JOURNAL OF VOICE
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2024
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IF 2.5
Zhe Chen,Ke-Da Li,Min Gao,Shui-Hong Zhou,Hong-Tian Yao,Jiang-Tao Zhong,Yang-Yang Bao,Zi-Ming Fu,Zai-Zai Cao
Summary Objective We assessed the expression of glucose transporter (GLUT)-1 and hexokinase (HK)-Ⅱ in vocal cord leukoplakia (VCL) and investigated its clinical significance. Methods We collected 127 archival pathological specimens from patients with VCL, 29 from vocal cord polyps, and 31 with laryngeal carcinoma at our hospital between December 2018 and December 2022. GLUT-1 and HK-II expression was detected using immunohistochemistry. Results Significant differences were observed between the VCL and vocal cord polyp groups according to sex ( P < 0.0001), smoking status ( P = 0.001), and alcohol consumption ( P = 0.007). GLUT-1 expression was observed in 36.2%, 20.7%, and 90.3% of patients with VCL, vocal cord polyps, and laryngeal carcinoma, respectively. GLUT-1 was highly expressed in severe dysplasia or carcinoma in situ (CIS) compared with vocal cord polyps ( P < 0.001). GLUT-1 expression was lower in the VCL group than in the laryngeal carcinoma group ( P < 0.001). HK-II expression was observed in 42.5%, 34.5%, and 80.6% of patients with VCL, vocal cord polyps, and laryngeal carcinoma, respectively. HK-II expression was significantly higher in severe dysplasia or CIS compared with vocal cord polyps ( P = 0.004). HK-II expression was lower in the VCL group than in the laryngeal carcinoma group ( P < 0.001). Both GLUT-1 expression ( P < 0.001) and HK-II expression ( P = 0.03) increased significantly with the degree of dysplasia. A significant correlation was observed between GLUT-1 and HK-II expression (r = 0.313, P < 0.001). Conclusion GLUT-1 and HK-II are significantly overexpressed in VCL patients. In VCL patients, GLUT-1 and HK-II expression levels increase proportionally with the degree of dysplasia.
研究领域:
耳鼻喉科学
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病理学
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肿瘤学
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DOI
PubMed
高影响因子
HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK
·
2020
·Vol. 42
·期 9
·2287-2297
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IF 2.538
Li-Bo Dai,Qi Yu,Shui-Hong Zhou,Yang-Yang Bao,Jiang-Tao Zhong,Li-Fang Shen,Zhong-Jie Lu,Jun Fan,Ya-Ping Huang
Background This study is to explore the role of curcumin and GLUT-1 antisense oligodeoxynucleotides (AS-ODN) on autophagy modulation-initiated radiosensitivity. Methods BALB/c mice were employed to establish xenograft model using Tu212 cell. The expression of autophagy- and apoptosis-related proteins was determined by WB. Autophagosome was observed under transmission electron microscope. Apoptosis of tumor tissue were detected by TUNEL staining. Results Combinations of curcumin and GLUT-1 AS-ODN with 10 Gy inhibited the tumor growth by inducing apoptosis of laryngeal cancer cells followed with the enhancement of autophagy. 3-MA also had a promotion effect on irradiation-mediated growth inhibition possibly by depressing PI3K and on curcumin/GLUT-1 AS-ODN-mediated growth inhibition potentially by regulating autophagic events. Of note, a de-escalation of radiotherapy dose (5 Gy) along with curcumin, GLUT-1 AS-ODN or 3-MA produced a stronger effect than high dosage of radiotherapy (10 Gy) alone. Conclusions Curcumin and GLUT-1 AS-ODN improve the radiosensitivity of laryngeal carcinoma through regulating autophagy and inducing apoptosis.
