Figure 1.
Figure 1. PGAM1 depletion selectively sensitizes cancer cells to DNA-damaging agents. (A and B) Clonogenic assay. PGAM1-depleted (shPGAM1#1, #2, #3) HeLa or scramble (Scr) cells were treated with indicated agents for 14 d. Knockdown efficiency was measured by immunoblotting. (C) Cell apoptosis assay. Cells as described in A were treated with CPT (1 µM), CDDP (10 µM), ADR (3 µM), or VP-16 (0.1 µM) for 48 h, and apoptotic cells were analyzed by Annexin V–PI dual staining. (D) Reconstitution of PGAM1 in PGAM1 knockdown cells. PGAM1 stable knockdown cells expressing shRNA-resistant WT PGAM1 or empty vector (EV) were treated with CPT (1 µM) for 48 h. Apoptotic cells were measured as in C. Error bars represent mean ± SD of triplicates. ***, P < 0.001.

PGAM1 depletion selectively sensitizes cancer cells to DNA-damaging agents. (A and B) Clonogenic assay. PGAM1-depleted (shPGAM1#1, #2, #3) HeLa or scramble (Scr) cells were treated with indicated agents for 14 d. Knockdown efficiency was measured by immunoblotting. (C) Cell apoptosis assay. Cells as described in A were treated with CPT (1 µM), CDDP (10 µM), ADR (3 µM), or VP-16 (0.1 µM) for 48 h, and apoptotic cells were analyzed by Annexin V–PI dual staining. (D) Reconstitution of PGAM1 in PGAM1 knockdown cells. PGAM1 stable knockdown cells expressing shRNA-resistant WT PGAM1 or empty vector (EV) were treated with CPT (1 µM) for 48 h. Apoptotic cells were measured as in C. Error bars represent mean ± SD of triplicates. ***, P < 0.001.

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