Regulome of cancer epithelial-mesenchymal transition (EMT)

During metastasis, cancer cells employ autophagy to meet elevated energy demands, of which the adaptor protein 14-3-3γ may play a role in this autophagic mechanism. It is hypothesized that 14-3-3γ activity promotes autophagy and EMT, and inhibition of 14-3-3γ may lead to the prevention of metastasis...

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Main Author: See, Benedict
Other Authors: Tan Nguan Soon
Format: Final Year Project
Language:English
Published: Nanyang Technological University 2020
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Online Access:https://hdl.handle.net/10356/140680
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Institution: Nanyang Technological University
Language: English
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spelling sg-ntu-dr.10356-1406802023-02-28T18:08:41Z Regulome of cancer epithelial-mesenchymal transition (EMT) See, Benedict Tan Nguan Soon School of Biological Sciences NSTan@ntu.edu.sg Science::Biological sciences::Molecular biology During metastasis, cancer cells employ autophagy to meet elevated energy demands, of which the adaptor protein 14-3-3γ may play a role in this autophagic mechanism. It is hypothesized that 14-3-3γ activity promotes autophagy and EMT, and inhibition of 14-3-3γ may lead to the prevention of metastasis by suppressing EMT genes or starving the cancer cells of nutrients through autophagy suppression. To elucidate any differentially expressed genes (DEGs) after EMT induction that are involved in autophagy and may potentially be 14-3-3 protein targets, RNA-Seq was carried out and a pipeline was established to determine the differences in expression of the genes regulated directly or indirectly through 14-3-3γ interaction with transcription factors or repressors. A number of genes that are known to play various roles in autophagy were found to be differentially expressed after treatment with DMOG and TGFβ, which suggests a correlation between autophagy and metastasis. These genes are predicted to interact with 14-3-3 proteins, which suggests 14-3-3γ may have a significant role in regulating autophagy and metastasis, thereby contributing to cancer progression. Bachelor of Science in Biological Sciences 2020-06-01T06:46:56Z 2020-06-01T06:46:56Z 2020 Final Year Project (FYP) https://hdl.handle.net/10356/140680 en application/pdf Nanyang Technological University
institution Nanyang Technological University
building NTU Library
continent Asia
country Singapore
Singapore
content_provider NTU Library
collection DR-NTU
language English
topic Science::Biological sciences::Molecular biology
spellingShingle Science::Biological sciences::Molecular biology
See, Benedict
Regulome of cancer epithelial-mesenchymal transition (EMT)
description During metastasis, cancer cells employ autophagy to meet elevated energy demands, of which the adaptor protein 14-3-3γ may play a role in this autophagic mechanism. It is hypothesized that 14-3-3γ activity promotes autophagy and EMT, and inhibition of 14-3-3γ may lead to the prevention of metastasis by suppressing EMT genes or starving the cancer cells of nutrients through autophagy suppression. To elucidate any differentially expressed genes (DEGs) after EMT induction that are involved in autophagy and may potentially be 14-3-3 protein targets, RNA-Seq was carried out and a pipeline was established to determine the differences in expression of the genes regulated directly or indirectly through 14-3-3γ interaction with transcription factors or repressors. A number of genes that are known to play various roles in autophagy were found to be differentially expressed after treatment with DMOG and TGFβ, which suggests a correlation between autophagy and metastasis. These genes are predicted to interact with 14-3-3 proteins, which suggests 14-3-3γ may have a significant role in regulating autophagy and metastasis, thereby contributing to cancer progression.
author2 Tan Nguan Soon
author_facet Tan Nguan Soon
See, Benedict
format Final Year Project
author See, Benedict
author_sort See, Benedict
title Regulome of cancer epithelial-mesenchymal transition (EMT)
title_short Regulome of cancer epithelial-mesenchymal transition (EMT)
title_full Regulome of cancer epithelial-mesenchymal transition (EMT)
title_fullStr Regulome of cancer epithelial-mesenchymal transition (EMT)
title_full_unstemmed Regulome of cancer epithelial-mesenchymal transition (EMT)
title_sort regulome of cancer epithelial-mesenchymal transition (emt)
publisher Nanyang Technological University
publishDate 2020
url https://hdl.handle.net/10356/140680
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