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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| Format: | Monograph |
| Language: | English |
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Pusat Pengajian Sains Kesihatan, Universiti Sains Malaysia
2016
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| Online Access: | http://eprints.usm.my/57499/ http://eprints.usm.my/57499/1/DR%20NOOR%20FATIMAWATI%20MAKHTAR-Eprints.pdf |
| _version_ | 1848883639485464576 |
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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. |
| first_indexed | 2025-11-15T18:54:00Z |
| format | Monograph |
| id | usm-57499 |
| institution | Universiti Sains Malaysia |
| institution_category | Local University |
| language | English |
| last_indexed | 2025-11-15T18:54:00Z |
| publishDate | 2016 |
| publisher | Pusat Pengajian Sains Kesihatan, Universiti Sains Malaysia |
| recordtype | eprints |
| repository_type | Digital Repository |
| 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 |