School Of Health Sciences

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Author: search.filters.author.Bhatti, Jasvinder SinghSubject: search.filters.subject.ROS

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    Targeting Mitochondria as a Novel Disease-Modifying Therapeutic Strategy in Cancer
    (Springer Singapore, 2022-09-28T00:00:00) Bhatti, Gurjit Kaur; Pahwa, Paras; Gupta, Anshika; Sidhu, Inderpal Singh; Navik, Uma Shanker; Reddy, P. Hemachandra; Bhatti, Jasvinder Singh
    Mitochondria are essential for the metabolism of energy, regulation of apoptosis, and cell signaling. Overproduction of reactive oxidation species (ROS) in mitochondria is one of the indications of cancer cells. Moreover, this boosts the proliferation of cancerous cells by causing genomic instability and altering gene expressions. Mitochondrial and nuclear DNA mutations caused by oxidative damage impair the mechanism of oxidative phosphorylation and can lead to more mitochondrial ROS output, genome instability, and cancer development. The classic approach to target mitochondria of cancerous cells with novel targeted therapeutics helps in targeting the mitochondrial apoptotic proteins and changing energy metabolism. A key benefit of selective drug delivery is that it reduces the drug�s toxicity and increases specificity. A better understanding of the mitochondrial role in tumor growth will help design more therapeutic agents with better selectivity. � Springer Nature Singapore Pte Ltd. 2022.
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    Targeting Mitochondria as a Novel Disease-Modifying Therapeutic Strategy in Cancer
    (Springer Nature, 2022-01-31T00:00:00) Bhatti, Gurjit Kaur; Pahwa, Paras; Gupta, Anshika; Navik, Uma Shanker; Reddy, P. Hemachandra; Bhatti, Jasvinder Singh
    Mitochondria are important for the metabolism of energy, regulation of apoptosis and cell signaling. Overproduction of reactive oxidation species (ROS) in mitochondria is one of the indications of cancer cells; moreover, this boosts the proliferation of cancerous cells by causing genomic instability and altering gene expressions. Mitochondrial and nuclear DNA mutations, caused by oxidative damage which impairs the mechanism of oxidative phosphorylation, can lead to more mitochondrial ROS output, genome instability, and the development of the cancer. Classic approach to target mitochondria of cancerous cells with novel-targeted therapeutics helps in targeting the mitochondrial apoptotic proteins and changing energy metabolism. Key benefit of selective drug delivery is it reduces the toxicity of drug and increases specificity. Better understanding of mitochondrial role in tumor growth will help to design more therapeutic agents with better selectivity. � Springer Nature Singapore Pte Ltd. 2022.
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    ALK and ERBB2 Protein Inhibition is Involved in the Prevention of Lung Cancer Development by Vincamine
    (Bentham Science Publishers, 2023-04-13T00:00:00) Verma, Aarti; Yadav, Poonam; Rajput, Sonu; Verma, Saloni; Arora, Sahil; Kumar, Raj; Bhatti, Jasvinder Singh; Khurana, Amit; Navik, Umashanker
    Background: According to the WHO report of 2022, 2.21 million new cases and 1.80 million deaths were reported for lung cancer in the year 2020. Therefore, there is an urgent need to explore novel, safe, and effective therapeutic interventions for lung cancer. Objective: To find the potential targets of vincamine using a network pharmacology approach and docking studies and to evaluate the anti-cancer effect of vincamine on A549 cell line. Methods: Hence, in the present study, we explored the anti-cancer potential of vincamine by using network pharma-cology, molecular docking, and in vitro approaches. Network pharmacology demonstrated that the most common targets of vincamine are G-protein coupled receptors, cytosolic proteins, and enzymes. Among these targets, two targets, ALK and ERBB2 protein, were common between vincamine and non-small cell lung cancer. Results: We discovered a link between these two targets and their companion proteins, as well as cancer-related pathways. In addition, a docking investigation between the ligand for vincamine and two targeted genes revealed a strong affinity toward these targeted proteins. Further, the in vitro study demonstrated that vincamine treatment for 72 h led to dose-dependent (0-500 ?M) cytotoxicity on the A549 lung cancer cell line with an IC50 value of 291.7 ??. The wound-healing assay showed that vincamine treatment (150 and 300 ?M) significantly inhibited cell migration and invasion. Interestingly, acridine orange/ethidium bromide dual staining demonstrated that vincamine treatment induces apoptosis in A549 cells. Additionally, the dichloro-dihydro-fluorescein diacetate (DCFH-DA) assay showed an increased level of reactive oxygen species (ROS) after the vincamine treatment, indicating ROS-mediated apoptosis in A549 cells. Conclusion: Altogether, based on our findings, we hypothesize that vincamine-induced apoptosis of lung cancer cells via ALK and ERBB2 protein modulation may be an attractive futuristic strategy for managing lung cancer in combination with chemotherapeutic agents to obtain synergistic effects with reduced side effects. � 2023 Bentham Science Publishers.