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Background <p>Esophageal cancer (EC) is a predominant and extremely aggressive malignant tumor with increased clinical incidences. It is a sixth major reason of cancer-related mortalities globally.</p> Objective <p>The current work was aimed to investigate the anticancer potentials of apocynin against EC KYSE-150 cells through the regulation of apoptotic gene expressions.</p> Methodology <p>The MTT test was employed to investigate the apocynin (1, 2, 5, 7.5, 10, 25, 50, &amp; 100 µM)-treated KYSE-150 cell viability. The ROS accumulation in the apocynin-exposed cells were analyzed by a DCFH-DA staining assay, while the apoptosis was analyzed by fluorescent staining assays, including DAPI, Annexin V-FITC/PI, and dual staining (AO/EB) assays. The level of MMP was examined by the Rh-123 staining technique. The Bax, Bcl-2, Cytochrome c, Cleaved Caspase-9, and Caspase-3 were investigated using Western Blot analysis.</p> Results <p>The findings of the MTT test demonstrated that KYSE-150 cell growth was substantially reduced by the apocynin treatment, and the IC50 concentration was noted at 10 µM. The results of the DCFH-DA staining revealed increased endogenous ROS production in 10 and 25 µM of apocynin-treated KYSE-150 cells. The apocynin also promoted the apoptotic rate in the KYSE-150 cells, which is confirmed by DAPI, Annexin V-FITC/PI, and dual staining assays. The result of RH-123 staining demonstrated the considerable decrease in the MMP level. The pro-apoptotic proteins Bax, Cytochrome c, Cleaved Caspase-9, and Caspase-3 levels were considerably increased, while anti-apoptotic Bcl-2 level was decreased in the apocynin-treated KYSE-150 cells.</p> Conclusion <p>Overall, the findings of this work highlighted that apocynin remarkably decreased the viability and promoted apoptosis in EC cells. Henceforth, it can be a promising anticancer agent to treat EC.</p>

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Apocynin Inhibits Cell Viability and Promotes Apoptotic Cell Death in Esophageal Cancer KYSE-150 Cells by Regulating Bax/Bcl-2 Signaling and Caspase Activation

  • 期刊论文

  • 发表日期：

    2026年3月17日

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  • Xiaolei Xue,
  • Mingwei Liu,
  • Hesham S. Almoallim,
  • Tahani Awad Alahmadi,
  • Wei Wang

摘要

Background

Esophageal cancer (EC) is a predominant and extremely aggressive malignant tumor with increased clinical incidences. It is a sixth major reason of cancer-related mortalities globally.

Objective

The current work was aimed to investigate the anticancer potentials of apocynin against EC KYSE-150 cells through the regulation of apoptotic gene expressions.

Methodology

The MTT test was employed to investigate the apocynin (1, 2, 5, 7.5, 10, 25, 50, & 100 µM)-treated KYSE-150 cell viability. The ROS accumulation in the apocynin-exposed cells were analyzed by a DCFH-DA staining assay, while the apoptosis was analyzed by fluorescent staining assays, including DAPI, Annexin V-FITC/PI, and dual staining (AO/EB) assays. The level of MMP was examined by the Rh-123 staining technique. The Bax, Bcl-2, Cytochrome c, Cleaved Caspase-9, and Caspase-3 were investigated using Western Blot analysis.

Results

The findings of the MTT test demonstrated that KYSE-150 cell growth was substantially reduced by the apocynin treatment, and the IC50 concentration was noted at 10 µM. The results of the DCFH-DA staining revealed increased endogenous ROS production in 10 and 25 µM of apocynin-treated KYSE-150 cells. The apocynin also promoted the apoptotic rate in the KYSE-150 cells, which is confirmed by DAPI, Annexin V-FITC/PI, and dual staining assays. The result of RH-123 staining demonstrated the considerable decrease in the MMP level. The pro-apoptotic proteins Bax, Cytochrome c, Cleaved Caspase-9, and Caspase-3 levels were considerably increased, while anti-apoptotic Bcl-2 level was decreased in the apocynin-treated KYSE-150 cells.

Conclusion

Overall, the findings of this work highlighted that apocynin remarkably decreased the viability and promoted apoptosis in EC cells. Henceforth, it can be a promising anticancer agent to treat EC.