It is shown that S100A6 is present at elevated levels in ovarian cancer and promotes cancer cell proliferation, migration, and invasion while suppressing cell death, and a small regulatory RNA molecule, Let-7c-3p, that directly suppresses S100A6 production is identified.
Abstract
Simple Summary Ovarian cancer is a highly aggressive disease often diagnosed at advanced stages, leading to limited treatment options and poor patient outcomes. Identifying key molecules that drive tumor growth and spread may help develop more effective diagnostic and therapeutic strategies. In this study, we investigated the role of a protein called S100A6 in ovarian cancer cells and tumor tissues. Our findings show that S100A6 is present at elevated levels in ovarian cancer and promotes cancer cell proliferation, migration, and invasion while suppressing cell death. We further identified a small regulatory RNA molecule, Let-7c-3p, that directly suppresses S100A6 production, and we uncovered that S100A6 exerts its effects by activating a cellular communication pathway known as JAK-STAT. Importantly, restoring Let-7c-3p function reversed the cancer-promoting effects of S100A6. These results highlight a new regulatory axis that drives ovarian cancer progression and suggest that targeting this pathway may offer new opportunities for diagnosis and treatment of this devastating disease.
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