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. 2023 Aug 9;14:1162786. doi: 10.3389/fendo.2023.1162786

Figure 10.

Figure 10

The working hypothesis for the mechanism of miR-10a-5p overexpression in OCCC G0 or G1/S Checkpoint. (A) Simplified representation of cell cycle progression function in non-cancerous cells, whereby CDK6 phosphorylates Rb freeing E2F for DNA replication in the S phase. (B) Infographic representation of cell cycle progression in non-malignant cells treated with platinum and/or taxane-containing agents. Cells will sustain DNA and/or microtubule damage resulting in no continued progression through the cell cycle and subsequent cell death. (C) Represents the working hypothesis for cell cycle progression in miR-10a-5p overexpressing OCCC cells. MiR-10a-5p downregulates CDK6 and other important regulators of the cell cycle slowing or halting phosphorylation of Rb leading to inactive or prolonged inactivation of E2F and transition to S Phase and DNA replication. Cells slowed in G1 or senescing in G0 miss the critical chemotherapeutic effects in the S and M phases (red “X”s).