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. 2021 Apr 27;13(9):2116. doi: 10.3390/cancers13092116

Figure 2.

Figure 2

A combination of LUT and I3C induces G1 cycle arrest and apoptosis in ER+ breast cancer cells. (A) The time course (24 h, 48 h, and 72 h) of cell growth inhibition by individual or combination of LUT and I3C in MCF7and T47D cells. (B) MCF7 cells were arrested in different stages of cell cycle (percentage indicated) by the individual or the combination of LUT and I3C at 24 h and 48 h. Cycle phases were analyzed by flow cytometry after propidium iodide (PI) staining. (C) Combined LUT and I3C significantly induced MCF7 cell apoptosis at 48 h. Apoptotic cells were counted by flow cytometry after Annexin V staining. (D) Cell cycle main regulator p21 protein level (measured by Immunoblot) was significantly increased by L30I40 in MCF7cellsat 24 h and 48hbut only at 48 h inT47D cells. The MCF7 and T47D cells at 24h and 48h were the same samples on the same membrane and share the same GAPDH bands, after detecting one protein, the membrane was stripped and reprobed the second or third proteins. (E) Apoptotic effector Bcl-xL and Bax protein levels (by Immunoblot) were significantly changed by L30I40 at 24 h and 48 h treatment in MCF7 and T47D cells. (F) L30I40 decreased CDK4/6 in complex with Cyclin D1 (by immunoprecipitation assay) in MCF7 and T47D cells. (G) Proposed mechanism of the G1 cell-phase arrest induced by the combination of LUT and I3C. Data are means ± SEM of at least three independent experiments performed in duplicate. * p < 0.05; ** p < 0.01.