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3. Glucagon Enhances Chemotherapy Efficacy By Inhibition of Tumor Vessels in Colorectal Cancer

Author

Xu, Yuxue, primary, Ni, Feixue, additional, Sun, Daxi, additional, Peng, Yue, additional, Zhao, Yaxuan, additional, Wu, Xiaojun, additional, Li, Shasha, additional, Qi, Xiangyu, additional, He, Xinkang, additional, Li, Min, additional, Zhou, Yizi, additional, Zhang, Chao, additional, Yan, Miao, additional, Yao, Cuifang, additional, Zhu, Shuaishuai, additional, Yang, Yang, additional, An, Baijiao, additional, Yang, Chunhua, additional, Zhang, Guilong, additional, Jiang, Wenguo, additional, Mi, Jia, additional, Chen, Xinju, additional, Wei, Pengfei, additional, Tian, Geng, additional, and Zhang, Yin, additional

Published
2023
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4. Glucagon Enhances Chemotherapy Efficacy By Inhibition of Tumor Vessels in Colorectal Cancer.

Author

Xu, Yuxue, Ni, Feixue, Sun, Daxi, Peng, Yue, Zhao, Yaxuan, Wu, Xiaojun, Li, Shasha, Qi, Xiangyu, He, Xinkang, Li, Min, Zhou, Yizi, Zhang, Chao, Yan, Miao, Yao, Cuifang, Zhu, Shuaishuai, Yang, Yang, An, Baijiao, Yang, Chunhua, Zhang, Guilong, and Jiang, Wenguo

Subjects
NEOVASCULARIZATION, GLUCAGON, COLORECTAL cancer, COLON tumors, VASCULOGENIC mimicry, LIPOSOMES, CANCER chemotherapy
Abstract

Chemotherapy is widely used to treat colorectal cancer (CRC). Despite its substantial benefits, the development of drug resistance and adverse effects remain challenging. This study aimed to elucidate a novel role of glucagon in anti‐cancer therapy. In a series of in vitro experiments, glucagon inhibited cell migration and tube formation in both endothelial and tumor cells. In vivo studies demonstrated decreased tumor blood vessels and fewer pseudo‐vessels in mice treated with glucagon. The combination of glucagon and chemotherapy exhibited enhanced tumor inhibition. Mechanistic studies demonstrated that glucagon increased the permeability of blood vessels, leading to a pronounced disruption of vessel morphology. Signaling pathway analysis identified a VEGF/VEGFR‐dependent mechanism whereby glucagon attenuated angiogenesis through its receptor. Clinical data analysis revealed a positive correlation between elevated glucagon expression and chemotherapy response. This is the first study to reveal a role for glucagon in inhibiting angiogenesis and vascular mimicry. Additionally, the delivery of glucagon‐encapsulated PEGylated liposomes to tumor‐bearing mice amplified the inhibition of angiogenesis and vascular mimicry, consequently reinforcing chemotherapy efficacy. Collectively, the findings demonstrate the role of glucagon in inhibiting tumor vessel network and suggest the potential utility of glucagon as a promising predictive marker for patients with CRC receiving chemotherapy. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Additional file 1 of PDGFB-targeted functional MRI nanoswitch for activatable T1–T2 dual-modal ultra-sensitive diagnosis of cancer

Author

Zhang, Ya’nan, Liu, Lu, Li, Wenling, Zhang, Caiyun, Song, Tianwei, Wang, Peng, Sun, Daxi, Huang, Xiaodan, Qin, Xia, Ran, Lang, Tian, Geng, Qian, Junchao, and Zhang, Guilong

Abstract

Additional file 1: Figure S1. The hydrodynamic sizes of different samples. Figure S2. TG curves, XPS spectra, FT-IR spectra, and zeta potential of different samples. STEM image of FMS. Figure S3. Hydrodynamic size variation of PDGFB-FMS in different media. Figure S4. TEM images of FMS after different treatments and corresponding hydrodynamic size distribution. Figure S5. T1WI and T2WI of FMS. Figure S6. r1 and r2 values of FMS. Figure S7. r1 value of free Mn2+ ions at 3.0 T, hydrodynamic size distribution of FMS-1 to FMS-5, r1 linear fit curves and r2 linear fit curves of FMS-1 to FMS-5. Figure S8. N2 adsorption–desorption isotherms and corresponding pore size distribution of FS, and FMS-1 to FMS-5. Figure S9. T1–T2WI of FMS with different Fe3O4 to Mn2+ ratios. Figure S10. Fe content of 4T1 cells. Figure S11. CLSM observation: the internalization of PC-3 cells. Figure S12. Colocalization and particle uptake ratios of 4T1 cells. Figure S13. Representative color-coded T1 and T2 map images of 4T1 tumor-bearing mice and T1 and T2 map values analysis. Figure S14. Cytotoxicity of PDGFB-FMS against PC-3 cells. Figure S15. Blood routine examination of mice. Figure S16. The viabilities of THLE-3, 293 T, PC-12, and SH-SY5Y cells. Table S1. ∆r1 and ∆r2 value of FMS under different pH conditions. Table S2. ∆r1 and ∆r2 value of FMS under different GSH conditions. Table S3. In vitro ∆R1 and ∆R2 of 4T1 cells treated with PDGFB-FMS at the presence of different concentrations of GSH.

