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https://scholarbank.nus.edu.sg/handle/10635/143304
DC Field | Value | |
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dc.title | THE STUDY OF THE RELATIONSHIP OF HS6ST2 WITH CXCL14 AND IFIT1 IN BREAST CANCER | |
dc.contributor.author | VICTORIA KING PEY CHING | |
dc.date.accessioned | 2018-06-19T18:01:04Z | |
dc.date.available | 2018-06-19T18:01:04Z | |
dc.date.issued | 2016-01-22 | |
dc.identifier.citation | VICTORIA KING PEY CHING (2016-01-22). THE STUDY OF THE RELATIONSHIP OF HS6ST2 WITH CXCL14 AND IFIT1 IN BREAST CANCER. ScholarBank@NUS Repository. | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/143304 | |
dc.description.abstract | FROM PREVIOUS STUDY, THE SILENCING OF HS6ST2 IN MCF7 DEMONSTRATED ENHANCED MIGRATION AND INVASION, WHILE THE DNA MICROARRAY PICKED OUT TWO CANDIDATE GENES: CXCL14 AND IFIT1. PRIMARILY, FINDINGS FROM HS6ST2 SILENCING WAS CORROBORATED VIA HS6ST2 OVER-EXPRESSION IN MDA-MB-231 AND MCF7. THROUGH LITERATURE STUDY, CXCL14 HAS A ROLE IN PROMOTING MIGRATION AND INVASION, INDICATIVE OF CXCL14?S INVOLVEMENT IN HS6ST2-SILENCED CELLS. USING DOUBLE SILENCING, THE RELATIONSHIP BETWEEN HS6ST2 AND CXCL14 THAT AFFECTS INVASION AND MIGRATION CAPABILITIES WAS SHOWN. DNA MICROARRAY TOGETHER WITH GENE ONTOLOGY POSTULATED THAT THE CHANGES OBSERVED COULD BE FURTHER ATTRIBUTED TO THE TGF-? PATHWAY THROUGH SMAD2/3 SIGNALLING. ON THE CONTRARY, IFIT1 HAS UNREPORTED FUNCTIONS IN BREAST CANCER. NOVEL FINDINGS OF IFIT1 HAVE SHOWN THE PROTEIN TO BE PRO-TUMOUR ADVANCEMENT. THROUGH IFIT1 SILENCING IN MDA-MB-231 AND MCF7, THERE WERE SIGNIFICANT DECREASE IN MIGRATION, INVASION AND PROLIFERATION. ADDITIONALLY, IHC OF HS6 | |
dc.language.iso | en | |
dc.subject | HS6ST2, CXCL14, IFIT1, breast cancer | |
dc.type | Thesis | |
dc.contributor.department | ANATOMY | |
dc.contributor.supervisor | YIP WAI CHEONG, GEORGE | |
dc.description.degree | Ph.D | |
dc.description.degreeconferred | DOCTOR OF PHILOSOPHY | |
Appears in Collections: | Ph.D Theses (Open) |
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KingPCV.pdf | 4.15 MB | Adobe PDF | OPEN | None | View/Download |
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