Background:There is discrepancy of results among various individual and me-ta-analytical studies about the effect of metformin on cancer risk and patients’ survival. Therefore, we have conducted a comprehensive, updated meta-analysis to evaluate the preventive and therapeutic effects of metformin for cancer patients, as well as the inci-dence of adverse reactions, among metformin users.Methods:A total of 18 studies (10 cohort studies and 8 randomized controlled trials) in-volving 1,300,820 participants from Europe, North America, and Asia were included in this meta-analysis.Results:No significant association was found between metformin use and overall survival (Hazard ratio = 1.02; 95% CI, 0.80 – 1.30) and progressive-free survival (Hazard ratio = 1.00; 95% CI, 0.76 – 1.31). In addition, the summary risk estimates for adverse reactions of metformin were not statistically significant between intervention and control groups (Risk Ratio = 1.11; 95% CI, 0.94 – 1.31). However, metformin use was associated with a reduction in cancer risk (Hazard ratio = 0.90, 95% CI, 0.86 – 0.94).Conclusion:Metformin does not significantly prolong the overall survival and progressive-free survival of cancer patients, but it may effectively reduce the risk of cancer occurrence.

01 Jun 2024·Cancer Letters

NUCB2 inhibition antagonizes osteosarcoma progression and promotes anti-tumor immunity through inactivating NUCKS1/CXCL8 axis

Article

Author: Zhao, Wenzhi ; Zhang, Lu ; Wang, Yuan ; Zheng, Shuo ; Wang, Yiping ; Li, Xiaojie ; Pan, Deyue ; Han, Chuanchun ; Han, Jian ; Ji, Renchen

The oncogenic properties of Nucleobindin2 (NUCB2) have been observed in various cancer types. Nevertheless, the precise understanding of the biological functions and regulatory mechanisms of NUCB2 in osteosarcoma remains limited. This investigation reported that NUCB2 was significantly increased upon glucose deprivation-induced metabolic stress. Elevated NUCB2 suppressed glucose deprivation-induced cell death and reactive oxygen species (ROS) increase. Depletion of NUCB2 resulted in a reduction in osteosarcoma cell proliferation as well as metastatic potential in vitro and in vivo. Mechanically, NUCB2 ablation suppressed C-X-C Motif Chemokine Ligand 8 (CXCL8) expression which then reduced programmed cell death 1 ligand 1 (PD-L1) expression and stimulated anti-tumor immunity mediated through cytotoxic T cells. Importantly, a combination of NUCB2 depletion with anti-PD-L1 treatment improved anti-tumor T-cell immunity in vivo. Moreover, we further demonstrated that NUCB2 interacted with NUCKS1 to inhibit its degradation, which is responsible for the transcriptional regulation of CXCL8 expression. Altogether, the outcome emphasizes the function of NUCB2 in osteosarcoma and indicates that NUCB2 elevates osteosarcoma progression and immunosuppressive microenvironment through the NUCKS1/CXCL8 pathway.

01 Apr 2024·Journal of Bone Oncology

BMS-794833 reduces anlotinib resistance in osteosarcoma by targeting the VEGFR/Ras/CDK2 pathway

Article

Author: Guan, Mingyang ; Jia, Chenxu ; Meng, Qingtao ; Zhao, Wenzhi ; Han, Jian ; Zhang, Bolun ; Wang, Peng

BackgroundOsteosarcoma, a tumor that originates from bone cells, has a poor prognosis and a high degree of malignancy. Anlotinib, a small-molecule multi-target tyrosine kinase inhibitor (TKI), is the first-line drug in treating osteosarcoma, especially in late-stage osteosarcoma. However, patients often develop resistance after using anlotinib for a certain period, which poses a challenge to its further clinical application. Recently, several TKIs, for instance regorafenib and cabozantinib, have showed clinical interest in treating osteosarcoma and target both vascular endothelial growth factor receptor (VEGFR) and mesenchymal epithelial transition factor (c-MET). Therefore, the identification of new TKI warrants further investigation.MethodsWe performed CCK8 aasays to confirm that BMS-794833 sensitization osteosarcoma cells to anlotinib. Bioinformatics analysis and rescue experiments showed that the reduce of resistance were dependent on the VEGFR/Ras/CDK2 pathway. Cell line based xenograft model were used to demonstrate that BMS-794833 and anlotinib could synergistically treat OS.ResultsHere, we found that BMS-794833 reduced anlotinib resistance in osteosarcoma by targeting the VEGFR/Ras/CDK2 pathway. CCK8 assay showed that BMS-794833 significantly improved the resistance of osteosarcoma cells to anlotinib. The results of rescue experiments showed that the regulatory effects of BMS-794833 on the proliferation and drug resistance of osteosarcoma cells were dependent on the VEGFR/Ras/CDK2 pathway. In addition, BMS-794833 affected the resistance of osteosarcoma cells to anlotinib through epithelial-mesenchymal transition (EMT) and apoptosis pathways. More importantly, BMS-794833 and anlotinib exerted synergistic therapeutic effects against osteosarcoma in vivo.ConclusionAltogether, this study reveals a new (VEGFR)-targeting drug that can be combined with anlotinib for the treatment of osteosarcoma, which provides an important theoretical basis for overcoming anlotinib resistance.

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