Fig. 1: The effects of ADA and PTX long-term exposure on cell cycle dynamics and proliferation in HGSOC models. | Cell Death & Disease

Fig. 1: The effects of ADA and PTX long-term exposure on cell cycle dynamics and proliferation in HGSOC models.

From: ROR1-PI3K/AKT signaling drives adaptive resistance to cell cycle blockade in TP53 mutated ovarian cancer

Fig. 1: The effects of ADA and PTX long-term exposure on cell cycle dynamics and proliferation in HGSOC models.

a Schematic representation of the mechanisms by which adavosertib (ADA) and paclitaxel (PTX) affect the cell cycle in high-grade serous ovarian cancer (HGSOC). Right, clinical trials where ADA and PTX were used in HGSOC. b Representative brightfield microscopy images of drug-naïve (parental) and long-term resistant (lt-res) HGSOC cell models. Scale bar: 100 µm. Below, dose–response curves for ADA and PTX in drug-naïve and lt-res cells following 3-day treatment. Cell viability was assessed using the CellTiter-Glo (CTG) assay. Data are presented as relative proliferation (normalized to untreated control = 1). c Half-maximal effective concentration (EC50) calculated from dose–response curves, with fold changes comparing lt-res to drug-naïve cells. d Baseline proliferation rates determined from luminescence values at day 0 and day 6 (CTG assay). Fold change was calculated relative to day 0. Data represent mean ± SD; n = 4 replicates. Statistical analysis was performed using unpaired two-tailed Student’s t-test (*P < 0.05, **P < 0.01, ***P < 0.001).

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