ANALYTICAL AND BIOANALYTICAL CHEMISTRY
·
2025
·
IF 3.8
Si Mengyao,Han Guo,Liu Tianwen,Wang Xiaoying
Aberrant overexpression of c-Myc protein (c-Myc) serves as a critical biomarker for aggressive lymphomas, yet its trace-level quantification remains challenging due to insufficient sensitivity in conventional assays. Here, we present an electrochemical immunosensor leveraging homogeneous gold–palladium (AuPd) nanohybrids for dual amplification, achieving both simplified fabrication and enhanced analytical performance. A chitosan–graphene oxide–AuPd nanorod composite (CS-GO-AuPd) was engineered as an electrode modifier, offering high conductivity, biocompatibility, and abundant antibody immobilization sites. Prussian blue-doped AuPd nanoparticles (PB-AuPd@Ab 2 ) were simultaneously designed as catalytic signal probes, synergistically amplifying responses through electron mediation and nanozyme activity. This homogeneous material strategy eliminated heterogeneous nanomaterial interfaces, streamlining sensor assembly while ensuring signal reproducibility. The sandwich-type immunocomplex formation triggered a PB-derived differential pulse voltammetry signal proportional to c-Myc concentration, yielding a 0.5 pg mL −1 –1 ng mL −1 linear range, with a detection limit of 0.25 pg mL −1 . Comparative validation against clinical methods confirmed robust accuracy, highlighting the platform’s potential for dynamic monitoring of lymphoma progression and therapy response. This work establishes a paradigm for unifying material homogeneity with dual-amplification mechanisms in biosensing, extensible to diverse low-abundance biomarkers. Graphical
研究领域:
生物传感器
·
纳米材料
·
电化学
·
癌症诊断
·
生物医学工程
✓ 已验证
产品关联
DOI
PubMed
高影响因子
SENSORS AND ACTUATORS B-CHEMICAL
·
2020
·
IF 7.1
Bo-Xin Zheng,Wei Long,Yi-Han Zhang,Xuan-He Huang,Cui-Cui Chen,Dong-Xiao Zhong,Meng-Ting She,Ze-Xin Chen,Dong-Peng Cai,Yu-Jing Lu,Wing-Leung Wong
Red fluorescent G-quadruplex DNA selective organic binding probe is relatively underdeveloped. In the present study, we designed a series of new fluorescent probes that exhibit large Stokes shift (112−131 nm), high quantum yield (up to 0.56), robust against photo-bleaching and high selectivity towards quadruplex structures of c-MYC and telomere DNA with strong binding affinity . The discrimination ability of the probes towards G-quadruplex structures against single-/double-stranded DNA or RNA was investigated by analyzing their structural property with respect to their binding specificity. From the sensing application of the probe targeting pu27, an excellent linear relationship (R 2 = 0.9997) with respect to the pu27- A3 interaction signal was observed. The LOD was found down to 4.0 nM, which is superior to thiazole orange dye. The probe is able to realize real-time fluorescence visualization in aqueous, PAGE staining and live cell imaging. In addition, from the immunofluorescence analysis using the probe and BG4 antibody, the A3 foci and BG4 staining co-localized well in PC3 cells, which suggest that the probe is G-quadruplex selective and is useful for visualizing G-quadruplex DNA structures in live cells. Cytotoxicity assays also demonstrated that the probe has low cytotoxicity against both PC3 cancer cells and 16HBE normal cells.
