Fig 2: The quantified parameters of MDA-MB-231 cells following DOX treatment: (A) the cell growth curves of three independent experiments with a mean (a dashed line); (B) the reciprocal relationship between mitotic (2C) and polyploid (>4C) cell numbers overtime for three independent experiments (with SD); (C) representative differential mitotic counts (from Experiment 3, shown in (A) by the green line); (D) viability test with trypan blue from Experiment 3 (green curve in (A) and in (C)); (E) results of gene transcription evaluation obtained by Selfie digital PCR for three gene transcripts quantified per gene copy and per cell (as transcripts per gene copy multiplied by the average ploidy in the same experiment)—the average of three technical replicates with SEM; and (F) the dynamics of the senescence marker Sa-ß-gal and proliferation marker Ki-67 along with DNA double-strand breaks (?H2AX) in three independent experiments and their repair by homologous recombination—cells with colocalized Rad51/?H2AX foci. (ANOVA with post hoc analysis (Tukey’s HSD test), *** p < 0.001.

Fig 3: Representative pictures of DNA repair of telomere DNA double-strand breaks by RAD51-dependent homologous recombination (HR) involving promyelocytic leukemia (PML) bodies, a sign of alternative lengthening of telomeres (ALT) in giant post-DOX cell nuclei undergoing MS cycles with sorting the damage signaling DNA out into the cytoplasm and reconstituting subnuclei free of it: (A–D) Days 5–8 post-DOX (n = 3). The typical HR configurations are boxed, the extranuclear damaged DNA on (D) arrowed. (E,F) Reconstitution of subnuclei in two similar cells (DOX-D8-9): (E) the extranuclear damaged DNA (arrowed) does not contain PML bodies; and (F) FISH with the telomere and cen#2 probes (n = 3) showing the telomere label cluster in the extranuclear DNA (arrowed). (G–I) The release of four repaired subnuclei (boxed) from a defect in the giant mother nucleus (reconstructed in J); high Ki-67 positivity of the sorted DNA signaling damage by ?H2AX-label on DOX-D19 (n = 3). Bars = 10 µm.

Fig 4: Summary of ovarian cancer response to compressive stimulus within a 3D agarose-collagen I hydrogel. Arrows indicate the applied compressive force (applied from the bottom) and its reactive force (represented by the top arrow). Ovarian cancer cells under compressive stimulus display an invasive morphology through their elongation and increase in aspect ratio. They also enhance proliferation and reduce overall cell death as shown in the immunohistochemical staining of ki67 and caspase-3 respectively. Compressive stimulus consistently upregulates CDC42 and chemoresistance to standard ovarian cancer drug treatments paclitaxel and carboplatin. Treatment with the CDC42 inhibitor ML141 facilitates chemotherapeutic response through enhanced cell death and reduced proliferation.

Fig 5: Effect of the selected extracts on ECFC proliferation and differentiation. (A) Representative images of Ki67 and vWF staining of ECFCs treated 48 h with the ethanolic extracts of mango (4.99 µg/mL) and olive (46.67 µg/mL) leaves, and red grape pomace (11.67 µg/mL). (B) Box and whisker diagrams of the effect of the selected extracts on the proliferation and differentiation of ECFCs after 48 h of treatment. * p-value: * p < 0.05; ** p < 0.01; *** p < 0.001.