Caprin-1 silencing enhances cisplatin sensitivity in CC by suppressing the YY1/HSP90α axis, accelerating IDH1 degradation, and activating ferroptosis.

LA-based IMS demonstrate significant potential as chemotherapeutic agents for the treatment of breast cancer.

In this study, SP94-LCP/DOX&Bcl-2 siRNA was successfully prepared. It exhibited remarkable targeting ability and antitumor activity, significantly enhancing the therapeutic effect of doxorubicin and siRNA on HCC. The construction of this drug delivery system provided a novel strategy for the clinical treatment of HCC.

KRT5+ cells form cancer organoids over successive passages, are tumorigenic in serial dilution xenograft assays, and are resistant to the antineoplastic agents, doxorubicin and cisplatin. Together, these findings support a model in which HGSC contains two hierarchically related cell populations: KRT5+, OPN-responsive CPCs and KRT5-, non-tumorigenic cells that form a niche producing OPN. Inhibiting pathways that sustain this niche may enable reduced dosing of highly toxic chemotherapeutic agents while enhancing therapeutic efficacy in HGSC.

P=N/A, N=12, Completed, UMC Utrecht | Not yet recruiting --> Completed | Trial completion date: Dec 2025 --> Mar 2026 | Trial primary completion date: Dec 2025 --> Mar 2026

However, these effects were not consistently supported by functional or histopathological findings. Further studies using more severe or longer-term cardiotoxicity models are warranted to clarify its cardioprotective potential.

Herein, we developed a pH-responsive nanocascade reactor (DOX@Cu-SKH) based on a copper infinite coordination polymer, which was functionalized with hyaluronic acid (HA) to deliver doxorubicin (DOX) for achieving efficient synergistic chemotherapy and chemodynamic therapy (CT/CDT)...At the same time, sulfasalazine effectively inhibited glutathione peroxidase 4 (GPX4) activity, further amplifying oxidative stress in tumor cells. In vivo studies utilizing H22 tumor-bearing mouse model demonstrated that the combination of CT/CDT significantly suppressed tumor growth with 88.7% tumor inhibition. This study introduces a novel strategy for the direct construction of a nanocascade reactor that achieves efficient CT/CDT combination therapy.

Based on a biomimetic "core-shell" nanoplatform (siXkr8/Dox@PMLC), this system initiates a cascade within the TME where Doxorubicin (Dox) induces tumour cells to generate drug-loaded apoptotic bodies (ApoBDs)...Furthermore, through targeted blockade of the CD24/Siglec-10 immune axis, the nanoplatform enhances macrophage-mediated phagocytosis of CSCs. In summary, this strategy achieves deep eradication of CSCs and synergistically enhances anti-tumour immunotherapy, demonstrating significant translational potential.

Recurrent disease caused by drug-tolerant persister cells (DTPs) that evade chemotherapeutic agents (e.g., doxorubicin hydrochloride (DOX) and paclitaxel (PTX)) is a significant challenge in treating TNBC...The results revealed that pharmacological inhibition of autophagy (hydroxychloroquine) or lysosomal activity (bafilomycin A1) compromised DTPs' survival...Our results demonstrated that increased autophagy-lysosomal process renders DTP cell survival in TNBC by maintaining mitochondrial reactive oxygen species (mROS) generation, which, in turn, contributes to chemotherapy resistance. A potential treatment strategy for eradicating DTP cells and preventing tumor recurrence in TNBC involves targeting these mechanisms.

In a 4T1 murine model, Lip CBB@DOX produced the greatest tumor growth inhibition without aggravating systemic toxicity; histology revealed reduced tumor-associated extramedullary hematopoiesis and extensive tumor necrosis. Collectively, these results indicate that CBB is a safe and effective liposomal excipient that enhances DOX delivery and amplifies ICD-mediated antitumor immunity, offering a promising strategy to improve TNBC therapy and informing future optimization of biguanide-modified liposomal carriers.

Although the combination of glucose oxidase (GOx)-based starvation therapy and chemodynamic therapy (CDT) has shown great potential, the severe systemic toxicity caused by the non-specific activity of GOx in the blood circulation and the insufficient immunogenic cell death (ICD) effect induced by doxorubicin (DOX) jointly restrict its clinical transformation...The severe oxidative stress caused by this process and DOX synergistically enhances the ICD effect, successfully triggering calreticulin (CRT) exposure, high mobility group protein B1 (HMGB1), and ATP release, thereby promoting dendritic cell maturation and cytotoxic T lymphocyte infiltration, and stimulating a strong anti-tumor immune response in the 4T1 tumor-bearing mouse model. In this study, the problems of safety and synergistic efficacy were solved simultaneously through ingenious chemical design, providing a new paradigm for the development of intelligent tumor combination therapy.

Our study identified key gene-based genotypes (Type II/III) of distinct GEPNEC patients and yielded their prognosis and therapeutic utility.