研究领域:
生物化学
·
分子生物学
·
医学诊断
✓ 已验证
DOI
高影响因子
Marine Drugs
·
2021
·Vol. 19
·期 2
·79
·
IF 5.118
Hengju Ge,Di Zhang,Muran Shi,Xiaoyuan Lian,Zhizhen Zhang
In 2019, streptoglutarimide H (SGH) was characterized as a new glutarimide from the secondary metabolites produced by a marine-derived actinomyceteStreptomycessp. ZZ741 and shown to have in vitro antiglioma activity. However, the antiproliferative activity and potential mechanism of SGH against lung cancer cells have not yet been characterized. This study demonstrated that SGH significantly inhibited the proliferation of different lung cancer cells. In terms of mechanism of action, SGH downregulated cell cycle- and nucleotide synthesis-related proteins to block cell cycle at G0/G1 phase, reduced the expression levels of glycolytic metabolic enzymes to inhibit glycolysis, and downregulated the important cancer transcription factor c-Myc and the therapeutic target deubiquitinase USP28. Potent anticancer activity and multiple mechanisms indicated SGH to be a novel antitumor compound against lung cancer cells.Keywords:Streptoglutarimide H;lung cancer cells;antiproliferative activity;cell cycle block;glycolysis;USP28;c-Myc
研究领域:
肿瘤学
·
药理学
·
海洋生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Oncology
·
2021
·
IF 4.375
Xiaodan Sun,Peiyan Zhao,Hui Li,Yan Liu,Tianming Wang,Ying Cheng
Ginsenoside Rh2 (Rh2) is one of the pharmacologically active components of ginseng with an antitumor effect. However, its effect on non-small-cell lung cancer (NSCLC), especially on aerobic glycolysis, which plays a crucial role in the proliferation and progression of tumor cells, has not been characterized. Here, we demonstrated that Rh2 inhibited the proliferation and metastasis of NSCLC cells by promoting apoptosis and suppressing epithelial-mesenchymal transition, respectively. Notably, Rh2 exerted a glycolysis inhibition effect through regulating GLUT1, PKM2, and LDHA, which are key enzymes of the glycolysis process. Furthermore, the metabolic shift function of Rh2 was dependent on the STAT3/c-Myc axis in NSCLC. This novel regulatory role of Rh2 provides a new perspective for NSCLC treatment and highlights the potentiality of Rh2 to be used as a tumor energy blocker. The combination of Rh2 with an STAT3 or c-Myc inhibitor revealed a promising therapeutic approach for patients with NSCLC.
研究领域:
肿瘤学
·
药理学
·
代谢途径
✓ 已验证
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2022
·
IF 6.656
Mengyang Wang,Wu Luo,Tianxiang Yu,Shiqi Liang,Chunpeng Zou,Jinfeng Sun,Gao Li,Guang Liang
Background Heart failure is a common event in the course of hypertension. Recent studies have highlighted the key role of the non-hemodynamic activity of angiotensin II (Ang II) in hypertension-related cardiac inflammation and remodeling. A naturally occurring compound, diacerein , exhibits anti-inflammatory activities in various systems. Hypothesis/Purpose In this study, we have examined the potential effects of diacerein on Ang II-induced heart failure. Methods C57BL/6 mice were administered Ang II by micro-osmotic pump infusion for 4 weeks to develop hypertensive heart failure. Mice were treated with diacerein by gavage for final 2 weeks. RNA-sequencing analysis was performed to explore the potential mechanism of diacerein. Results We found that diacerein could inhibit inflammation, myocardial fibrosis , and hypertrophy to prevent heart dysfunction, without the alteration of blood pressure. To explore the potential mechanism of diacerein, RNA-sequencing analysis was performed, indicating that MAPKs/c-Myc pathway is involved in that cardioprotective effects of Diacerein. We further confirmed that diacerein inhibits Ang II-activated MAPKs/c-Myc pathway to reduce inflammatory response in mouse hearts and cultured cardiomyocytes . Deficiency of MAPKs or c-Myc in cardiomyocytes abolished the anti-inflammatory effects of diacerein. Conclusion Our results indicate that diacerein protects hearts in Ang II-induced mice through inhibiting MAPKs/c-Myc-mediated inflammatory responses, rendering diacerein a potential therapeutic candidate agent for hypertensive heart failure.
