The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness

This study was designed mainly to investigate the role of transcription factor, hypoxia inducible factor- 1a (HIF -1a) in enhancing Nav1.5 and nNav1.5 expression in breast cancer that transforms it to become aggressive. siRNA was conducted to knockdown HIF -1 a expression in the aggressive MDAMB-...

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Main Author: Makhtar, Noor Fatmawati
Format: Monograph
Language:English
Published: Pusat Pengajian Sains Kesihatan, Universiti Sains Malaysia 2016
Subjects:
Online Access:http://eprints.usm.my/57499/
http://eprints.usm.my/57499/1/DR%20NOOR%20FATIMAWATI%20MAKHTAR-Eprints.pdf
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author Makhtar, Noor Fatmawati
author_facet Makhtar, Noor Fatmawati
author_sort Makhtar, Noor Fatmawati
building USM Institutional Repository
collection Online Access
description This study was designed mainly to investigate the role of transcription factor, hypoxia inducible factor- 1a (HIF -1a) in enhancing Nav1.5 and nNav1.5 expression in breast cancer that transforms it to become aggressive. siRNA was conducted to knockdown HIF -1 a expression in the aggressive MDAMB- 231 cells whilst hypoxia-mimetic agent. cobalt chloride (CoCI 2) was used to stabilize HIF-1a in the less aggressive MCF-7 cells . Total RNA and protein were extracted and subjected to real-time PCR and Western blotting . Migration and motility assays were carried out to study effect of treatments (siRNA and CoCI2) on metastatic cell behaviours. Nav1 .5 , nNav1 .5, HIF-1a and CA9 expression were all hiqhlv expressed in MDA-MB-231 cells . siRNA caused a siqnificant decreased in HIF -1 a expression (mRNA and protein) and HIF-1 a-common target gene. CA9. mRNA expression of Nav1 .5 but not nNav1.5 was significantly downregulated by siRNA-HIF-1a followed by suppression of migration. When MCF-7 cells were treated with CoCI2 , HIF-1a protein, CA9 and Nav1.5mRNA expression was increased significantly but not nNav1 .5 followed by enhanced motility and migration. In conclusion. transcription factor, HIF-1a able to regulate Nav1 .5 (but not nNav1.5) in breast cancer to promote its aggressiveness.
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format Monograph
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institution Universiti Sains Malaysia
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language English
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publishDate 2016
publisher Pusat Pengajian Sains Kesihatan, Universiti Sains Malaysia
recordtype eprints
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spelling usm-574992023-03-26T00:25:13Z http://eprints.usm.my/57499/ The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness Makhtar, Noor Fatmawati RC254-282 Neoplasms. Tumors. Oncology (including Cancer) This study was designed mainly to investigate the role of transcription factor, hypoxia inducible factor- 1a (HIF -1a) in enhancing Nav1.5 and nNav1.5 expression in breast cancer that transforms it to become aggressive. siRNA was conducted to knockdown HIF -1 a expression in the aggressive MDAMB- 231 cells whilst hypoxia-mimetic agent. cobalt chloride (CoCI 2) was used to stabilize HIF-1a in the less aggressive MCF-7 cells . Total RNA and protein were extracted and subjected to real-time PCR and Western blotting . Migration and motility assays were carried out to study effect of treatments (siRNA and CoCI2) on metastatic cell behaviours. Nav1 .5 , nNav1 .5, HIF-1a and CA9 expression were all hiqhlv expressed in MDA-MB-231 cells . siRNA caused a siqnificant decreased in HIF -1 a expression (mRNA and protein) and HIF-1 a-common target gene. CA9. mRNA expression of Nav1 .5 but not nNav1.5 was significantly downregulated by siRNA-HIF-1a followed by suppression of migration. When MCF-7 cells were treated with CoCI2 , HIF-1a protein, CA9 and Nav1.5mRNA expression was increased significantly but not nNav1 .5 followed by enhanced motility and migration. In conclusion. transcription factor, HIF-1a able to regulate Nav1 .5 (but not nNav1.5) in breast cancer to promote its aggressiveness. Pusat Pengajian Sains Kesihatan, Universiti Sains Malaysia 2016-07 Monograph NonPeerReviewed application/pdf en http://eprints.usm.my/57499/1/DR%20NOOR%20FATIMAWATI%20MAKHTAR-Eprints.pdf Makhtar, Noor Fatmawati (2016) The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness. Project Report. Pusat Pengajian Sains Kesihatan, Universiti Sains Malaysia. (Submitted)
spellingShingle RC254-282 Neoplasms. Tumors. Oncology (including Cancer)
Makhtar, Noor Fatmawati
The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness
title The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness
title_full The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness
title_fullStr The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness
title_full_unstemmed The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness
title_short The role of hypoxia in controlling Volatagegated Sodium Channels (VGSCS) induced breast cancer invasiveness
title_sort role of hypoxia in controlling volatagegated sodium channels (vgscs) induced breast cancer invasiveness
topic RC254-282 Neoplasms. Tumors. Oncology (including Cancer)
url http://eprints.usm.my/57499/
http://eprints.usm.my/57499/1/DR%20NOOR%20FATIMAWATI%20MAKHTAR-Eprints.pdf