Yue Zhou’s research while affiliated with Guizhou University and other places

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Publications (14)


Synthesis and antitumor activity of a novel class of covalent inhibitors of EGFR with 2-indolone backbone
  • Article

February 2025

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5 Reads

Bioorganic Chemistry

Huayuan Tan

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Yue Zhou

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Fulian Li

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[...]

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Benzimidazole derivatives found in literature research, previous related works, and the design strategy of this work
A. DAPI staining results of compound 5 m and 5-Fluorouracil. B. Apoptosis graphs and statistical graphs of compound 5 m and 5-Fluorouracil. **** p < 0.0001
A. Inhibition of 5 m and 5-Fluorouracil on migration of A549. B. Effect of 5 m treatment for 10 days on colony formation of A549. ** p < 0.01
The level of reactive oxygen species in A549 cells increased after treatment with compound 5 m for 24 h. **** p < 0.0001
The mitochondrial membrane potential of A549 cells decreased after treatment with compound 5 m for 24 h. **** p < 0.0001

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Design, synthesis, and in vitro antitumor evaluation of novel benzimidazole acylhydrazone derivatives
  • Article
  • Publisher preview available

January 2025

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2 Reads

Molecular Diversity

This study focuses on the design, synthesis, and evaluation of benzimidazole derivatives for their anti-tumor activity against A549 and PC-3 cells. Initial screening using the MTT assay identified compound 5m as the most potent inhibitor of A549 cells with an IC50 of 7.19 μM, which was superior to the positive agents 5-Fluorouracil and Gefitinib. Cellular mechanism studies elucidated 5m arrests cell cycle at G2/M phase, induces apoptosis along with the decrease of mitochondrial membrane potential and increased reactive oxygen species. Colony formation and wound healing assays demonstrated that 5m markedly inhibited the clonogenic and migratory abilities of A549 cells. Western blot analysis showed an upregulation of pro-apoptotic protein Bax, downregulation of anti-apoptotic protein Bcl-2, and significant downregulation of cell cycle proteins CyclinB1 and CDK-1. These findings suggest that compound 5m effectively suppresses A549 cell proliferation and migration through multiple mechanisms, highlighting its potential as a novel anti-lung cancer agent. Graphical abstract

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Synthesis, anticancer evaluation, preliminary mechanism study of novel 1, 2, 3-triazole-piperlongumine derivatives

Molecular Diversity

Piperlongumine, a natural product from traditional Chinese medicine, shows promising antitumor effects but suffers from high toxicity. In this study, X and Q series Piperlongumine derivatives containing 1, 2, 3-triazole were designed and synthesized using the principle of molecular hybridization. The antitumor activity of these target compounds was evaluated, revealing significant activity compared to piperlongumine across four cancer cell lines. The structure–activity relationship of these compounds was analyzed using 3D-QSAR. Among these derivatives, compound 6Q demonstrated the highest antitumor activity against human chronic myeloid leukemia (K562) cells, with an IC50 value of 0.31 μM, low toxicity to normal cells, and a selectivity index (SI) of 11.2. Further in vitro experiments confirmed that 6Q induced apoptosis in K562 cells by disrupting mitochondrial membrane potential, activating the MAPK signaling pathway, and causing cell cycle arrest in the G2/M phase. These findings underscored the potential of the natural product derivative 6Q as a promising candidate for further development in cancer therapy. Graphical abstract



Figure 4. (A) Compound 8q at 10 µM and Harmine at 30 µM concentrations induced apoptosis of PC-3 cells. (B) Quantitative analysis of PC-3 cell apoptosis using Flow Jo-V10 software. One-way ANOVA followed by Dunnett's multiple-comparisons test was performed using GraphPad Prism 9 (**** p < 0.0001). (C) Compound 8q at 10 µM concentration and Harmine at 30 µM increased the level of reactive oxygen species in PC-3 cells. (D) Quantitative analysis of reactive oxygen species in PC-3 cells using Flow Jo-V10 software. One-way ANOVA followed by Dunnett's multiplecomparisons test was performed using GraphPad Prism 9 (* p < 0.05, **** p < 0.001).
Figure 5. (A) Flow cytometry detection of the effect of compound 8q on the distribution of PC-3 cell cycle at concentrations of 10 µM, 20 µM and 30 µM. (B) Quantitative analysis of cell cycles in PC-3 cells using Flow Jo-V10 software. β-Tubulin as an internal reference. One-way ANOVA followed by Dunnett's multiple-comparisons test was performed using GraphPad Prism 9. (C) Western blot analysis of the effect of 8q on the expression of Cyclin D1 in cells. (D) Analyzed protein grayscale values using Image J software (2.1.0/1.53c). β-Tubulin as an internal reference. One-way ANOVA followed by Dunnett's multiple-comparisons test was performed using GraphPad Prism 9 (* p < 0.05).
In vitro cytotoxicity (10 µM) of the compound 8 series.
In vitro cytotoxicity (IC 50 ) of the compounds.
Design, Synthesis and Biological Activity Evaluation of β-Carboline Derivatives Containing Nitrogen Heterocycles

