School Of Basic And Applied Sciences

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    Herbal Remedies for Improving Cancer Treatment Through Modulation of Redox Balance
    (Springer Singapore, 2022-09-28T00:00:00) Kaur, Sukhchain; Verma, Harkomal; Kaur, Sharanjot; Singh, Subham; Mantha, Anil K.; Dhiman, Monisha
    The redox modulation induced by oxidative stress is one of the major cause of the metabolic and inflammatory disorders including cancer. The reactive oxygen species (ROS) produced by various sources in the cell shift the redox homeostasis of cells towards more oxidizing or acidic environment. This shift results in the alterations of normal physiologic functioning of biomolecules as well as causes damage to these biomolecules (proteins, lipids, and DNA/RNA). The excessive ROS and redox modulation are the key factors that support growth, progression, and survival of cancer cells. ROS-induced redox modulation further activates pro-tumorigenic cellular pathways for e.g., PI3K/AKT, HIF-1, and MAPK signaling pathways as well as hinders epigenetic signaling. Increasing evidences demonstrate that long-term side effects of anti-cancer chemotherapy are major concern of medical sciences although modern treatments are quite effective. The combination of various herbal formulations with anti-cancer therapy shows improvement in treatment effectiveness in cancer patients. Bioactive compounds present in herbal formulations possess antioxidant and anti-cancer properties that help in the regulation of redox status of cancer cells. The synergetic effects of herbal remedies along with conventional treatment are proven as novel therapeutics in cancer progression management. Clinical studies have shown that broad range of herbs and bioactive compounds from various plants having antioxidant, anti-inflammatory properties can suppress the carcinogenesis. In this chapter we will discuss the role of various plants such as Glycyrrhiza glabra, Picrorhiza kurroa, Tinospora cordifolia, Curcuma longa, Ocimum sanctum, Viola odorata, and bioactive compound ferulic acid found in various cereals. The chapter will also focus on various mechanisms involved in the modulation of chemo-toxicity and improvement of efficacy of conventional anti-cancer therapies by these plants. � Springer Nature Singapore Pte Ltd. 2022.
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    Methods to Detect Nitric Oxide and Reactive Nitrogen Species in Biological Sample
    (Humana Press Inc., 2022-01-19T00:00:00) Kaur, Sharanjot; Gupta, Kunj Bihari; Kumar, Sandeep; Upadhyay, Shishir; Mantha, Anil Kumar; Dhiman, Monisha
    Oxidative stress has been implicated in various human diseases, including cancer, mainly through the generation of reactive nitrogen species (RNS), such as nitric oxide (NO), nitrite, nitroxyl, s-nitrosothiols, and reactive oxygen species (ROS) such as peroxides, superoxide, and hydroxyl radicals. NO being the main player among RNS induced altered cellular molecules and metabolisms, thus making it important to understand and detect the generation of NO in biological samples. There are many methods for direct and indirect detection of NO; out of these most commonly used are spectrophotometric-based Griess assay and fluorescence probe-based assays. In this chapter, we summarize these routinely used methods to detect NO and various challenges associated with these methods. � 2022, Springer Science+Business Media, LLC, part of Springer Nature.
