Skip to main content
. 2022 May 21;127(4):637–648. doi: 10.1038/s41416-022-01835-1

Fig. 6. TXN inhibitor overcomes the decreased ALDH1L2 expression mediated radioresistance through promoting the downstream NF-κB signaling pathway.

Fig. 6

a, b Western blotting of indicated proteins with/ without ALDH1L2 knockdown after 6 Gy irradiation. c, d) Western blotting of indicated proteins with/ without ALDH1L2 overexpression after 6 Gy irradiation. Histone H3 was a nuclear marker and β-actin was served as a cytoplasmic marker. e, f Western blotting of proteins with/without PX-12 (20 μM, 16 h) treatment. g Colony formation assays in HCT-15 cell lines with/without PX-12 (20 μM, 16 h) treatment before irradiation. h The survival curves of multi-target single-hit model. i Colony formation assays in HCT 116 cell lines with/without PX-12 (20 μM, 16 h) treatment before irradiation. j The survival curves of multi-target single-hit model. k Overlay of histograms by flow cytometry. l Mean of DHE intensity in cells with/without ALDH1L2 knockdown and with/ without PX-12, after 6 Gy irradiation. m Apoptosis of different cell lines by flow cytometry. n Bar graph to show the percentage of apoptosis cells. o Image of tumours from nude mice. p Weight of tumours harvested in nude mice. q Schematic diagram summarising our working model, namely, decreased ALDH1L2 can interact less with and inhibit the protein degradation of TXN, thereby promoting NF-κB-CAT/SOD2 signaling, followed by increasing ROS scavenge and radioresistance after irradiation. PX-12 inhibits the interaction between ALDH1L2 and TXN and promotes the protein degradation of TXN, and therefore inhibiting the downstream signaling pathway and CRC cells become radiosensitive again. *P < 0.05; **P < 0.01; ***P < 0.001.