October 2024

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14 Reads

Molecules

A series of β-carboline derivatives containing nitrogen heterocycles were designed and synthesized. All compounds were screened for their antitumor activity against four human tumor cell lines (A549, K562, PC-3, T47D). Notably, compound N-(4-(morpholinomethyl)phenyl)-2-((5-(1-(3,4,5-trimethoxyphenyl)-9H-pyrido[3,4-b]indol-3-yl)-1,3,4-oxadiazol-2-yl)thio)acetamide (8q) exhibited significant inhibitory activity against PC-3 cells with an IC50 value of 9.86 µM. Importantly, compound 8q effectively suppressed both the proliferation and migration of PC-3 cells. Mechanistic studies revealed that compound 8q induced cell apoptosis and caused the accumulation of reactive oxygen species (ROS), leading to cell cycle arrest in the G0/G1 phase in PC-3 cells.


Figure 1
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Synthesis, evaluation, and mechanism study of novel benzimidazole acylhydrazone derivatives for antitumor activity

October 2024

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22 Reads

This study focuses on the design, synthesis, and evaluation of benzimidazole derivatives for their anti-tumor activity against A549 and PC-3 cells. Initial screening using the MTT assay identified compound 5m as the most potent inhibitor of A549 cells with an IC 50 of 7.19 μM, which was superior to the positive agents 5-Fluorouracil and Gefitinib . Cellular mechanism studies elucidated 5m arrests cell cycle at G2/M phase, induces apoptosis along with the decrease of mitochondrial membrane potential and increased reactive oxygen species. Colony formation and wound healing assays demonstrated that 5m markedly inhibited the clonogenic and migratory abilities of A549 cells. Western blot analysis showed an upregulation of pro-apoptotic protein Bax, downregulation of anti-apoptotic protein Bcl-2, and significant downregulation of cell cycle proteins CyclinB1 and CDK-1. These findings suggest that compound 5m effectively suppresses A549 cell proliferation and migration through multiple mechanisms, highlighting its potential as a novel anti-lung cancer agent.


EGCG enhances antitumor effect of apatinib in nonsmall cell lung cancer by targeting VEGF signaling to inhibit glycolysis

October 2024

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2 Reads

Drug Development Research

Nonsmall cell lung cancer (NSCLC), one of the most aggressive malignancies globally, is characterized by poor prognosis and limited life expectancy. Epigallocatechin‐3‐gallate (EGCG), a natural polyphenol found in green tea, has emerged as a promising anticancer agent due to its potent antitumor properties. However, the role and the underlying mechanisms of EGCG in NSCLC remain poorly understood. Hence, this research aimed to explore the effect of EGCG on the antitumor effect of apatinib in NSCLC through vascular endothelial growth factor (VEGF)‐regulated glycolysis. Cell Counting Kit‐8 (CCK‐8), 5‐ethynyl‐2'‐deoxyuridine staining, wound healing, transwell, terminal deoxynucleotidyl transferase dUTP nick‐end labeling, and flow cytometry assays were carried out to evaluate the proliferation, migration, invasion, and apoptosis of H1299 cells, respectively. Furthermore, western blot analysis was used to detect the expressions of VEGF, p‐vascular endothelial growth factor receptor‐2, hypoxia‐inducible factor 1α, neuropilin‐1, phosphorylated‐phosphatidylinositol 3‐kinase, and phosphorylated‐AKT. The transfection efficiency of H1299 cells with VEGF overexpression plasmid was also assessed by western blot analysis. Glycolysis was analyzed by estimating extracellular acidification rate, lactate concentration, glucose uptake, and the expressions of lactate dehydrogenase A, pyruvate kinase M2, and hexokinase 2. The results demonstrated that VEGF activated glycolysis in NSCLC cells. EGCG alone and apatinib alone or in combination inhibited cell viability, proliferation, invasion, migration, and glycolysis whereas promoted apoptosis in NSCLC cells. EGCG regulated glycolysis levels in NSCLC through VEGF overexpression, and enhanced the antitumor effect of apatinib in NSCLC through VEGF‐regulated glycolysis. Taken together, EGCG strengthened the protective effects of apatinib in NSCLC through glycolysis mediated by VEGF.


