Fig. 9: Prolyl 4-hydroxylase (P4H) inhibitors stall proliferation, migration, and invasion and promotes apoptosis of PTC cells. | Cell Death & Disease

Fig. 9: Prolyl 4-hydroxylase (P4H) inhibitors stall proliferation, migration, and invasion and promotes apoptosis of PTC cells.

From: Prolyl 4-hydroxylase subunit alpha-2 acts as a TRIM21 ubiquitination substrate to promote papillary thyroid cancer progression via the glycolytic pathway

Fig. 9

A After treating BCPAP cells with 10 μM and TPC-1 cells with 30 μM 1,4-dihydrophenonthrolin-4-one-3-carboxylic acid (1,4-DPCA), respectively, the cell proliferation was detected by colony formation assay. B After treating BCPAP and TPC-1 cells with 150 μM dimethyloxalylglycine (DMOG), the cell proliferation was detected by colony formation assay. The BCPAP cells were treated with 10 μM 1,4-DPCA and TPC-1 cells were treated with 30 μM 1,4-DPCA, and the cell migration (C), invasion (E) and apoptosis (G) were detected by Transwell assay and flow cytometry. The BCPAP and TPC-1 cells were treated with 150 μM DMOG for 48 h, and cell migration (D), invasion (F) and apoptosis (H) were detected by Transwell assay and flow cytometry. I The mechanistic diagram of this study is presented here. On the one hand, P4HA2, as a substrate of TRIM21, undergoes K48 and K63 linked ubiquitination, leading to its degradation. On the other hand, P4HA2 can cause malignant changes in PTC cells by promoting the expression of key enzymes of the glycolysis pathway, such as PGK1, ENO1, and LDHA, while the use of P4H inhibitors can reverse this change. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

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