研究领域:
心脏病学
·
药理学
·
分子生物学
·
炎症
✓ 已验证
DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2025
·
IF 4.7
Qianqian Zheng,Gui Mei,Ping Cheng,Yahong Li,Qingfeng Zhang,Mingwei Ye
Given the demonstrated mitigating effect of omega-9 monounsaturated fatty acids (ω-9MUFAs) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), we deeply explored corresponding mechanisms. Sprague-Dawley rats experienced ALI modeling, and received ω-9 MUFAs (3 mg/kg) injection via the tail vein. Post incubation in 100 ng/mL phorbol-12-myristate-13-acetate and 100 ng/mL LPS for 24 h each, THP-1 macrophages were transfected with shHSPH1 and c-MYC overexpression plasmid. Lung injury detection depended on H&E staining. Levels of inflammation-related factors were detected by ELISA. Levels of inflammation-related factors, heat shock protein family H (Hsp110) member 1 (HSPH1), c-MYC, stimulator of interferon response CGAMP interactor 1 (STING) and NOD-like receptor thermal protein domain associated protein 3 (NLRP3) were measured by qRT-PCR. Levels of pyroptosis-related factors, HSPH1, c-MYC, STING, NLRP3, and M1 macrophage biomarkers were assayed by Western blot. Proportion of M1 macrophages and pyroptosis were detected by flow cytometry. Localization of HSPH1 and CD68 was measured by immunofluorescence assay. ω-9MUFAs reduced the inflammation, the proportion of M1 and pyroptotic macrophages and levels of HSPH1, c-MYC, STING and NLRP3 in ALI rats. The expression positions of HSPH1 and CD68 were overlapped in ALI rat lung tissue. HSPH1 silencing reversed the changes in inflammation, the proportion of M1 and pyroptotic macrophages and levels of c-MYC, STING and NLRP3 in LPS-induced THP-1 macrophages, and c-MYC overexpression offset these effects of HSPH1 silencing. Collectively, ω-9MUFAs ameliorated LPS-induced ALI by regulating HSPH1/c-MYC expression, down-regulating M1 macrophage polarization and pyroptosis.
研究领域:
免疫学
·
分子生物学
·
病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CELL BIOCHEMISTRY AND FUNCTION
·
2026
·Vol. 44
·期 10
·e70320
·
IF 3.5
Caifang Sun,Meijuan Yue,Yuxiang Chen,Jiaying Zhang,Yunyun Mai,Yuhang Zhang,Bingyu Ye
The transcription factor zinc finger protein 143 (ZNF143) plays a crucial role in regulating diverse biological processes, including cell cycle progression, development, and cellular differentiation. Similarly, c-Myc is well-established as a key regulator of cell proliferation, differentiation, and metabolic homeostasis. While studies have demonstrated ZNF143's involvement in the proliferation of both normal hepatocytes and hepatoma cells, the precise mechanisms underlying ZNF143-mediated regulation of hepatocyte proliferation, as well as its potential functional interplay with c-Myc in this process, remain to be fully elucidated. In this study, we investigated the dynamic expression patterns of ZNF143 and c-Myc during distinct phases of liver regeneration using a 2/3 partial hepatectomy (PHx) mouse model. To elucidate the regulatory roles of these factors in hepatocyte proliferation, we employed the mouse normal hepatocyte line AML12 and the human hepatoma cell line Huh7 as experimental models. Through MTT, CCK-8, EdU, quantitative real-time PCR (qRT-PCR), and Western blot, we examined the individual and combined effects of ZNF143 and c-Myc on hepatocyte proliferation. Our findings reveal that ZNF143 inhibits proliferation and cell cycle progression in AML12 cells but promotes these processes in Huh7 cells. Notably, co-overexpression (OE) of ZNF143 and c-Myc in AML12 cells inhibited proliferation and cell cycle progression, suggesting that ZNF143 exerts a dominant regulatory effect over c-Myc in normal hepatocytes. This study establishes a critical foundation for investigating the role of ZNF143 in hepatocyte proliferation in vivo, with potential implications for liver regeneration and transplantation therapies. Significance Statement The transcription factor ZNF143, which contains seven zinc finger domains, has been extensively studied in various cancers. However, its role and underlying mechanisms in liver regeneration remain largely unexplored. Here, we report the dynamic expression pattern of ZNF143 in a mouse liver regeneration model, suggesting its potential involvement in hepatocyte proliferation. Utilizing two cell lines, AML12 and Huh7, our study revealed that ZNF143 exerts opposing effects on cell proliferation and the cell cycle in normal hepatocytes versus hepatocellular carcinoma cells. Mechanistically, ZNF143 regulates these processes by suppressing c-Myc expression. Future work focused on designing targeted therapies based on the regulatory model of ZNF143 could represent a significant strategy for addressing challenges in both liver regeneration and liver disease.
