Muhammad Faraz Arshad Malik1, Lucy K Satherley2, Eleri L Davies3, Lin Ye2, Wen G Jiang4. 1. Metastasis and Angiogenesis Research Group, Cardiff University-Peking University Cancer Institute, Cardiff University School of Medicine, Cardiff, U.K. Department of Biosciences, COMSATS-Institute of Information Technology, Islamabad, Pakistan. 2. Metastasis and Angiogenesis Research Group, Cardiff University-Peking University Cancer Institute, Cardiff University School of Medicine, Cardiff, U.K. 3. Cardiff Breast Centre, University Hospital Llandough, Cardiff and Vale University Health Board, Cardiff, U.K. 4. Metastasis and Angiogenesis Research Group, Cardiff University-Peking University Cancer Institute, Cardiff University School of Medicine, Cardiff, U.K. JiangW@Cardiff.ac.uk.
Abstract
BACKGROUND: The aim of the current study was to examine the role of semaphorin 3C (SEMA3C) in breast cancer. MATERIALS AND METHODS: SEMA3C transcripts expressed by breast tissues were determined using real-time polymerase chain reaction (PCR). Knock-down of SEMA3C was performed in MDA-MB-231 and MCF-7 breast cancer cell lines using anti-SEMA3C hammerhead ribozyme transgenes. The effect of SEMA3C knockdown on cancer cells was determined using in vitro cellular function assays. RESULTS: Higher SEMA3C transcript levels were significantly associated with poor differentiation of cancer cells, and transcript levels were significantly reduced in oestrogen receptor-positive tumours. Knock-down of SEMA3C expression resulted in a decrease in cell proliferation, adhesion and invasion of breast cancer cells. CONCLUSION: Higher SEMA3C expression is correlated with tumour differentiation. Inhibition of SEMA3C reduces adhesion and invasion of breast cancer cells. This suggests that SEMA3C may play a significant role in morphological changes of cancer cells, leading to enhanced growth and dissemination. Copyright
BACKGROUND: The aim of the current study was to examine the role of semaphorin 3C (SEMA3C) in breast cancer. MATERIALS AND METHODS:SEMA3C transcripts expressed by breast tissues were determined using real-time polymerase chain reaction (PCR). Knock-down of SEMA3C was performed in MDA-MB-231 and MCF-7 breast cancer cell lines using anti-SEMA3C hammerhead ribozyme transgenes. The effect of SEMA3C knockdown on cancer cells was determined using in vitro cellular function assays. RESULTS: Higher SEMA3C transcript levels were significantly associated with poor differentiation of cancer cells, and transcript levels were significantly reduced in oestrogen receptor-positive tumours. Knock-down of SEMA3C expression resulted in a decrease in cell proliferation, adhesion and invasion of breast cancer cells. CONCLUSION: Higher SEMA3C expression is correlated with tumour differentiation. Inhibition of SEMA3C reduces adhesion and invasion of breast cancer cells. This suggests that SEMA3C may play a significant role in morphological changes of cancer cells, leading to enhanced growth and dissemination. Copyright
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