Targeting miR-506 in leiomyosarcoma therapy: simultaneous suppression of metastatic potential and potentiation of pirarubicin efficacy
Year: 2026
Type: article
Abstract: Background: Extensive studies have established that miR-506 inhibits epithelial-mesenchymal transition (EMT) in epithelial ovarian cancer by upregulating E-cadherin while suppressing vimentin and N-cadherin. Additionally, miR-506 has been shown to enhance the therapeutic response of serous ovarian cancer to cisplatin and olaparib via modulation of RAD51. However, the functional role of miR-506 in leiomyosarcoma (LMS) remains unexplored. This study aims to investigate the expression and functional role of miR-506 in soft tissue LMS, focusing on its clinical relevance and impact on tumor progression and chemosensitivity. Methods: functional assays were performed to elucidate the role of miR-506 in soft tissue LMS pathogenesis and its underlying mechanism in modulating chemosensitivity. Results: functional studies showed that miR-506 upregulated epithelial markers (E-cadherin and β-catenin) while suppressing mesenchymal markers (vimentin and N-cadherin), consequently inhibiting LMS cell proliferation, migration, and invasion. Moreover, miR-506 enhanced pirarubicin sensitivity by dual mechanisms: (I) By downregulating DNA damage homologous repair proteins (ATM, ATR, RAD51, and RAD52), and (II) modulating EMT via targeting EMT-associated regulatory protein Slug and mesenchymal marker vimentin. Conclusions: and modulates homologous recombination repair pathways, effectively inhibiting LMS cell proliferation, migration, and invasion while enhancing chemosensitivity.
Source: Translational Cancer Research
Authors: Ting Li, Ruwei Xing, Feng Li, Jilong Yang
Language: English
Subfield: Cancer Research
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W7223321453