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    Understanding the multifaceted role of miRNAs in Alzheimer�s disease pathology
    (Springer, 2023-07-28T00:00:00) Kaur, Sharanjot; Verma, Harkomal; Kaur, Sukhchain; Gangwar, Prabhakar; Yadav, Anuradha; Yadav, Bharti; Rao, Rashmi; Dhiman, Monisha; Mantha, Anil Kumar
    Small non-coding RNAs (miRNAs) regulate gene expression by binding to mRNA and mediating its degradation or inhibiting translation. Since miRNAs can regulate the expression of several genes, they have multiple roles to play in biological processes and human diseases. The majority of miRNAs are known to be expressed in the brain and are involved in synaptic functions, thus marking their presence and role in major neurodegenerative disorders, including Alzheimer�s disease (AD). In AD, amyloid beta (A?) plaques and neurofibrillary tangles (NFTs) are known to be the major hallmarks. The clearance of A? and tau is known to be associated with miRNA dysregulation. In addition, the ?-site APP cleaving enzyme (BACE 1), which cleaves APP to form A?, is also found to be regulated by miRNAs, thus directly affecting A? accumulation. Growing evidences suggest that neuroinflammation can be an initial event in AD pathology, and miRNAs have been linked with the regulation of neuroinflammation. Inflammatory disorders have also been associated with AD pathology, and exosomes associated with miRNAs are known to regulate brain inflammation, suggesting for the role of systemic miRNAs in AD pathology. Several miRNAs have been related in AD, years before the clinical symptoms appear, most of which are associated with regulating the cell cycle, immune system, stress responses, cellular senescence, nerve growth factor (NGF)�signaling, and synaptic regulation. Phytochemicals, especially polyphenols, alter the expression of various miRNAs by binding to miRNAs or binding to the transcriptional activators of miRNAs, thus control/alter various metabolic pathways. Awing to the sundry biological processes being regulated by miRNAs in the brain and regulation of expression of miRNAs via phytochemicals, miRNAs and the regulatory bioactive phytochemicals can serve as therapeutic agents in the treatment and management of AD. � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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    Methods to Assess Oxidative DNA Base Damage Repair of Apurinic/Apyrimidinic (AP) Sites Using Radioactive and Nonradioactive Oligonucleotide-Based Assays
    (NLM (Medline), 2022-01-19T00:00:00) Gupta, Kunj Bihari; Kaur, Sharanjot; Dhiman, Monisha; Mantha, Anil Kumar
    Reactive oxygen species (ROS) overproduction results in oxidative stress leading to genomic instability via the generation of small base lesions in the genome, and this unrepaired DNA base damage leads to various cellular consequences. The oxidative stress-mediated DNA base damage is involved in various human disorders like cancer, cardiovascular, ocular, and neurodegenerative diseases. Base excision repair (BER) pathway, one of the DNA repair pathways, is majorly involved in the repair of oxidative DNA base lesions, which utilizes a different set of enzymes, including endonuclease viz Apurinic/apyrimidinic endonuclease 1 (APE1). APE1 is a well-known multifunctional enzyme with DNA repair, REDOX regulatory, and protein-protein interaction/cross-talk functions associated with the cell survival mechanisms. APE1 acts as an important player in both normal and cancerous cell survival; thus, evaluating its endonuclease activity in the biological samples provide useful readout of the DNA repair capacity/ability, which can be used to tune for the development of therapeutic candidates via either stimulating or blocking its DNA repair function in normal vs. cancer cells, respectively. This chapter enlists two methods used for the determination of APE1's endonuclease activity by oligonucleotide-based radioactive P32-labeled and nonradioactive fluorescence dyes using the cell extracts and recombinant APE1 protein. � 2022. Springer Science+Business Media, LLC, part of Springer Nature.
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    Brain Exosomes: Friend or Foe in Alzheimer�s Disease?
    (Springer, 2021-09-30T00:00:00) Kaur, Sharanjot; Verma, Harkomal; Dhiman, Monisha; Tell, Gianluca; Gigli, Gian Luigi; Janes, Francesco; Mantha, Anil K.
    Alzheimer�s disease (AD) is the most common neurodegenerative disease. It is known to be a multifactorial disease and several causes are associated with its occurrence as well as progression. However, the accumulation of amyloid beta (A?) is widely considered its major pathogenic hallmark. Additionally, neurofibrillary tangles (NFT), mitochondrial dysfunction, oxidative stress, and aging (cellular senescence) are considered as additional hits affecting the disease pathology. Several studies are now suggesting important role of inflammation in AD, which shifts our thought towards the brain�s resident immune cells, microglia, and astrocytes; how they interact with neurons; and how these interactions are affected by intra and extracellular stressful factors. These interactions can be modulated by different mechanisms and pathways, in which exosomes could play an important role. Exosomes are multivesicular bodies secreted by nearly all types of cells. The exosomes secreted by glial cells or neurons affect the interactions and thus the physiology of these cells by transmitting miRNAs, proteins, and lipids. Exosomes can serve as a friend or foe to the neuron function, depending upon the carried signals. Exosomes, from the healthy microenvironment, may assist neuron function and health, whereas, from the stressed microenvironment, they carry oxidative and inflammatory signals to the neurons and thus prove detrimental to the neuronal function. Furthermore, exosomes can cross the blood�brain barrier (BBB), and from the blood plasma they can enter the brain cells and activate microglia and astrocytes. Exosomes can transport A? or Tau, cytokines, miRNAs between the cells, and alter the physiology of recipient cells. They can also assist in A? clearance and regulation of synaptic activity. The exosomes derived from different cells play different roles, and this field is still in its infancy stage. This review advocates exosomes� role as a friend or foe in neurodegenerative diseases, especially in the case of Alzheimer�s disease. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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    A short review on cross-link between pyruvate kinase (PKM2) and Glioblastoma Multiforme
    (Springer, 2021-03-02T00:00:00) Verma, Harkomal; Cholia, Ravi P.; Kaur, Sharanjot; Dhiman, Monisha; Mantha, Anil K.
