Oxidative stress and innate immune response in A549 lung carcinoma cells

dc.contributor.authorUpadhyay, Shishir
dc.contributor.supervisorDhiman, Manisha
dc.date.accessioned2018-08-30T05:10:37Z
dc.date.accessioned2018-08-30T06:09:23Z
dc.date.accessioned2024-08-13T10:50:37Z
dc.date.available2018-08-30T05:10:37Z
dc.date.available2018-08-30T06:09:23Z
dc.date.available2024-08-13T10:50:37Z
dc.date.issued2014
dc.description.abstractCancer immunology is the study of cross-talk between the immune response and cancer cells. The immune response, including the recognition of cancer-specific antigens is of particular interest as knowledge gained drives the development of new vaccines and antibody therapies. The molecular mechanisms which are disturbed in the susceptible patients who proceed to develop cancer are very complicated and still largely unknown. It proposed that apart from the reported genetic modifications on tumor cells there are modifications due to oxidative stress (resulting in the formation of chemical adducts, e.g. 3-hydroxynonenal, 3- nitrotyrosine, carbonyl etc.) at the vicinity of tumor where the immune cells infiltrate. The central hypothesis of the present work is that respiratory burst which is host?s mechanism to kill the foreign particles (tumor cells) is used as defence mechanism by the tumor cells by forming neoantigen which in turn make them undetectable and can further help them to escape the host immune surveillance. The lung carcinoma A549 cells were treated with100μM H2O2 and using 1-D gel electrophoresis the oxidized tumor proteins in normal and treated cells were visualized. To confirm the oxidized modifications at membrane levels and at proteins levels the lipid peroxidation and protein carbonyls were detected respectively. It was observed that the oxidative stress induces the lipid peroxidation and protein carbonyls in tumor cells. To determine if neo (oxidized) tumor antigens elicit any alteration in immune responses where they show compromised phagocytosis, thus resulting in a failure to elicit effector immune functions were analyzed via phagocytosis and respiratory burst using spectrophotometry and microscopic techniques. The present study has identified a novel mechanism(s) of carcinogenesis initiation and which can further provide directions for the development of adjunct therapies to control cancer in its initial stages and at the same time it advocates for new ventures to increase the efficacy of the chemotherapeutic drugs.en_US
dc.identifier.accessionnoT00129
dc.identifier.citationUpadhyay, Shishir(2014) Oxidative stress and innate immune response in A549 lung carcinoma cells.en_US
dc.identifier.urihttp://10.2.3.109/handle/32116/1739
dc.language.isoen_USen_US
dc.publisherCentral University of Punjaben_US
dc.subjectCancer Immunologyen_US
dc.subjectNeoantigensen_US
dc.subjectProtein carbonylsen_US
dc.subjectPhagocytosisen_US
dc.titleOxidative stress and innate immune response in A549 lung carcinoma cellsen_US
dc.typeMphil Dissertationen_US

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