Published
2023
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7. PDGFB-targeted functional MRI nanoswitch for activatable T1–T2 dual-modal ultra-sensitive diagnosis of cancer.

Author

Zhang, Ya'nan, Liu, Lu, Li, Wenling, Zhang, Caiyun, Song, Tianwei, Wang, Peng, Sun, Daxi, Huang, Xiaodan, Qin, Xia, Ran, Lang, Tian, Geng, Qian, Junchao, and Zhang, Guilong

Subjects
FUNCTIONAL magnetic resonance imaging, CANCER diagnosis, MAGNETIC resonance imaging, TUMOR diagnosis, EARLY diagnosis, ENDORECTAL ultrasonography
Abstract

As one of the most significant imaging modalities currently available, magnetic resonance imaging (MRI) has been extensively utilized for clinically accurate cancer diagnosis. However, low signal-to-noise ratio (SNR) and low specificity for tumors continue to pose significant challenges. Inspired by the distance-dependent magnetic resonance tuning (MRET) phenomenon, the tumor microenvironment (TME)-activated off–on T1–T2 dual-mode MRI nanoswitch is presented in the current study to realize the sensitive early diagnosis of tumors. The tumor-specific nanoswitch is designed and manufactured on the basis of PDGFB-conjugating ferroferric oxide coated by Mn-doped silica (PDGFB-FMS), which can be degraded under the high-concentration GSH and low pH in TME to activate the T1–T2 dual-mode MRI signals. The tumor-specific off–on dual-mode MRI nanoswitch can significantly improve the SNR and is used successfully for the accurate diagnosis of early-stage tumors, particularly for orthotopic prostate cancer. In addition, the systemic delivery of the nanoswitch did not cause blood or tissue damage, and it can be excreted out of the body in a timely manner, demonstrating excellent biosafety. Overall, the strategy is a significant step in the direction of designing off–on dual-mode MRI nanoprobes to improve imaging accuracy, which opens up new avenues for the development of new MRI probes. [ABSTRACT FROM AUTHOR]

Published
2023
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12. MRP4: a previously unidentified factor in resistance to nucleoside-based antiviral drugs

Author

Schuetz, John D., Connelly, Michele C., Sun, Daxi, Paibir, Sheela G., Flynn, Patricia M., Srinivas, R.V., Kumar, Alok, and Fridland, Arnold

Subjects
Drug resistance -- Research, HIV infection -- Research
Abstract

Researchers have identified a protein produced by mammalian cells that pumps drugs out of the cell. The protein, MRP4, could explain why some HIV patients become resistant to some AIDS drugs even though their viral isolate shows no sign of drug resistance.

Published
1999

19. Mrp4 Confers Resistance to Topotecan and Protects the Brain from Chemotherapy

Author

Leggas, Markos, primary, Adachi, Masashi, additional, Scheffer, George L., additional, Sun, Daxi, additional, Wielinga, Peter, additional, Du, Guoqing, additional, Mercer, Kelly E., additional, Zhuang, Yanli, additional, Panetta, John C., additional, Johnston, Brad, additional, Scheper, Rik J., additional, Stewart, Clinton F., additional, and Schuetz, John D., additional

Published
2004
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20. Interactions between Hepatic Mrp4 and Sult2a as Revealed by the Constitutive Androstane Receptor and Mrp4 Knockout Mice

Author

Assem, Mahfoud, primary, Schuetz, Erin G., additional, Leggas, Markos, additional, Sun, Daxi, additional, Yasuda, Kazuto, additional, Reid, Glen, additional, Zelcer, Noam, additional, Adachi, Masashi, additional, Strom, Stephen, additional, Evans, Ronald M., additional, Moore, David D., additional, Borst, Piet, additional, and Schuetz, John D., additional

Published
2004
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