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Role of BACH1 in regulation of antioxidant mediated metastasis in lung cancer
Högskolan i Skövde, Institutionen för biovetenskap.
2018 (engelsk)Independent thesis Advanced level (degree of Master (One Year)), 20 poäng / 30 hpOppgave
Abstract [en]

Consumption of antioxidant supplements is widely popular worldwide mainly because of their supposed anticancer benefits. Though these benefits against cancer are highly advertised by supplement industry and a well stablished perception in general population, there are not enough studies to support those claims. In fact, several studies have pinpointed antioxidants’ role in promoting tumor proliferation and migration in multiple types of cancer. Nevertheless, the mechanisms behind how antioxidants are actually mediating these events is largely unknown. This study aims to investigate how antioxidants are affecting lung cancer cells migration and to decipher the involvement of the transcription factor BACH1 in it. In this study, effect of antioxidant supplementation on three human Non-small-cell lung carcinoma (NSCLC) cell lines were investigated. Antioxidant administration was found to increase cell migration and BACH1 expression in all of them. Effect of inactivation and over activation of BACH1 confirmed significant relation between antioxidant induced migration and BACH1 expression. Along with increased migration, antioxidants increased glycolysis in the cells in a Bach1 dependent manner. Activation of NRF2, the master regulator of endogenous antioxidant expression had also been found to increase migration through up regulation of BACH1. Overall findings of this study confirm Bach1’s role in antioxidant-induced migration in lung cancer from different directions and provides a broader understanding how redox status of cancer cells influence their metastatic ability.

sted, utgiver, år, opplag, sider
2018. , s. 27
HSV kategori
Identifikatorer
URN: urn:nbn:se:his:diva-16578OAI: oai:DiVA.org:his-16578DiVA, id: diva2:1281304
Fag / kurs
Molecular Biology
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Tilgjengelig fra: 2019-01-29 Laget: 2019-01-22 Sist oppdatert: 2019-01-29bibliografisk kontrollert

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