    Pyruvate kinase (PK) catalyzes the last irreversible reaction of glycolysis pathway, generating pyruvate and ATP, from Phosphoenol Pyruvate (PEP) and ADP precursors. In mammals, four different tissue-specific isoforms (M1, M2, L and R) of PK exist, which are translated from two genes (PKL and PKR). PKM2 is the highly expressed isoform of PK in cancers, which regulates the aerobic glycolysis via reprogramming cancer cell�s metabolic pathways�to provide an anabolic�advantage to the tumor cells. In addition to the established role of PKM2 in aerobic glycolysis of multiple cancer types, various recent findings have highlighted the non-metabolic functions of PKM2 in brain tumor development. Nuclear PKM2 acts as a co-activator and directly regulates gene transcription. PKM2 dependent transactivation of various oncogenic genes is instrumental in the progression and aggressiveness of Glioblastoma Multiforme (GBM). Also, PKM2 acts as a protein kinase in histone modification which regulates gene expression and tumorigenesis. Ongoing research has explored novel regulatory mechanisms of PKM2 and its association in GBM progression. This review enlists and summarizes the metabolic and non-metabolic roles of PKM2 at the cellular level, and its regulatory function highlights the importance of the nuclear functions of PKM2 in GBM progression, and an emerging role of PKM2 as novel cancer therapeutics. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.
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    Understanding the multifaceted role of miRNAs in Alzheimer�s disease pathology
    (Springer, 2023-07-28T00:00:00) Kaur, Sharanjot; Verma, Harkomal; Kaur, Sukhchain; Gangwar, Prabhakar; Yadav, Anuradha; Yadav, Bharti; Rao, Rashmi; Dhiman, Monisha; Mantha, Anil Kumar
    Small non-coding RNAs (miRNAs) regulate gene expression by binding to mRNA and mediating its degradation or inhibiting translation. Since miRNAs can regulate the expression of several genes, they have multiple roles to play in biological processes and human diseases. The majority of miRNAs are known to be expressed in the brain and are involved in synaptic functions, thus marking their presence and role in major neurodegenerative disorders, including Alzheimer�s disease (AD). In AD, amyloid beta (A?) plaques and neurofibrillary tangles (NFTs) are known to be the major hallmarks. The clearance of A? and tau is known to be associated with miRNA dysregulation. In addition, the ?-site APP cleaving enzyme (BACE 1), which cleaves APP to form A?, is also found to be regulated by miRNAs, thus directly affecting A? accumulation. Growing evidences suggest that neuroinflammation can be an initial event in AD pathology, and miRNAs have been linked with the regulation of neuroinflammation. Inflammatory disorders have also been associated with AD pathology, and exosomes associated with miRNAs are known to regulate brain inflammation, suggesting for the role of systemic miRNAs in AD pathology. Several miRNAs have been related in AD, years before the clinical symptoms appear, most of which are associated with regulating the cell cycle, immune system, stress responses, cellular senescence, nerve growth factor (NGF)�signaling, and synaptic regulation. Phytochemicals, especially polyphenols, alter the expression of various miRNAs by binding to miRNAs or binding to the transcriptional activators of miRNAs, thus control/alter various metabolic pathways. Awing to the sundry biological processes being regulated by miRNAs in the brain and regulation of expression of miRNAs via phytochemicals, miRNAs and the regulatory bioactive phytochemicals can serve as therapeutic agents in the treatment and management of AD. � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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    Methods to Assess Oxidative DNA Base Damage Repair of Apurinic/Apyrimidinic (AP) Sites Using Radioactive and Nonradioactive Oligonucleotide-Based Assays
    (NLM (Medline), 2022-01-19T00:00:00) Gupta, Kunj Bihari; Kaur, Sharanjot; Dhiman, Monisha; Mantha, Anil Kumar
    Reactive oxygen species (ROS) overproduction results in oxidative stress leading to genomic instability via the generation of small base lesions in the genome, and this unrepaired DNA base damage leads to various cellular consequences. The oxidative stress-mediated DNA base damage is involved in various human disorders like cancer, cardiovascular, ocular, and neurodegenerative diseases. Base excision repair (BER) pathway, one of the DNA repair pathways, is majorly involved in the repair of oxidative DNA base lesions, which utilizes a different set of enzymes, including endonuclease viz Apurinic/apyrimidinic endonuclease 1 (APE1). APE1 is a well-known multifunctional enzyme with DNA repair, REDOX regulatory, and protein-protein interaction/cross-talk functions associated with the cell survival mechanisms. APE1 acts as an important player in both normal and cancerous cell survival; thus, evaluating its endonuclease activity in the biological samples provide useful readout of the DNA repair capacity/ability, which can be used to tune for the development of therapeutic candidates via either stimulating or blocking its DNA repair function in normal vs. cancer cells, respectively. This chapter enlists two methods used for the determination of APE1's endonuclease activity by oligonucleotide-based radioactive P32-labeled and nonradioactive fluorescence dyes using the cell extracts and recombinant APE1 protein. � 2022. Springer Science+Business Media, LLC, part of Springer Nature.
