ArticleOncotarget2017
A novel benzimidazole derivative, MBIC inhibits tumor growth and promotes apoptosis via activation of ROS-dependent JNK signaling pathway in hepatocellular carcinoma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 99 citations in OpenAlex.
- From Scaffold to Therapy: Benzimidazole Pharmacophore Evolution in Breast Cancer Research.Chemistry & biodiversity · 2026Review
- Anticancer and Antimicrobial Activities of New Cobalt and Zinc Complex-Derived Benzimidazole Containing Nitro or Methyl Groups.ACS omega · 2026Article
- Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen-Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells.Cancer medicine · 2026Article
- Evaluating the Cytotoxic Potential of 3-(2-(3,4 dimethoxyphenyl)-2-oxoethylidene) indolin-2-one) (RAJI) on Triple Negative Breast Cancer Cells.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Synergistic Effects of 2-Deoxyglucose and Diclofenac Sodium on Breast Cancer Cells: A Comparative Evaluation of MDA-231 and MCF7 Cells.International journal of molecular sciences · 2025Article
- Benzimidazole scaffold as a potent anticancer agent with different mechanisms of action (2016-2023).Molecular diversity · 2025Review
- Anticancer Activity of Ether Derivatives of Chrysin.Molecules (Basel, Switzerland) · 2025Review
- Autophagy in doxorubicin resistance: basic concepts, therapeutic perspectives and clinical translation.Frontiers in immunology · 2025Review
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- Fluoride-Induced Mitochondrial Dysfunction and Approaches for Its Intervention.Biological trace element research · 2024Review
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- Drug target therapy and emerging clinical relevance of exosomes in meningeal tumors.Molecular and cellular biochemistry · 2024Review
- MiRNAs function in the development of resistance against doxorubicin in cancer cells: targeting ABC transporters.Frontiers in pharmacology · 2024Review
- Hypoxia signaling in hepatocellular carcinoma: Challenges and therapeutic opportunities.Cancer metastasis reviews · 2023Review
- Discovery of Pyrimidine- and Coumarin-Linked Hybrid Molecules as Inducers of JNK Phosphorylation through ROS Generation in Breast Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
- Baicalein as Promising Anticancer Agent: A Comprehensive Analysis on Molecular Mechanisms and Therapeutic Perspectives.Cancers · 2023Review
- Benzimidazole and its derivatives as cancer therapeutics: The potential role from traditional to precision medicine.Acta pharmaceutica Sinica. B · 2023Review
- Skin Improvement with Antioxidant Effect of Yuja (Antioxidants (Basel, Switzerland) · 2022Article
- Potential Application of Leelamine as a Novel Regulator of Chemokine-Induced Epithelial-to-Mesenchymal Transition in Breast Cancer Cells.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
15 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A prior screening programme carried out using MTT assay by our group identified a series of novel benzimidazole derivatives, among which Methyl 2-(5-fluoro-2-hydroxyphenyl)-1H- benzo[d]imidazole-5-carboxylate (MBIC) showed highest anticancer efficacy compared to that of chemotherapeutic agent, cisplatin. In the present study, we found that MBIC inhibited cell viability in different hepatocellular carcinoma (HCC) cell lines without exerting significant cytotoxic effects on normal liver cells. Annexin V-FITC/PI flow cytometry analysis and Western blotting results indicated that MBIC can induce apoptosis in HCC cells, which was found to be mediated through mitochondria associated proteins ultimately leading to the activation of caspase-3. The exposure to MBIC also resulted in remarkable impairment of HCC cell migration and invasion. In addition, treatment with MBIC led to a rapid generation of reactive oxygen species (ROS) and substantial activation of c-Jun-N-terminal kinase (JNK). The depletion of ROS by N-Acetyl cysteine (NAC) partially blocked MBIC-induced apoptosis and JNK activation in HCC cells. Finally, MBIC significantly inhibited tumor growth at a dose of 25 mg/kg in an orthotopic HCC mouse model. Taken together, these results demonstrate that MBIC may inhibit cell proliferation via ROS-mediated activation of the JNK signaling cascade in HCC cells.
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