Background: Breast cancer remains a leading cause of cancer-related mortality worldwide, with therapeutic outcomes frequently limited by drug resistance, toxicity, and metastatic progression. Quinoline-based heterocycles have emerged as promising anticancer scaffolds owing to their diverse pharmacological properties and amenability to structural modification. This study evaluated the antiproliferative and cell migration inhibitory activities of a novel quinoline compound and its derivative against human breast adenocarcinoma (MCF-7) cells.
Methods: MCF-7 cells were treated with quinoline (8OHQ/BA/3-PYr) and its hydroxyphenyl derivative (8OHQ/BA/4-HOBA) at concentrations ranging from 25–400 µg/mL for 48 h. Cell viability was determined using the MTT assay, and IC₅₀ values were estimated by nonlinear regression analysis. Treatment-induced morphological alterations were examined by phase-contrast microscopy. The more potent derivative was further evaluated for its effect on cell migration using an in vitro scratch wound-healing assay, in which wound closure was quantified at 24 and 48 h relative to untreated controls.
Results: Both compounds demonstrated concentration-dependent cytotoxicity against MCF-7 cells. The quinoline derivative exhibited greater activity across all tested concentrations, with cytotoxicity increasing from 53.86% to 63.60%, compared with 31.13% to 57.17% for the parent compound. The derivative showed significantly enhanced potency, with an IC₅₀ of 6.28 µM compared with 20.73 µM for quinoline. Phase-contrast microscopy revealed concentration-dependent cell rounding, detachment, reduced confluence, and increased cellular debris, which were more pronounced following derivative treatment. In the scratch assay, untreated cells achieved 88.4 ± 3.1% and 96.2 ± 2.4% wound closure at 24 and 48 h, respectively, whereas derivative-treated cells showed significantly reduced wound closure of 46.7 ± 2.8% and 61.5 ± 3.6% at the respective time points (p < 0.001), corresponding to approximately 47% and 36% inhibition of cell migration.
Conclusion: Structural modification of the quinoline scaffold significantly enhanced its biological activity against MCF-7 breast cancer cells. The hydroxyphenyl-substituted derivative demonstrated superior cytotoxicity, a threefold lower IC₅₀, pronounced morphological evidence of reduced cell viability, and significant inhibition of cell migration. These findings suggest that quinoline structural optimization may yield compounds with dual antiproliferative and migration-inhibitory properties, supporting further mechanistic studies and preclinical evaluation as potential therapeutic agents for breast cancer.