Regulation of TGF and#946;1 Stimulated Activating Transcription Factor 3 by Micrornas in Human Breast Cancer Cells

dc.contributor.guideSelvamurugan, N
dc.coverage.spatial
dc.creator.researcherAkshaya, R L
dc.date.accessioned2023-08-25T10:19:37Z
dc.date.available2023-08-25T10:19:37Z
dc.date.awarded2023
dc.date.completed2023
dc.date.registered
dc.description.abstractBreast cancer (BC) is the primary cause of cancer-associated deaths among females globally. There is an alarming increase in the BC incidence, which exhibits a vast ethnic disparity in mortality. Bone metastasis of BC is the most pernicious condition characterized by bone pain, pathological fractures, other skeletal complications, etc., and critically affects the life expectancy of metastatic BC patients. Bone metastases of BC are primarily osteolytic and lead to increased osteoclastic bone resorption, which results in the release of transforming growth factor-beta1 (TGF-and#946;1). TGF-and#946;1 is the abundant cytokine in the bone matrix that drives the malignant feed-forward loop of tumor growth in bone. Earlier reports suggested that TGF-and#946;1 induces a continuous and persistent expression of activating transcription factor 3 (ATF3), thereby regulating BC progression and bone metastasis. Recently, several studies have highlighted the importance of dysregulation of small non-coding microRNAs (miRs) in driving BC pathogenesis newline
dc.description.note
dc.format.accompanyingmaterialDVD
dc.format.dimensions
dc.format.extent
dc.identifier.urihttp://hdl.handle.net/10603/508594
dc.languageEnglish
dc.publisher.institutionDepartment of Biotechnology
dc.publisher.placeKattankulathur
dc.publisher.universitySRM Institute of Science and Technology
dc.relation
dc.rightsuniversity
dc.source.universityUniversity
dc.subject.keywordBiotechnology and Applied Microbiology
dc.subject.keywordLife Sciences
dc.subject.keywordMicrobiology
dc.titleRegulation of TGF and#946;1 Stimulated Activating Transcription Factor 3 by Micrornas in Human Breast Cancer Cells
dc.title.alternative
dc.type.degreePh.D.

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