研究领域:
肿瘤学
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药理学
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放射生物学
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DOI
PubMed
高影响因子
Polymers
·
2021
·Vol. 13
·期 17
·2929
·
IF 4.329
Jing Miao,Liwen Zhang,Peng Gao,Huawei Zhao,Xianji Xie,Junyan Wang
Glucose Transporter-1 (GLUT-1) is considered to be a possible intrinsic marker of hypoxia in malignant tumors, which is an important factor in radioresistance of laryngocarcinoma. We speculated that the inhibition of GLUT-1 expression might improve the radiosensitivity of laryngocarcinoma. GLUT-1 siRNA was designed to inhibit the GLUT-1 expression, but the high molecular weight and difficult drug delivery limited the application. Herein, we constructed a glycolipid polymer chitosan oligosaccharide grafted stearic acid (CSSA) to conjugate siRNA via electrostatic interaction. The characteristics of CSSA and CSSA/siRNA were studied, as well as the radiosensitization effect of siRNA on human laryngocarcinoma epithelial (Hep-2) cells. Compared with the traditional commercial vector LipofectamineTM2000 (Lipo), CSSA exhibited lower cytotoxicity, more efficiently cellular uptake. Incubating with CSSA/siRNA, the survival rates of Hep-2 cells were significantly decreased comparing with either the group before transfection or Lipo/siRNA. CSSA is a promising carrier for efficient siRNA delivery and radiosensitization of laryngocarcinoma.Keywords:GLUT-1;siRNA;chitosan oligosaccharide grafted stearic acid;laryngocarcinoma;radiosensitization
研究领域:
癌症生物学
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药学
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分子生物学
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DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2026
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IF 8.3
Chong Gao,Wei Liu,Sai-Hu Liu,Shuang Zheng,Chen-Yu Wang,Xu Dai,Li-Hua Lian,Zhen-Yu Cui,Ji-Xing Nan,Yan-Ling Wu
Background Reprogramming of aerobic glycolysis occurs with HSCs activation and is associated with regression of liver fibrosis. Trigonelline (TRG), a plant alkaloid extracted from Trigonella foenum-graecum L seeds, has a variety of pharmacological effect. Purpose The current study investigated the hepatoprotective effect and mechanism of TRG against hepatic fibrosis by regulating glycolysis. Methods Anti-hepatic fibrosis effects of TRG were detected in thioacetamide (TAA)-induced hepatic fibrosis mice. HSCs or LX-2 were stimulated with TGF-β or conditioned medium (CM) from LPS-stimulated THP-1, then incubated with TRG, phloretin (PHL), rosiglitazone (RGZ), siRNA Glut-1 or plasmid with Glut-1. Results TRG significantly reduced serum transaminase levels, liver histopathological changes, excessive collagen deposition, inflammatory response, and neutrophil recruitment in TAA-induced mice. TAA increased hepatic Glut-1, HIF-1α and key enzymes of glycolysis expressions, while TRG completely reversed this effect. TRG also obviously regulated the combination of Glut-1 and HIF-1α to affect glycolysis in activated HSCs. TRG could inhibit α-SMA, IL-6, IL1R1, and HIF-1α expressions accompanying inhibition of Glut-1, function as PHL (Glut-1 inhibitor). Glut-1 silencing weakened α-SMA, IL-6, IL1R1, and HIF-1α expressions and enhanced the effect of TRG in activated LX-2. TRG inhibited LX-2 activation caused by Glut-1 overexpression, even demonstrated in interaction between LX-2 and macrophages. Further, TRG shown that improved fibrogenesis and inflammatory response by inhibiting Glut-1 compared with PHL in vivo . Conclusion TRG could ameliorate hepatic fibrosis through inhibiting ECM excessive deposition and inflammatory response. Inhibiting Glut-1-HIF-1α axis and glycolysis was a potential therapeutic strategy for TRG ameliorating liver microenvironment, further against hepatic fibrosis.
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PubMed
高影响因子
Food & Function
·
2022
·Vol. 13
·期 8
·4612-4623
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IF 6.317
Xiang Ye,Wen Chen,Pengcheng Tu,Ruoyi Jia,Yangyang Liu,Qiong Tang,Chuan Chen,Caihong Yang,Xiaodong Zheng,Qiang Chu
Cyanidin-3-O-glucoside (C3G), an essential representative of anthocyanins, has been proved to possess a myriad of biological activities. However, the effects of C3G on glucose metabolism and its underlying molecular mechanisms remain elusive. The aim of the present study was to investigate the metabolic impact of C3G on db/db mice and to determine whether its consequent anti-diabetic effects were related to glucose transporter-1 (GLUT-1) by in vivo and in vitro studies. As a result, through diabetic db/db mice, C3G treatment was found to significantly reduce the fasting blood glucose level and increase glycogen synthesis, which were associated with upregulation of GLUT-1 expression in the liver of the mice. In addition, in liver cells of the HepG2 and L02 lines, we further discovered that C3G could effectively promote glucose consumption by regulating the Wnt/β-catenin-WISP1 signaling pathway. Nevertheless, such effects would be restricted when the expression of GLUT-1 was blocked by the inhibitor IWR-1. Meanwhile, molecular docking technology was applied to simulate the possible action sites of C3G at the molecular level, and the results indicated that C3G might bind to β-catenin. In conclusion, our study provided evidence of the antihyperglycemic effect of C3G in vivo and in vitro via regulating GLUT-1 expression and the related signaling pathways.
