| Autor: |
Fei-Lin Cao, Yixing Zhou, Zenggui Wu, Jin-Xi Hu, Lijie Chen, Jia-Xiang An, Fanshuang Zhu, Zhaosheng Ma |
| Rok vydání: |
2020 |
| Předmět: |
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| DOI: |
10.21203/rs.3.rs-24717/v1 |
| Popis: |
Background Aquaporin 3 (AQP3) and Cellular-mesenchymal to epithelial transition factor (c-Met) are both overexpressed in human breast cancer and highly related to proliferation and migration. However, it is still unclear whether c-Met is associated with AQP3. The study objective was to explore the relationship between c-Met and AQP3 in human breast cancer. Methods We used immunohistochemistry to determine the expression of AQP3 and c-Met in breast cancer tissue specimens and analysed whether there was any correlation between the two molecules. Real-time quantitative polymerase chain reaction and Western blotting were used to detect AQP3 expression in MCF-7 and MDA-MB-231 cells after human hepatocyte growth factor (hHGF) treatment and/or transfection with c-Met silencing small interfering (si)RNA. Additionally, cell migration was examined with a wound scratch assay. Results Based on the immunohistochemical results combined with the clinicopathological data of 59 breast cancer patients, c-Met exhibited a significant correlation with AQP3 in breast cancer tissue. Studies have shown that hHGF can increase c-Met phosphorylation, and we discovered that the hHGF-induced increase in AQP3 expression was dose dependent. However, after reducing c-Met expression with c-Met-specific siRNA, AQP3 expression decreased accordingly. Additionally, the wound scratch assay showed that AQP3-specific siRNA or c-Met-specific siRNA significantly inhibited breast cancer cell migration, which was promoted by hHGF. Conclusions Our study indicated that AQP3 expression was regulated by c-Met in human breast cancer. These discoveries may help us comprehend the mechanisms underlying breast cancer development and invasion and offer another possibility for targeted treatment of breast cancer. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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