This system is self-assembled from a pentavalent arsenate prodrug (AsO₄³⁻), the hydrogen sulfide (H₂S) donor GYY4137, and the lactate export inhibitor diclofenac (DCF), enabling precise responsiveness to the acidic and reductive tumor microenvironment...This is evidenced by the release of damage-associated molecular patterns (DAMPs), dendritic cell maturation, and T cell activation. By integrating lactate metabolism regulation, prodrug activation, and immune remodeling, this strategy provides a promising avenue for combined chemo-immunotherapy of HCC.

Mechanistically, SUN5 activates the NF-κB signaling pathway, which can be inhibited by the IKK inhibitor BAY11-7082...Moreover, xenograft transplantation experiments reveal that the knockdown of SUN5 inhibits glycolysis and tumorigenesis in vivo. Taken together, these findings indicate that SUN5 enhances the glycolysis and tumorigenesis of CRC cells via interaction with TRIM28, which provides a potential target for the diagnosis and treatment of CRC.

P1/2, N=50, Not yet recruiting, Tanta University

This study investigates the characterization and biological effects of Dual Drug-Loaded Nanoparticles on HepG2/doxorubicin (DOX) cells, focusing on the anti-cancer ability of Doxorubicin/Curcumin-Polyethylene Glycol-Polycaprolactone Nanoparticles (DOX/Cur-PEG-PCL-NPs)...These results demonstrate that DOX/Cur-PEG-PCL-NPs effectively reverse chemoresistance and suppress tumor progression through modulation of the Nrf2 pathway and apoptosis induction, offering a promising strategy for targeted liver cancer therapy. The online version contains supplementary material available at 10.1007/s10616-025-00855-y.

Four immune metabolism-associated diagnostic genes were identified, including TRAF3IP2, RIPK1, KEAP1, and DPP4 for OMAS.

Furthermore, CHL reduced p-p65 expression by 5-fold, indicating its effective inhibition of NF-κB transcriptional activity and thereby alleviating inflammatory responses. Therefore, the LAP-activable co-prodrug CHL holds promising potential as a candidate for the synergistic treatment of liver injury.

P3, N=270, Not yet recruiting, Affiliated Cancer Hospital of Shandong First Medical University (Shandong Institute of Cancer Prevention and Treatment and Shandong Cancer Hospital);

P1, N=72, Completed, Merry Life Biomedical Co., Ltd. | Recruiting --> Completed | Trial primary completion date: Apr 2025 --> Jul 2025

Kanglaite injection (KLT) combined with CCRT (SUCRA: 85.1%; 90.1%) was optimal for enhancing performance status and one-year survival rate...Nevertheless, the findings shall be validated in multicenter, better-designed RCTs. The PRISMA registration details for this study can be found at: https://www.crd.york.ac.uk/PROSPERO/view/CRD42024574242.

Kanglaite Injection (KLT) combined with chemotherapy had the best effect on reducing tumor markers CEA and CA153. Although a 2021 network meta-analysis (Comparative Efficacy and Safety of Chinese Herbal Injections Combined With Cyclophosphamide and 5-Fluorouracil Chemotherapies in Treatment of Breast Cancer: A Bayesian Network Meta-Analysis) examined chemotherapy combined with Chinese medicine injections for breast cancer, it was limited to the CF regimen and assessed few outcomes, with some lower-quality studies included (excluded herein)...This provides more comprehensive results, identifying SQFZ as most effective for improving response rate and Karnofsky Performance Status (KPS), thereby enhancing clinical utility. https://www.crd.york.ac.uk/PROSPERO/myprospero, identifier [CRD42024589306].

These findings indicate that γT3 and δT3 inhibit HCC2998 cell proliferation by activating the DDR pathway, highlighting their potential as therapeutic agents to overcome cell cycle arrest resistance in CRC. This study provides critical insights into the molecular actions of γT3 and δT3, supporting their further investigation as promising candidates for CRC intervention.

These dual actions-tumor chemosensitization via ZWINT/NF-κB inhibition and immune reprogramming via KLF2 activation-were functionally interconnected, as cytokines released by PLB-primed T cells reinforced NF-κB suppression in tumor cells. Collectively, our findings identify PLB as a low-cost small molecule that integrates cisplatin sensitization with immune activation, offering a promising adjunctive strategy for cisplatin-refractory TSCC.