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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Expressions of 14-3-3 gamma in Human Malignant Brain Tumors

Kao, Chiu-li 09 September 2004 (has links)
The family of 14-3-3 proteins is crucial for various physiological cellular processes such as signaling, cell growth, division, differentiation, and apoptosis. One of the 14-3-3 proteins members, 14-3-3 gamma, is abundantly expressed in brain and had been detected in the cerebrospinal fluid of patients with different neurological disorders. Although 14-3-3 gamma played critical physiological or pathological role in brain, it has not been reported on brain tumorigenesis. To test expression of 14-3-3 gamma in brain tumor, 3 brain tumor cell lines and 4 normal brain tissues, 24 astrocytoma, 14 glioblastoma mutiform, 2 oligodenroglioma, 1 ependymoma were analyzed using RT-PCR, western blotting, immunohistochemistry, real-time quantitative PCR. The study found that the expressions of 14-3-3 gamma mRNA in all of tumor three cell lines was greater than normal brain tissue, but the 14-3-3 gamma proteins expressed were lower than normal brain tissue. In brain tumor tissues, higher 14-3-3 gamma mRNA expression was detected in 20 of 24 astrocytoma (83%) and higher 14-3-3 gamma protein expression was detected in 9 of 24 astrocytoma (37%). The expression of 14-3-3 gamma mRNA is higher than normal brain tissue in all 14 glioblastoma multiforme (100%), and the 14-3-3 gamma protein was expressed higher in 9 of 14 glioblastoma multiforme than normal brain tissue (64.3%). Besides, the 14-3-3 gamma protein expressed much higher in glioblastoma multiforme than astrocytoma .The copy number of the 14-3-3 gamma gene was higher in astrocytoma and glioblastoma multiforme than normal brain tissue. Thus, this study evidenced that the 14-3-3 gamma protein may play a crucial role during tumorigenesis of brain tumors.
2

Overexpression of 14-3-3 gamma protein in human breast carcinoma

Chen, Chien-min 07 July 2004 (has links)
The chaperone proteins designated 14-3-3 are expressed in all eukaryotic cells; they help to regulate signal transduction pathways controlling proliferation, differentiation, and survival. They associated directly or indirectly with proliferative signal-transducing proteins such as PKC, MEK kinases, PI3-kinase and Raf. In human, there are seven isotypes of 14-3-3 genes: £]¡]beta¡^¡B£^¡]gamma¡^¡B£`¡]epsilon¡^¡B£b¡]eta¡^¡B£m¡]sigma¡^¡B£n/£c¡]tau/theta¡^ and£a¡]zeta¡^, some of which would be pseudogenes, and yeast and plant each have two and fifteen genes. Althought these genes are diverse, all 14-3-3 isotypes share many conservation domains in amino acid sequences. The previous studies have suggested that 14-3-3 sigma is most directly linked to cancer because it is thought to function as a tumor suppressor by inhibiting cell-cycle progression. In tumor formation, inactivation of 14-3-3 sigma occurs with high frequency. More importantly, expression of 14-3-3 sigma is silenced in most breast cancer cells. The 14-3-3 sigma protein is associated with cyclin E-CDK2 complex as well as cyclin B-CDC2 complex and mediated their inactivation by cytoplasmic localization and causing cell-cycle arrest in G2 and G1. However, the roles of other 14-3-3 isotypes in the formation of breast cancer are controversial in published reference. The aim of this study was to determine the differential expressions of 14-3-3 gamma in non-tumor tissues and corresponding tumor tissues. Amplification and overexpression of 14-3-3 gamma in DNA, RNA, and protein of breast tumor tissues were found by experiments of RT-PCR, Western blot analysis, immunohistochemistry and Real-time PCR. However, the role of 14-3-3 gamma in the formation of breast cancer requires further study.

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