Synthesis of novel 4-substituted isatin Schiff base derivatives as potential autophagy inducers and evaluation of their antitumour activity

August 2024

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11 Reads

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1 Citation

Molecular Diversity

Induction of autophagic death in cancer cells is one of the promising strategies for the development of anti-cancer therapeutics. In the present study, we designed and synthesized a series of isatin Schiff base derivatives containing thioether structures. After discovering the highly active target compound H13 (IC50 = 4.83 μM) based on in vitro antiproliferation, we also found it had a high safety against normal cells HEK293 with CC50 of 69.01 μM, indicating a sufficient therapeutic window. In addition, to provide reference for subsequent studies, a model was successfully constructed by Sybyl software. Preliminary mechanistic studies suggested that H13-induced apoptosis may be closely related to ROS accumulation and mitochondrial dysfunction. Subsequent studies revealed that H13 inhibited cell proliferation by inducing cellular autophagy mainly through blocking signal of the PI3K/AKT/mTOR pathway. Altogether, these results suggested that H13 was potentially valuable as a lead compound. Graphical abstract A novel class of 4-substituted insatin Schiff base derivatives as potential autophagy inducers and evaluation of their antitumour activity


A Novel Tryptanthrin Derivative D6 Induces Apoptosis and DNA Damage in Non-small-cell Lung Cancer Cells Through Regulating the EGFR Pathway

July 2024

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6 Reads

Anti-Cancer Agents in Medicinal Chemistry

Background Non-small-cell lung cancer is a prevalent malignancy associated with significant morbidity and mortality rates. Tryptanthrin and its derivatives have exhibited potent antitumor activity. Objective This study aims to investigate the inhibitory effect of a novel synthesized tryptanthrin derivative D6 on proliferation and the possible mechanism of human non-small cell lung cancer cell lines (A549) in vitro. Methods In this study, MTT assay, cell migration, colony formation assay, cell cycle analysis, cell apoptosis, JC- 1 staining assay, reactive oxygen species analysis, proteomics, western blotting, high content screening and absorption titrations analysis were performed. Results We found that D6 inhibited both the proliferation and migration, induced cell cycle arrest in the G2/M phase, increased levels of ROS, decreased mitochondrial membrane potential, and promoted apoptosis in A549 cells. Further mechanistic studies found that D6 reduced EGFR expression in A549 cells and inhibited the EGFR pathway by decreasing phosphorylation levels of EGFR, Stat3, AKT and Erk1/2. Moreover, DNA damage induced by D6 involved an increase in p53/MDM2 ratio and concentration-dependent accumulation of micronuclei. Conclusion D6 demonstrated significant antitumor activity against A549 cells by inhibiting the EGFR signaling pathway, inducing DNA damage, and subsequently leading to oxidative stress, apoptosis, and cell cycle arrest. Our findings suggest that D6 exhibits potential as an NSCLC drug, owing to its attributes such as antiproliferative activity and ability to induce apoptosis by attenuating the EGFR-mediated signaling pathway.


Citations (1)


... In Figs. 4 and 5, the comparison of the cytotoxic effects of template compounds C and D against A549 cell line with their corresponding analogs among the new compounds 5 are shown 19 . Although the cell lines used in the study of series C and D are different from our report, it seems that the majority of the new compounds can produce better cytotoxic effects. ...

Reference:

Design, synthesis, and cytotoxic activity of 2-amino-1,4-naphthoquinone-benzamide derivatives as apoptosis inducers
Novel 2-Amino-1,4-Naphthoquinone Derivatives Induce A549 Cell Death through Autophagy

Molecules