研究领域:
药理学
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分子生物学
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糖尿病研究
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细胞生物学
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DOI
PubMed
高影响因子
MOLECULES
·
2023
·Vol. 28
·期 9
·3824
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IF 4.6
Lei Meng,Fangshu Liu,Chenchen Du,Jiaying Zhu,Qian Xiong,Jing Li,Weitong Sun
In this work, glucose transporter-1 (GLUT-1) and glutathione (GSH) over-expression in liver cancer was utilized to design a reduction-responsive and active targeting drug delivery system AG-PEG-SS-PCL (APSP) for the delivery of sorafenib (SF). The SF-APSP micelles were prepared using the thin film hydration method and characterized by various techniques. In vitro release experiments showed that the cumulative release of SF-APSP micelles in the simulated tumor microenvironment (pH 7.4 with GSH) reached 94.76 ± 1.78% at 48 h, while it was only 20.32 ± 1.67% in the normal physiological environment (pH 7.4 without GSH). The in vitro study revealed that glucosamine (AG) enhanced the antitumor effects of SF, and SF-APSP micelles inhibited proliferation by targeting HepG2 cells and suppressing cyclin D1 expression. The in vivo antitumor efficacy study further confirmed that the SF-APSP micelles had excellent antitumor effects and better tolerance against nude mouse with HepG2 cells than other treatment groups. All in all, these results indicated that SF-APSP micelles could be a promising drug delivery system for anti-hepatoma treatment.Keywords:liver cancer;glucosamine;sorafenib;reduction-responsive;polymer micelles
研究领域:
药学
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癌症研究
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纳米技术
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药物递送系统
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PubMed
高影响因子
Journal of Advanced Research
·
2022
·
IF 12.822
Ying Zhu,Anni Wang,Shuya Zhang,Jisu Kim,Jiaxuan Xia,Fengxue Zhang,Dan Wang,Qi Wang,Jianxin Wang
Introduction Inherent or acquired resistance to paclitaxel (PTX) is a pivotal challenge for chemotherapy treatment of multidrug-resistant (MDR) breast cancer. Although various targeted drug-delivery systems, including nanoparticles and liposomes, are effective for MDR cancer treatment, their efficacy is restricted by immunosuppressive tumor microenvironment (TME). Methods Ginsenosides Rg3 was used to formulate unique Rg3-based liposomes loaded with PTX to establish Rg3-PTX-LPs, which were prepared by the thin-film hydration method. The stability of the Rg3-PTX-LPs was evaluated by particle size analysis through dynamic light scattering. The active targeting effect of Rg3-based liposomes was examined in an MCF-7/T xenograft model by an in a vivo imaging system. To evaluate the antitumor activity and mechanism of Rg3-PTX-LP, MTT, apoptosis assays, TAM regulation, and TME remodeling were performed in MCF-7/T cells in vitro and in vivo. Results Rg3-PTX-LPs could specifically distribute to MCF7/T cancer cells and TME simultaneously, mainly through the recognition of GLUT-1. The drug resistance reversing capability and in vivo antitumor effect of Rg3-PTX-LPs were significantly improved compared with conventional cholesterol liposomes. The TME remodeling mechanisms of Rg3-PTX-LPs included inhibiting IL-6/STAT3/p-STAT3 pathway activation to repolarize protumor M2 macrophages to antitumor M1 phenotype, suppressing myeloid-derived suppressor cells (MDSCs), decreasing tumor-associated fibroblasts (TAFs) and collagen fibers in TME, and promoting apoptosis of tumor cells. Hence, through the dual effects of targeting tumor cells and TME remodeling, Rg3-PTX-LPs achieved a high tumor inhibition rate of 90.3%. Conclusion Our multifunctional Rg3-based liposome developed in the present study offered a promising strategy for rescuing the drug resistance tumor treatment.
研究领域:
药学
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肿瘤学
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纳米技术
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癌症治疗
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DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
·
2017
·Vol. 15
·期 1
·1-17
·
IF 4.946
Zhou Yi,Wen Huaying,Gu Liang,Fu Jijun,Guo Jiayi,Du Lingran,Zhou Xiaoqin,Yu Xiyong,Huang Yugang,Wang He
Background Chemotherapeutic drugs used for cancer therapy frequently encounter multiple-drug resistance (MDR). Nanoscale carriers that can target tumors to accumulate and release drugs intracellularly have the greatest potential for overcoming MDR. Glucose transporter-1 (GLUT-1) and glutathione (GSH) overexpression in cancer cells was exploited to assemble aminoglucose (AG)-conjugated, redox-responsive nanomicelles from a single disulfide bond-bridged block polymer of polyethylene glycol and polylactic acid (AG-PEG-SS-PLA). However, whether this dual functional vector can overcome MDR in lung cancer is unknown. Results In this experiment, AG-PEG-SS-PLA was synthetized successfully, and paclitaxel (PTX)-loaded AG-PEG-SS-PLA (AG-PEG-SS-PLA/PTX) nanomicelles exhibited excellent physical properties. These nanomicelles show enhanced tumor targeting as well as drug accumulation and retention in MDR cancer cells. Caveolin-dependent endocytosis is mainly responsible for nanomicelle internalization. After internalization, the disulfide bond of AG-PEG-SS-PLA is cleaved in the presence of high intracellular glutathione levels, causing the hydrophobic core to become a polar aqueous solution, which subsequently results in nanomicelle disassembly and the rapid release of encapsulated PTX. Reduced drug resistance was observed in cancer cells in vitro. The caspase-9 and caspase-3 cascade was activated by the AG-PEG-SS-PLA/PTX nanomicelles through upregulation of the pro-apoptotic proteins Bax and Bid and suppression of the anti-apoptotic protein Bcl-2, thereby increasing apoptosis. Furthermore, significantly enhanced tumor growth inhibition was observed in nude mice bearing A549/ADR xenograft tumors after the administration of AG-PEG-SS-PLA/PTX nanomicelles via tail injection. Conclusions These promising results indicate that AG-PEG-SS-PLA/PTX nanomicelles could provide the foundation for a paradigm shift in MDR cancer therapy.
研究领域:
药学
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癌症生物学
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纳米技术
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药物递送系统
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）