Abstract 697
Background
Breast cancer is the most common cancer among women worldwide. TBC1D3 (also referred to as prostate cancer gene 17, PRC17), a hominoid-specific gene, was originally found expressing in breast cancer, Ewing sarcoma and leiomyosarcoma, etc. Thyroid cancer gene-1 (TC-1, also known as C8orf4) is highly expressed in gastric cancer, lung cancer, and breast cancer, which can cause malignant transformation of normal thyroid cells.
Methods
Human breast cancer MCF-7 cells were transfected with or without the Flag-TBC1D3 plasmid, then transwell migration experiment and scratches assays were made to analyze the effect. Total RNA was extracted from MCF-7 cells, and the full-length open reading frame (ORF) of TC-1 cDNA was amplified by RT-PCR and inserted into the eukaryotic expression vector Flag-pcDNA3.0 to construct the TC-1 eukaryotic expression plasmid FIag- TC-l/pcDNA3.0. Western blot was used to detect the TC-1 expression.
Results
The transwell results showed that the migration number of MCF-7 cells which was transfected with Flag-TBC1D3 was significantly greater than that of MCF-7 cells transfected with Flg-pcDNA3.0 empty vector. Similarly, the migration ability of MCF-7 cells with high expression of TBC1D3 was also significantly stronger than that of the control group. These results indicated that high expression of TBC1D3 promotes cell migration. At the same time, the expression level of TC1 in overexpressed Flg-TBC1D3 group was higher than the control group. Similarly, the transwell results showed the migration ability of MCF-7 cells with high expression of Flag-TC-1 was significantly stronger than that of the control group. However, we used a shRNA that specifically inhibited TC1 expression to infect the MCF-7 cells with the viral vector TC-1(1566) shRNA. The migration ability of MCF-7 cells with high expression of TBC1D3 was not significantly different from the control group.
Conclusions
High expression of TBC1D3 oncogene may promote migration of human MCF-7 cells by regulating the expression of TC-1 in human MCF-7 cells.
Editorial acknowledgement
Legal entity responsible for the study
Medical School of Southeast University.
Funding
Natural Science Foundation of China (81272261).
Disclosure
All authors have declared no conflicts of interest.