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    Application of curcumin nanoformulations to target folic acid receptor in cancer: Recent trends and advances
    (Academic Press Inc., 2023-06-20T00:00:00) Hussain, Arif; Kumar, Ajay; Uttam, Vivek; Sharma, Uttam; Sak, Katrin; Saini, Reena V.; Saini, Adesh K.; Haque, Shafiul; Tuli, Hardeep Singh; Jain, Aklank; Sethi, Gautam
    Curcumin, derived from turmeric, has a strong anticancer potential known for millennia. The development of this phytochemical as a medicine has been hampered by several significant deficiencies, including its poor water solubility and low bioavailability. This review article discusses possibilities to overcome these bottlenecks by focusing on this natural polyphenol's nanoformulation. Moreover, preparation of curcumin conjugates containing folates as ligands for folic acid receptors can add a new important dimension in this field, allowing specific targeting of cancer cells, considering the significantly higher expression of these receptors in malignant tissues compared to normal cells. It is highly expected that simultaneous improvement of different aspects of curcumin in fighting against such a complex and multifaceted disease like cancer. Therefore, we can better comprehend cancer biology by developing a mechanistic understanding of curcumin, which will also inspire the scientific community to develop new pharmacological models, and exploration of emerging directions to revitalize application of natural products in cancer therapy. � 2023 Elsevier Inc.
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    Role of curcumin on monoamine oxidase(MAO) enzyme expression and activity against Amyloid Beta (A?)-induced oxidative stress in human glioblastoma U-87 MG cell.
    (Central University of Punjab, 2018) Behera, Nishibala N; Mantha,Anil K.
    Glioblastoma (GBM) is the most common brain tumor in humans. The major factor responsible for its progression is oxidative stress. Oxidative stress leads to disruption of signaling pathways and damage to cells and tissues. Monoamine oxidase (MAO) is involved in oxidative deamination of endogenous biogenic amine neurotransmitters such as dopamine, serotonin, norepinephrine, and epinephrine. Therefore, MAO plays a key role in initiation and progression of GBM through oxidative stress. In the present study, A?(25-35) peptide treatment was used to induce oxidative stress in human glioblastoma (U-87 MG) cells. A?(25-35) is known to induce oxidative stress through altering the expression and activity of various antioxidant and mitochondrial enzymes. In this study, the expression and activity of MAO was evaluated through induction of oxidative stress by A?(25-35) and antioxidant treatment of Curcumin. It was found that Curcumin decreases the mRNA expression of MAO but its protein expression increases, whereas A?(25-35) showed little decrease in the mRNA expression of MAO and increase in its protein expression, thus pointing towards differential regulation of translation and transcription. The activity of MAO was found to be increased in A?(25-35), Cur and Cur+A?(25-35) . Therefore, Curcumin has little or no antioxidant effect in altering the expression and activity of MAO and A? showed its oxidative potential by increasing the expression and activity of MAO, although not very significant, possibly because it uses other pathways for inducing oxidative stress.
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    APE1/Ref-1 as an emerging therapeutic target for various human diseases: Phytochemical modulation of its functions
    (Nature Publishing Group, 2014) Thakur, Shweta; Sarkar, Bibekananda; Cholia, Ravi P.; Gautam, Nandini; Dhiman, Monisha; Mantha, Anil K.
    Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme involved in the base excision repair (BER) pathway, which repairs oxidative base damage caused by endogenous and exogenous agents. APE1 acts as a reductive activator of many transcription factors (TFs) and has also been named redox effector factor 1, Ref-1. For example, APE1 activates activator protein-1, nuclear factor kappa B, hypoxia-inducible factor 1a, paired box gene 8, signal transducer activator of transcription 3 and p53, which are involved in apoptosis, inflammation, angiogenesis and survival pathways. APE1/Ref-1 maintains cellular homeostasis (redox) via the activation of TFs that regulate various physiological processes and that crosstalk with redox balancing agents (for example, thioredoxin, catalase and superoxide dismutase) by controlling levels of reactive oxygen and nitrogen species. The efficiency of APE1/Ref-1's function(s) depends on pairwise interaction with participant protein(s), the functions regulated by APE1/Ref-1 include the BER pathway, TFs, energy metabolism, cytoskeletal elements and stress-dependent responses. Thus, APE1/Ref-1 acts as a 'hub-protein' that controls pathways that are important for cell survival. In this review, we will discuss APE1/Ref-1's versatile nature in various human etiologies, including neurodegeneration, cancer, cardiovascular and other diseases that have been linked with alterations in the expression, subcellular localization and activities of APE/Ref-1. APE1/Ref-1 can be targeted for therapeutic intervention using natural plant products that modulate the expression and functions of APE1/Ref-1. In addition, studies focusing on translational applications based on APE1/Ref-1-mediated therapeutic interventions are discussed. ? 2014 KSBMB.
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    An in vitro study ascertaining the role of H2O2 and glucose oxidase in modulation of antioxidant potential and cancer cell survival mechanisms in glioblastoma U-87 MG cells
    (Springer New York LLC, 2017) Cholia, Ravi P.; Kumari, Sanju; Kumar, Saurabh; Kaur, Manpreet; Kaur, Manbir; Kumar, Raj; Dhiman, Monisha; Mantha, Anil K.
    Glial cells protect themselves from the elevated reactive oxygen species (ROS) via developing unusual mechanisms to maintain the genomic stability, and reprogramming of the cellular antioxidant system to cope with the adverse effects. In the present study non-cytotoxic dose of oxidants, H2O2 (100??M) and GO (10??U/ml) was used to induce moderate oxidative stress via generating ROS in human glioblastoma cell line U-87 MG cells, which showed a marked increase in the antioxidant capacity as studied by measuring the modulation in expression levels and activities of superoxide dismutase (SOD1 and SOD2) and catalase (CAT) enzymes, and the GSH content. However, pretreatment (3?h) of Curcumin and Quercetin (10??M) followed by the treatment of oxidants enhanced the cell survival, and the levels/activities of the antioxidants studied. Oxidative stress also resulted in an increase in the nitrite levels in the culture supernatants, and further analysis by immunocytochemistry showed an increase in iNOS expression. In addition, phytochemical pretreatment decreased the nitrite level in the culture supernatants of oxidatively stressed U-87 MG cells. Elevated ROS also increased the expression of COX-2 and APE1 enzymes and pretreatment of Curcumin and Quercetin decreased COX-2 expression and increased APE1 expression in the oxidatively stressed U-87 MG cells. The immunocytochemistry also indicates for APE1 enhanced stress-dependent subcellular localization to the nuclear compartment, which advocates for enhanced DNA repair and redox functions of APE1 towards survival of U-87 MG cells. It can be concluded that intracellular oxidants activate the key enzymes involved in antioxidant mechanisms, NO-dependent survival mechanisms, and also in the DNA repair pathways for glial cell survival in oxidative-stress micro-environment. ? 2017, Springer Science+Business Media, LLC.