[Retracted] FXYD6 Regulates Chemosensitivity by Mediating the Expression of Na+/K+-ATPase α1 and Affecting Cell Autophagy and Apoptosis in Colorectal Cancer

Figure 4

FXYD6 mediated cell apoptosis and autophagy by mediating the Na+/K+-ATPase α1 pathway in chemosensitivity regulation of CRC cells. (a) Protein expression of ATP-α1 in SW620/Iri and SW620 cells was documented by western blotting. Relative abundance was analyzed by the ImageJ program (upper). Relative expression of ATP-α1 in SW620/Iri and SW620 cells was detected by RT-PCR (lower). (b) Western blotting was conducted in FXYD6 and ATP-α1 silenced SW620 cells and FXYD6 and ATP-α1 overexpressed SW620/Iri cells to understand the relationship of FXYD6 and ATP-α1. Relative abundance was analyzed by the ImageJ program. (c) Western blotting was performed in ATP-α1 silenced cells built on SW620/Iri-FXYD6 cells and ATP-α1 overexpressed cells built on SW620-siFXYD6 cells. Relative abundance was analyzed by the ImageJ program. (d) Autophagy and apoptosis elements were tested by western blotting. LC3I was the internal control of LC3II; β-actin was the internal control of P62, BAX, and Bcl-2. (e) MTT assays were carried out to measure the cell survival rate. (f) The autophagy was documented under different expressions of ATP-α1 by autophagy fluorescence analysis using a fluorescence microscope (200x magnification). Scale bar: 20 μm. Autophagic puncta were counted in 20 cells, and average puncta were used to quantify. (g) The apoptosis was tested by flow cytometric analysis under different expressions of ATP-α1. The apoptosis rate was analyzed by GraphPad Prism 7. LR: early apoptosis; UR: late apoptosis.

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