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Lung cancer cell viability is suppressed by Sch A in a concentration- and time-dependent manner. Sch A decreased (A) <t>A549</t> and (B) HCC827 cell viability in a concentration-dependent manner, according to Cell Counting Kit-8 analysis. Sch A significantly reduced the viability of (C) A549 and (D) HCC827 cells at 24, 48 and 72 h. ***P<0.001 vs. Con. Con, control; Sch A, Schisantherin A; OD, optical density.
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Lung cancer cell viability is suppressed by Sch A in a concentration- and time-dependent manner. Sch A decreased (A) <t>A549</t> and (B) HCC827 cell viability in a concentration-dependent manner, according to Cell Counting Kit-8 analysis. Sch A significantly reduced the viability of (C) A549 and (D) HCC827 cells at 24, 48 and 72 h. ***P<0.001 vs. Con. Con, control; Sch A, Schisantherin A; OD, optical density.
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Lung cancer cell viability is suppressed by Sch A in a concentration- and time-dependent manner. Sch A decreased (A) <t>A549</t> and (B) HCC827 cell viability in a concentration-dependent manner, according to Cell Counting Kit-8 analysis. Sch A significantly reduced the viability of (C) A549 and (D) HCC827 cells at 24, 48 and 72 h. ***P<0.001 vs. Con. Con, control; Sch A, Schisantherin A; OD, optical density.
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Lung cancer cell viability is suppressed by Sch A in a concentration- and time-dependent manner. Sch A decreased (A) A549 and (B) HCC827 cell viability in a concentration-dependent manner, according to Cell Counting Kit-8 analysis. Sch A significantly reduced the viability of (C) A549 and (D) HCC827 cells at 24, 48 and 72 h. ***P<0.001 vs. Con. Con, control; Sch A, Schisantherin A; OD, optical density.

Journal: Molecular Medicine Reports

Article Title: Schisantherin A induces ferroptosis in non-small cell lung cancer through activation of the YAP/ACSL4/TfR signaling pathway

doi: 10.3892/mmr.2025.13734

Figure Lengend Snippet: Lung cancer cell viability is suppressed by Sch A in a concentration- and time-dependent manner. Sch A decreased (A) A549 and (B) HCC827 cell viability in a concentration-dependent manner, according to Cell Counting Kit-8 analysis. Sch A significantly reduced the viability of (C) A549 and (D) HCC827 cells at 24, 48 and 72 h. ***P<0.001 vs. Con. Con, control; Sch A, Schisantherin A; OD, optical density.

Article Snippet: Procell Life Science & Technology Co., Ltd. provided the EGFR-mutant HCC827 cell line (human lung adenocarcinoma origin, harboring the classic EGFR Exon19del E746-A750 deletion mutation; cat. no. CL-0094) and the EGFR wild-type A549 cell line (cat. no. CL-0016).

Techniques: Concentration Assay, Cell Counting, Control

Sch A induces cell death and cell cycle arrest in A549 and HCC827 cells. Sch A considerably increased the death of (A) A549 and (B) HCC827 cells in comparison with the control group, according to flow cytometric analysis. Compared with Con, (C) A549 and (D) HCC827 cells presented a significant decrease in the number of G 2 + S-phase cells and a significant increase in the number of G 1 -phase cells. Fer-1 and DFO were able to significantly reverse the Sch A-induced decrease in (E) A549 and (F) HCC827 cell viability, according to the results of the Cell Counting Kit-8 analysis. *P<0.05, **P<0.01 and ***P<0.001 vs. Con; ## P<0.01 and ### P<0.001 vs. Sch A. DFO, deferoxamine; Con, control; Sch A, Schisantherin A; Fer-1, ferrostatin-1; Nec-1, necrostatin-1; 3-MA, 3-methyladenine.

Journal: Molecular Medicine Reports

Article Title: Schisantherin A induces ferroptosis in non-small cell lung cancer through activation of the YAP/ACSL4/TfR signaling pathway

doi: 10.3892/mmr.2025.13734

Figure Lengend Snippet: Sch A induces cell death and cell cycle arrest in A549 and HCC827 cells. Sch A considerably increased the death of (A) A549 and (B) HCC827 cells in comparison with the control group, according to flow cytometric analysis. Compared with Con, (C) A549 and (D) HCC827 cells presented a significant decrease in the number of G 2 + S-phase cells and a significant increase in the number of G 1 -phase cells. Fer-1 and DFO were able to significantly reverse the Sch A-induced decrease in (E) A549 and (F) HCC827 cell viability, according to the results of the Cell Counting Kit-8 analysis. *P<0.05, **P<0.01 and ***P<0.001 vs. Con; ## P<0.01 and ### P<0.001 vs. Sch A. DFO, deferoxamine; Con, control; Sch A, Schisantherin A; Fer-1, ferrostatin-1; Nec-1, necrostatin-1; 3-MA, 3-methyladenine.