✓ 已验证
DOI
高影响因子
Human Cell
·
2025
·Vol. 38
·期 6
·1-17
·
IF 3.1
Li Qingsheng,Liu Yuxi,Zhang Lin,Zheng Yi,Feng Xiaofan,Wang Yanjie
The occurrence of tumor metastasis is associated with the phenotype of tumor-associated macrophages (TAMs). Within the tumor microenvironment, TAMs undergo metabolic reprogramming. Aerobic glycolysis contributes to TAM polarization into an M2-like phenotype. Cedrol is a component extracted from herbal medicines. Anti-cancer activities of cedrol have been reported, however, its effect on the metabolic reprogramming and pro-metastatic ability of TAMs remains unclear. Here, we found that cedrol reduced THP-1-derived macrophage polarization into M2-like phenotypes. Cedrol impaired the promoting effects of TAMs on the migration and invasion of lung cancer cells. Tumor metastasis in C57BL/6 mice was reduced following cedrol treatment, accompanied by decreases in M2-like TAMs in the lung tissues. Cedrol treatment decreased glucose consumption and lactate production and downregulated glycolysis-associated gene expression. A glycolytic inhibitor (2-DG) was utilized to confirm that suppression of glycolysis in TAMs limited the metastasis of lung cancer cells. MYC was identified as a downregulated gene in cedrol-treated TAMs based on the mRNA sequencing analysis. MYC overexpression could reverse the effects of cedrol on TAMs. Cedrol treatment reduced MYC expression at least partly via the PI3K-Akt pathway. These findings suggest that cedrol exerts anti-tumor effects by inhibiting TAM polarization into an M2-like phenotype by modulating MYC-mediated aerobic glycolysis, indicating cedrol as a potential drug for lung cancer treatment.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
·
2020
·
IF 4.831
Qiong Wu,Yue Song,Ruotong Liu,Rui Wang,Wenjie Mei,Weiming Chen,Huanglan Yang,Xicheng Wang
Phenanthroimidazole derivatives containing phenanthroline and imidazole heterocyclic aromatic rings are effective agents to inhibit tumor cell growth. Herein, halogen element-modified imidazo[4,5 f ][1,10]phenanthroline derivatives 1–6 ( 1 , 4-fluorophenyl; 2 , 4-chlorophenyl; 3 , 4-bromobenyl; 4 , 2,3-dichlorophenyl; 5 , 3,4-dichlorophenyl; and 6 , 2,4-dichlorophenyl) were synthesized, and their antitumor activities were investigated. All of the compounds, especially 4 , exhibited an excellent inhibitory effect against nasopharyngeal carcinoma CNE-1 cells. This effect was better than that of doxorubicin. Compound 4 also markedly blocked the proliferation of the CNE-1 cells in a zebrafish xenograft model. The antitumor mechanisms might be attributed to apoptosis induction, which triggered ROS-mediated DNA damage and generated mitochondrial dysfunction by stabilizing c-myc G-quadruplex DNA structure. Results indicated that phenanthroimidazole derivatives could act as promising anticancer agents.
研究领域:
药理学
·
肿瘤学
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Xin-Yao Li,Bang-Yin Tan,Yue Zhang,Yan-Lin Lv,Yun-Li Zhao,Xiao-Dong Luo
Ethnopharmacological relevance Stemona sessilifolia (Miq.) Miq. has been employed in traditional medicine for its potential renal benefits, including anti-edema, diuretic, and anti-jaundice properties. However, the renoprotective effects related to these traditional uses remain to be fully elucidated. Aim of the study : To investigate the therapeutic efficacy of S . sessilifolia against hyperuricemic nephropathy and elucidate its underlying signaling pathway. Materials and methods A hyperuricemic nephropathy mouse model, induced by potassium oxonate and hypoxanthine, was employed to evaluate the renal protection of the extract of S. sessilifolia through biochemical tests and histopathological observation. Transcriptomic analysis was applied to explore potential signaling pathways. Subsequently, bioassay-guided isolation was conducted during phytochemical investigation. Uric acid-induced HK-2 cells were then employed to validate the renal cytoprotective effects of the isolated compounds. Results Treatment with S. sessilifolia extract significantly reduced serum uric acid, creatinine, and urea nitrogen levels by 65.15%, 47.95%, and 49.1%, respectively. Additionally, it decreased urinary protein excretion, and ameliorated renal injury and fibrosis in mice. The protective effects might be exerted by inhibiting the c-Myc/c-Fos/MAPK signaling pathway to maintain the homeostasis of renal tissue. Moreover, the bioactive compound stemoninine protected HK-2 cells against uric acid-induced oxidative stress, inflammatory response, proliferation, migration, and apoptosis. Conclusion The S. sessilifolia extract and its major bioactive compound, stemoninine, protected against hyperuricemic nephropathy by suppressing the c-Myc/c-Fos/MAPK signaling pathway.
