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University students usually consist of young people from culturally and linguistically diverse backgrounds, and a group recognised as being at increased risk of STI. This study found lower levels of STI knowledge and STI testing among international students and to a lesser extent, domestic overseas-born students, compared with domestic Australian-born students. International students exhibited lower risk sexual behaviour but were more likely to have had a HIV test than domestic students. This diversity in sexual health knowledge, sexual health services utilisation and sexual experience indicates the need for a variety of public health approaches to improve sexual health.

The current study aims to evaluate for the first time the inhibitory roles of miR-205 in the pathogenesis of anaplastic thyroid carcinoma. In addition, we investigated the mechanisms by which miR-205 regulates angiogenesis and epithelial-to-mesenchymal transition (EMT) in cancer. Two anaplastic thyroid carcinoma cell lines were transfected with the expression vector pCMV-MIR-205. Selected markers of angiogenesis and EMT including vascular endothelial growth factor A (VEGF-A) and zinc finger E-box-binding homeobox 1 (ZEB1) were investigated by Western blot. The interaction of miR-205 expression with EMT and angiogenesis were also investigated by assessment of matrix metalloproteinases 2 and 9 (MMP2 and MMP 9), SNAI1 (Snai1 family zinc finger 1), vimentin, E-cadherin and N-cadherin. The function of miR-205 was further tested with VEGF enzyme-linked immunosorbent assay (ELISA), wound healing, invasion and tube formation assays. Using an animal model, we studied the association of miR-205 with angiogenesis, proliferation and invasion. The following results were obtained. Permanent overexpression of miR-205 significantly suppressed angiogenesis and EMT by simultaneously targeting VEGF-A, ZEB1 and downstream products. Ectopic expression of miR-205 in cancer cells led to decreased migration, invasion and tube formation of endothelial cells. In addition, inhibition of tumour growth, vascularisation and invasion were noted in the mouse tumour xenografts. Our findings provide insights into simultaneous regulatory role of miR-205 in the pathogenesis of anaplastic thyroid carcinoma by suppressing both angiogenesis and EMT. This may open avenues to exploit miR-205 as an alternative cancer therapeutic strategy in the future.

Full Text, Thesis (PhD Doctorate), Doctor of Philosophy (PhD), School of Medical Science, Griffith Health, A variety of factors such as genetic and epigenetic alterations is known to be involved in initiation and progression of the malignant lesion. microRNA dysregulation is identified as one of the epigenetic changes during cancer development. They play important roles in modulating range of pathways including cell differentiation apoptosis, cell invasion, Epithelial-mesenchymal transition (EMT) and angiogenesis. Angiogenesis is a vital process for cancer survival. The process of angiogenesis in malignancy is initially and mainly promoted by vascular endothelial growth factors (VEGFs). Over-expression of VEGF-A in different carcinomas has been reported, and its cross-talk has been described in cancer between angiogenesis and epithelial-to-mesenchymal transition (EMT) process. EMT is a process which generates motile and invasive cells and converts epithelial cells into mesenchymal cells. Subsequently, cells acquire migratory abilities, accumulate resistance to different types of cancer therapies and gain stem-cell like properties.

Full Text, Thesis (PhD Doctorate), Doctor of Philosophy (PhD), School of Medical Science, Griffith Health, Cancer is a disease driven by complex genetic abnormalities. The ultimate outcome of these complex genetic disorders is uncontrolled cell proliferation. There are two major cellular proliferation and survival signalling pathways which are RAS-RAF- MEK-ERK and PI3K-AKT-mTOR proliferation-survival pathways. These proliferation-survival cell signalling pathways receive, carry and transfer important cell signals to the nucleus where the major transcription changes required for cell proliferation and survival occur. In normal cells, this proliferation cell signalling process is controlled, but this process becomes uncontrolled in cancer cells due to complex genetic changes like genetic mutations. One such genetic mutation is the BRAF V600E mutation which transforms the BRAF kinase into an auto-activated kinase. As a result, the RAS-RAF-MEK-ERK proliferation-survival pathway becomes truncated and auto-activated BRAF kinase continuously sends proliferation-survival signals to the nucleus through downstream MEK-ERK signalling molecules. Therefore, BRAF V600E mutated cells proliferate without control, invade & damage surrounding tissues and metastasise all over the body.