drug therapies, such as cancer immunotherapy. This paper outlines the pharmacy education required to produce pharmacists who can practice safe cancer drug therapy.

In Silico Optimization of Frizzled-8 Receptor Inhibition Activity of Carbamazepine: Designing New Anti-Cancer Agent.

BACKGROUND: Frizzled-8 (FZD8) receptor is a therapeutic target for cancer treatment and recent research has shown that carbamazepine (CBZ) can inhibit this receptor. OBJECTIVE: In this work, it has been tried to optimize CBZ to enhance its binding capacity to the N6W binding site of FZD8 by using structure-based drug design methods. METHODS: CBZ and its 83 derivatives were docked to the N6W binding site of FZD8. RESULTS: Docking results show that two compounds 79 and 82 have the smallest binding energies and are fitted to the N6W binding site. Compounds C79 and C82 have been synthesized by replacing a hydrogen atom of the seven-membered ring in CBZ with benzoate and nicotinate groups, respectively. In addition, docking results show that a trifluoromethyl on one of the phenyl rings is favorable for improving the FZD8 inhibition activity of the molecule. CONCLUSION: Both molecules C79 and C82 were subjected to molecular dynamics (MD) simulation. MD results show that FZD8-C82 complex is stable and this compound binds to the N6W binding site more strongly than compounds C79 and CBZ.

Seaweed-associated heterotrophic Bacillus altitudinis MTCC13046: a promising marine bacterium for use against human hepatocellular adenocarcinoma.

Since the report of the antibiotic with anticancer properties, scientists have been focusing to isolate and characterize novel anti-microbial natural products possessing anticancer activities. The current study describes the production of seaweed-associated heterotrophic Bacillus altitudinis MTCC13046 with potential anticancer properties. The bacterium was screened for its capacity to diminish the cell proliferation of the human hepatocellular adenocarcinoma (HepG2) cell line, without upsetting the normal cells. The bacterial extract showed anticancer properties in a dose-reactive form against HepG2 (IC50, half maximal inhibitory concentration ~ 29.5 µg/ml) on tetrazolium bromide analysis with less significant cytotoxicity on common fibroblast (HDF) cells (IC50 ~ 77 µg/ml). The potential antioxidant ability of the organic extract of B. altitudinis MTCC13046 (IC90 133 µg/ml) could corroborate its capacity to attenuate the pathophysiology leading to carcinogenesis. The results of the apoptosis assay showed that the crude extracts of B. altitudinis maintained 68% viability in normal cells compared to 11% in the cancer cells (IC50 76.9 µg/ml). According to the findings, B. altitudinis MTCC13046 could be used to develop prospective anticancer agents.

Binding characterization of anthraquinone derivatives by stabilizing G-quadruplex DNA leads to an anticancerous activity.

G-quadruplex is a non-canonical secondary structure identified in the telomeric region and the promoter of many oncogenes. Anthraquinone derivatives, a well-known inducer of telomere disruption in malignant cells and activate the apoptotic pathway. We used biophysical and biochemical studies to confirm the interaction of synthesized anthraquinone derivatives with the human telomeric G-quadruplex sequence. The binding affinity of N-2DEA and N-1DEA are K b = 4.8 × 106 M-1 and K b = 7.6 × 105 M-1, respectively, leading to hypochroism, fluorescence quenching with minor redshift and ellipticity variations indicating ligand binding in the external groove. We found that sodium ions induced stabilization more rather than potassium ions. Molecular docking of complex demonstrates a molecule's exterior binding to a quadruplex. The investigation of ROS activity indicated that the cell initiates mortality in response to the IC50 concentration. Cellular morphology, nuclear condensation, and fragmentation were altered in the treated cell, impairing cellular function. Finally, the transcriptional regulatory study paves the way for drug design as an anti-cancer agent because of the tremendous possibilities of changing substituent groups on anthraquinones to improve efficacy and selectivity for G-quartet DNA. Our research focused on how ligand binding to telomere sequences induces oxidative stress and inhibits the growth of malignant cells.

[Elucidation of Pathology in Urological Diseases and Creation of New Therapeutics].

Global increase in lifestyle-related diseases, such as type 2 diabetes mellitus and hypertension, and infertility rate due to late marriage has become alarming and problematic. Lifestyle-related diseases and infertility rate are strongly linked to urological diseases and are issues that must be resolved to maintain a high QOL. In this review, we elucidated the pathophysiology of urologic diseases, which authors have been researching, and demonstrated the creation of new therapeutic methods for clinical applications. We have clarified the effects of testosterone on the tissue structure and endothelial function of the corpus cavernosum using castrated rats. Additionally, we reported that the administration of testosterone to model rats with type 2 diabetes suppressed the inflammatory response in the corpus cavernosum and improved erectile function in rats. Furthermore, the effect of anti-cancer agents on erectile function was analyzed using the database obtained from the U.S. Food and Drug Administration (FDA) Adverse Event Reporting System (AERS). Finally, we found that the above-mentioned anti-cancer agents had an affected erectile function in rats. Our study may shed light on possible treatment strategies for improving the QOL of patients with erectile dysfunction, including maintenance of erectile function.

Tea Polyphenols and Their Preventive Measures against Cancer: Current Trends and Directions.

Cancer is exerting an immense strain on the population and health systems all over the world. Green tea because of its higher simple catechin content (up to 30% on dry weight basis) is greatly popular as an anti-cancer agent which is found to reduce the risks of cancer as well as a range of other diseases. In addition, several in vitro and in vivo studies have shown that green tea possesses copious health benefits like anti-diabetic, anti-obese, anti-inflammatory, neuro-protective, cardio-protective, etc. This review highlights the anti-carcinogenic effects of green tea catechins integrating the recent information to gain a clear concept. Special emphasis was given to the effectiveness of green tea polyphenols (GTP) in the prevention of cancer. Overall, green tea has been found to be effective to reduce the risks of breast cancer, ovarian cancer, liver cancer, colorectal cancer, skin cancer, prostate cancer, oral cancer, etc. However, sufficient information was not found to support that green tea consumption reduces the risk of lung cancer, esophageal cancer, or stomach cancer. The exciting data integrated into this article will increase interest in future researchers to garner more fruitful information on the relevant topics.

Metal complexes of benzimidazole-derived as potential anti-cancer agents: synthesis, characterization, combined experimental and computational studies.

In this study, a series of 14 Cu (II), Zn (II), Ni (II) and Ag (I) complexes containing bis-benzimidazole derivatives were successfully designed and synthesized from 2-(1H-benzimidazole-2-yl)-phenol derivatives and corresponding metal salt solutions. The compound structures were identified by FT-IR, 1H-NMR, powder X-ray diffraction and ESI-MS analyses, and the presence of the metal in the complexes was confirmed by ultraviolet-visible spectroscopy and ICP optical emission spectrometry. Electronic structure calculations were also carried out to describe the detailed structures in addition to the electronic absorption spectra of the ligands. The cytotoxic activity of the complexes was evaluated against three human cancer cell lines: lung (A549), breast (MDA-MB-231) and prostate (PC3) cancer cells. All complexes inhibited anti-proliferative cancer cells better than free ligands, especially Zn (II) and Ag (I) complexes, which are most sensitive to MDA-MB-231 cells. In addition, showing the growth inhibition of three cancer cell lines with IC50 < 10.4 µM, complexes C1 , C3 and C14 could be considered potential multi-targeted anti-cancer agents.