研究领域:
民族药理学
·
肾病学
·
植物化学
·
分子生物学
·
信号转导
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FASEB JOURNAL
·
2026
·Vol. 40
·期 14
·e72138
·
IF 4.3
Yong Sun,Huayue Wu,Yutong Zhou,Pengsheng Yin,Long Wu,Haiyang Li,Shi Zuo,Zhe Yang,Kun Cao
Liver fibrosis remains a major global health challenge, driving interest in bioactive metabolites from natural sources as potential therapies. Sodium butyrate (NaB), a gut microbiota–derived short‐chain fatty acid with notable anti‐fibrotic activity, shows promise, although its mechanisms remain unclear. This study aims to explore the molecular mechanisms through which NaB attenuates liver fibrosis. This study integrates bioinformatics and network pharmacology to predict the molecular targets through which NaB exerts its anti‐fibrotic effects. Candidate targets were validated through molecular docking, histopathology, CETSA, and SPR. The inferred mechanisms were further validated in vitro (LX‐2 cells) and in vivo (CCl 4 ‐induced mice) using Western blot, IF Co‐IP, RT‐qPCR, ELISA, and histopathological staining. HDAC3 was identified as a key driver of liver fibrosis. As a natural HDAC3 inhibitor, NaB markedly attenuated CCl 4 ‐induced hepatic injury and fibrosis, accompanied by reduced expression of HDAC3, c‐Myc, glycolytic enzymes (HK2, PFKFB3, and PKM2), and fibrotic markers (α‐SMA and type I collagen) in fibrotic liver tissues and LX‐2 cells. Mechanistically, NaB exerts its anti‐fibrotic effects by inhibiting HDAC3 expression and deacetylase activity, promoting c‐Myc acetylation and downregulating its expression, thereby suppressing glycolytic metabolic reprogramming in hepatic stellate cells. These findings indicate that NaB attenuates liver fibrosis by inhibiting HDAC3/c‐Myc–mediated metabolic reprogramming, revealing a gut‐derived anti‐fibrotic mechanism and potential therapeutic targets. This study explores the molecular mechanisms by which NaB ameliorates liver fibrosis from the perspectives of the gut–liver axis and metabolic reprogramming. In vivo and in vitro experiments demonstrate that gut‐derived NaB may alleviate liver injury and fibrosis by inhibiting hepatic stellate cell activation and aerobic glycolysis through the HDAC3/c‐Myc signaling axis.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ONCOLOGY REPORTS
·
2020
·Vol. 44
·期 3
·927-938
·
IF 3.417
Songhui Zhou,Ruicheng Wang,Hong Xiao
The resistance of cancer cells to carboplatin restricts their efficacy in the clinical setting, and a solution to reverse the resistance is urgently required for the treatment of ovarian cancer. An increasing number of studies have found associations between obesity and the incidence, and mortality rates of female cancer. However, the association between adipocytes and the resistance of ovarian cancer has rarely been reported. Based on this, the present study first revealed the inductive effect of adipocytes on the resistance of ovarian cancer to carboplatin using in vivo and in vitro experiments. Subsequently, it was identified that the angiopoietin‑like 4 (ANGPTL4) secreted by adipocytes played a vital role in the resistance of ovarian cancer using bioinformatics analysis, cellular and molecular biological experiments, as well as forward and backward validation. The glycosylated ANGPTL4 protein could bind with integrin α5β1 on the surface of ovarian cancer cells; following which, it could activate the c‑myc/NF‑κB pathway and stimulate the expression of the antiapoptotic protein Bcl‑xL, as well as the ABC transporter family members ABCB1, ABCC1 and ABCG2. Thus, inducing the resistance of ovarian cancer to carboplatin. In conclusion, targeting the adipocyte‑derived ANGPTL4 combined with the application of carboplatin contributes to the clinical treatment for ovarian cancer.
研究领域:
肿瘤学
·
分子生物学
·
药理学
✓ 已验证
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）