Harnessing nanomedicine for breast cancer therapy through the immunomodulatory activity of BCc1

Although BCc1 represents a novel nanochelating-based nanomedicine, its route- and dose-dependent impacts on mammary oncogenesis, immunoregulation, and non-coding RNA (ncRNA) dynamics remain poorly defined. Here, female BALB/c mice bearing subcutaneous 4T1 mammary carcinomas were treated with oral or intraperitoneal BCc1 at diverse doses for 24 days. BCc1 restricted primary tumor kinetics in a dose- and route-dependent manner without compromising systemic tolerability or body weight. Notably, oral administration at \(10\;\text{m}\text{g}/\text{k}\text{g}\) exerted the most profound antitumor efficacy, significantly reducing final tumor burden. This therapeutic outcome was associated with elevated interleukin-12 ( \(\text{I}\text{L-}12\) ) levels, an attenuated transforming growth factor-β1 \((\text{T}\text{G}\text{F-}\upbeta 1)/\text{I}\text{L-}12\) ratio, sustained tumor necrosis factor- \(\upalpha \) ( \(\text{T}\text{N}\text{F-}\upalpha \) ) expression, enhanced intratumoral immune infiltration, increased apoptotic indices, and heightened natural killer (NK) cell-mediated cytotoxicity. Furthermore, BCc1 modulated the expression of interleukin-27 ( \(\text{I}\text{L-}27)\) , \(\text{B}\text{A}\text{X}/\text{B}\text{C}\text{L-}2\) , microRNA-145-5p (miR-145-5p), and circular RNA Golgi phosphoprotein 3 (circGOLPH3), highlighting alterations in immunomolecular and apoptotic pathways, findings further supported by exploratory in silico molecular docking simulations. Collectively, these data show that oral BCc1 at \(10\;\text{m}\text{g}/\text{k}\text{g}\) mitigates breast tumor progression in association with immunomodulatory, apoptotic, and post-transcriptional changes, supporting its potential as a candidate nanomedicine for breast cancer therapy.