School Of Basic And Applied Sciences

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    Impact of noncoding RNAs on cancer directed immune therapies: Now then and forever
    (John Wiley and Sons Inc, 2022-04-30T00:00:00) Roy, Roshan Kumar; Yadav, Rakhi; Sharma, Uttam; Wasson, Mishi Kaushal; Sharma, Ashok; Tanwar, Pranay; Jain, Aklank; Prakash, Hridayesh
    Accumulating evidence demonstrates that the host genome's epigenetic modifications are essential for living organisms to adapt to extreme conditions. DNA methylation, covalent modifications of histone and interassociation of noncoding RNAs facilitate the cellular manifestation of epigenetic changes in the genome. Out of various factors involved in the epigenetic programming of the host, noncoding RNAs (ncRNAs) such as microRNA (miRNA), long noncoding RNA (lncRNA), circular RNA, snoRNA and piRNA are new generation noncoding molecules that influence a variety of cellular processes like immunity, cellular differentiation and tumor development. During tumor development, temporal changes in miRNA/lncRNA rheostat influence sterile inflammatory responses accompanied by the changes in the carcinogenic signaling in the host. At the cellular level, this is manifested by the upregulation of inflammasome and inflammatory pathways, which promotes cancer-related inflammation. Given this, we discuss the potential of lncRNAs, miRNAs, circular RNA, snoRNA and piRNA in regulating inflammation and tumor development in the host. � 2022 UICC.
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    Mitigation of Gliadin-Induced Inflammation and Cellular Damage by Curcumin in Human Intestinal Cell Lines
    (Springer, 2021-01-04T00:00:00) Gupta, Kunj Bihari; Mantha, Anil K.; Dhiman, Monisha
    Wheat is a major diet from many years; apart from its nutritious value, the wheat protein gliadin is responsible for many inflammatory diseases like celiac disease (CD), and non-celiac gluten sensitivity (NCGS). In this study, the gliadin-induced inflammation and associated cellular damage along with the protective role of curcumin was evaluated using human intestinal cell lines (HCT-116 and HT-29) as a model. Cells were cultured and exposed to 160 ?g/ml of gliadin, 100 ?M H2O2, and 10 ?M curcumin (3 h pretreatment) followed by the assessment of inflammation. Spectrophotometric methods, real-time-PCR, ELISA, Western blotting, and confocal microscopy techniques were used to assess inflammatory markers such as advanced oxidation protein products (AOPPs) level, activity of myeloperoxidase (MPO) and NADPH oxidase (NOX), cytokines, and cell damage markers. The results show that gliadin increases the AOPPs level and the activity of MPO and NOX expression. It enhances inflammation by increasing expression of pro-inflammatory cytokines, altered expression of anti-inflammatory, and regulatory cytokines. It exacerbates the cellular damage by increasing MMP-2 and 9 and decreasing integrin ? and ? expression. Gliadin promotes disease pathogenesis by inducing the inflammation and cellular damage which further alter the cellular homeostasis. The pretreatment of curcumin counteracts the adverse effect of gliadin and protect the cells via diminishing the inflammation and help the cell to regain the cellular morphology suggesting phytochemical-based remedial interventions against wheat allergies. � 2021, Springer Science+Business Media, LLC, part of Springer Nature.
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    Mycobacterium Tubercular Mediated Inflammation and Lung Carcinogenesis: Connecting Links
    (LIDSEN Publishing Inc, 2023-06-21T00:00:00) Vashishth, Abhay; Shuaib, Mohd; Bansal, Tanya; Kumar, Shashank
    Lung cancer is a leading cause of death among all the cancer worldwide and it has the highest occurrence and mortality rates. Mycobacterium tuberculosis (MTB) induced tuberculosis has been known as one of the risk factors for lung carcinogenesis. The exact mechanism of MTB is understood to date. Several research and epidemiological studies about the link between tuberculosis and lung cancer exist. It has been proposed that tuberculosis causes chronic inflammation, which increases the risk of lung cancer by creating a favorable environment. EGFR downstream signaling promotes constitutive activation of TKIs domain due to the mutation in exon 19 and exon 21 (L858R point mutation), which leads to cell proliferation, invasion, metastasis, and angiogenesis, causing lung adenocarcinoma. Several other studies have shown that human monocyte cells infected by MTB enhance the invasion and cause induction of epithelial-mesenchymal transition (EMT) characteristics in lung cancer cell co-culture. This review article has tried to draw a relationship between chronic tuberculosis and lung carcinogenesis. � 2023 by the author.