Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/143304
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dc.titleTHE STUDY OF THE RELATIONSHIP OF HS6ST2 WITH CXCL14 AND IFIT1 IN BREAST CANCER
dc.contributor.authorVICTORIA KING PEY CHING
dc.date.accessioned2018-06-19T18:01:04Z
dc.date.available2018-06-19T18:01:04Z
dc.date.issued2016-01-22
dc.identifier.citationVICTORIA 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.urihttp://scholarbank.nus.edu.sg/handle/10635/143304
dc.description.abstractFROM 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.isoen
dc.subjectHS6ST2, CXCL14, IFIT1, breast cancer
dc.typeThesis
dc.contributor.departmentANATOMY
dc.contributor.supervisorYIP WAI CHEONG, GEORGE
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY
Appears in Collections:Ph.D Theses (Open)

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