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    Brain Exosomes: Friend or Foe in Alzheimer�s Disease?
    (Springer, 2021-09-30T00:00:00) Kaur, Sharanjot; Verma, Harkomal; Dhiman, Monisha; Tell, Gianluca; Gigli, Gian Luigi; Janes, Francesco; Mantha, Anil K.
    Alzheimer�s disease (AD) is the most common neurodegenerative disease. It is known to be a multifactorial disease and several causes are associated with its occurrence as well as progression. However, the accumulation of amyloid beta (A?) is widely considered its major pathogenic hallmark. Additionally, neurofibrillary tangles (NFT), mitochondrial dysfunction, oxidative stress, and aging (cellular senescence) are considered as additional hits affecting the disease pathology. Several studies are now suggesting important role of inflammation in AD, which shifts our thought towards the brain�s resident immune cells, microglia, and astrocytes; how they interact with neurons; and how these interactions are affected by intra and extracellular stressful factors. These interactions can be modulated by different mechanisms and pathways, in which exosomes could play an important role. Exosomes are multivesicular bodies secreted by nearly all types of cells. The exosomes secreted by glial cells or neurons affect the interactions and thus the physiology of these cells by transmitting miRNAs, proteins, and lipids. Exosomes can serve as a friend or foe to the neuron function, depending upon the carried signals. Exosomes, from the healthy microenvironment, may assist neuron function and health, whereas, from the stressed microenvironment, they carry oxidative and inflammatory signals to the neurons and thus prove detrimental to the neuronal function. Furthermore, exosomes can cross the blood�brain barrier (BBB), and from the blood plasma they can enter the brain cells and activate microglia and astrocytes. Exosomes can transport A? or Tau, cytokines, miRNAs between the cells, and alter the physiology of recipient cells. They can also assist in A? clearance and regulation of synaptic activity. The exosomes derived from different cells play different roles, and this field is still in its infancy stage. This review advocates exosomes� role as a friend or foe in neurodegenerative diseases, especially in the case of Alzheimer�s disease. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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    A short review on cross-link between pyruvate kinase (PKM2) and Glioblastoma Multiforme
    (Springer, 2021-03-02T00:00:00) Verma, Harkomal; Cholia, Ravi P.; Kaur, Sharanjot; Dhiman, Monisha; Mantha, Anil K.
    Pyruvate kinase (PK) catalyzes the last irreversible reaction of glycolysis pathway, generating pyruvate and ATP, from Phosphoenol Pyruvate (PEP) and ADP precursors. In mammals, four different tissue-specific isoforms (M1, M2, L and R) of PK exist, which are translated from two genes (PKL and PKR). PKM2 is the highly expressed isoform of PK in cancers, which regulates the aerobic glycolysis via reprogramming cancer cell�s metabolic pathways�to provide an anabolic�advantage to the tumor cells. In addition to the established role of PKM2 in aerobic glycolysis of multiple cancer types, various recent findings have highlighted the non-metabolic functions of PKM2 in brain tumor development. Nuclear PKM2 acts as a co-activator and directly regulates gene transcription. PKM2 dependent transactivation of various oncogenic genes is instrumental in the progression and aggressiveness of Glioblastoma Multiforme (GBM). Also, PKM2 acts as a protein kinase in histone modification which regulates gene expression and tumorigenesis. Ongoing research has explored novel regulatory mechanisms of PKM2 and its association in GBM progression. This review enlists and summarizes the metabolic and non-metabolic roles of PKM2 at the cellular level, and its regulatory function highlights the importance of the nuclear functions of PKM2 in GBM progression, and an emerging role of PKM2 as novel cancer therapeutics. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.