Article Snippet: Procell Life Science & Technology Co., Ltd. provided the EGFR-mutant HCC827 cell line (human lung adenocarcinoma origin, harboring the classic EGFR Exon19del E746-A750 deletion mutation; cat. no. CL-0094) and the EGFR wild-type A549 cell line (cat. no. CL-0016).

Techniques: Comparison, Control, Cell Counting

In A549 and HCC827 cells, ferroptosis inhibitors prevent Sch A-induced apoptosis. Fer-1 and DFO were shown by JC-1 staining to reverse the Sch A-induced MMP reduction in (A) A549 and (B) HCC827 cells (scale bar, 30 µm). Fer-1 and DFO inhibited the Sch A-induced increase in MDA in (C) A549 and (D) HCC827 cells. Fer-1 and DFO counteracted the Sch A-induced reduction in GSH in (E) A549 and (F) HCC827 cells. Reverse transcription-quantitative PCR analysis revealed that Fer-1 and DFO reversed the Sch A-induced increase in Chac1 and ptgs2 levels in (G) A549 and (H) HCC827 cells. *P<0.05, **P<0.01 and ***P<0.001 vs. Con; # P<0.05, ## P<0.01 and ### P<0.001 vs. Sch A. Con, control; Chac1, glutathione-specific γ-glutamylcyclotransferase 1; ptgs2, prostaglandin-endoperoxide synthase 2; Fer-1, ferrostatin-1; DFO, deferoxamine; Sch A, Schisantherin A; MDA, malondialdehyde; GSH, glutathione.

Journal: Molecular Medicine Reports

Article Title: Schisantherin A induces ferroptosis in non-small cell lung cancer through activation of the YAP/ACSL4/TfR signaling pathway

doi: 10.3892/mmr.2025.13734

Figure Lengend Snippet: In A549 and HCC827 cells, ferroptosis inhibitors prevent Sch A-induced apoptosis. Fer-1 and DFO were shown by JC-1 staining to reverse the Sch A-induced MMP reduction in (A) A549 and (B) HCC827 cells (scale bar, 30 µm). Fer-1 and DFO inhibited the Sch A-induced increase in MDA in (C) A549 and (D) HCC827 cells. Fer-1 and DFO counteracted the Sch A-induced reduction in GSH in (E) A549 and (F) HCC827 cells. Reverse transcription-quantitative PCR analysis revealed that Fer-1 and DFO reversed the Sch A-induced increase in Chac1 and ptgs2 levels in (G) A549 and (H) HCC827 cells. *P<0.05, **P<0.01 and ***P<0.001 vs. Con; # P<0.05, ## P<0.01 and ### P<0.001 vs. Sch A. Con, control; Chac1, glutathione-specific γ-glutamylcyclotransferase 1; ptgs2, prostaglandin-endoperoxide synthase 2; Fer-1, ferrostatin-1; DFO, deferoxamine; Sch A, Schisantherin A; MDA, malondialdehyde; GSH, glutathione.

Article Snippet: Procell Life Science & Technology Co., Ltd. provided the EGFR-mutant HCC827 cell line (human lung adenocarcinoma origin, harboring the classic EGFR Exon19del E746-A750 deletion mutation; cat. no. CL-0094) and the EGFR wild-type A549 cell line (cat. no. CL-0016).

Techniques: Staining, Reverse Transcription, Real-time Polymerase Chain Reaction, Control

Sch A induces ferroptosis in lung cancer cells by activating YAP signaling. (A) GeneCards intersection analysis revealed 739 overlapping genes associated with both ferroptosis and NSCLC. (B) Transcription factors among the intersecting genes were analyzed to identify key node genes. Reverse-transcription-quantitative PCR analysis revealed that Sch A increased the mRNA expression levels of YAP1 in (C) A549 and (D) HCC827 cells. Western blot analysis revealed that Sch A increased the expression levels of TfR, ACSL4 and YAP in (E) A549 and (F) HCC827 cells. *P<0.05 and **P<0.01 vs. Con. Con, control; YAP, yes-associated protein; Sch A, Schisantherin A; TfR, transferrin receptor; ACSL4, acyl-CoA synthase long-chain family member 4; NSCLC, non-small cell lung cancer.

Journal: Molecular Medicine Reports

Article Title: Schisantherin A induces ferroptosis in non-small cell lung cancer through activation of the YAP/ACSL4/TfR signaling pathway

doi: 10.3892/mmr.2025.13734

Figure Lengend Snippet: Sch A induces ferroptosis in lung cancer cells by activating YAP signaling. (A) GeneCards intersection analysis revealed 739 overlapping genes associated with both ferroptosis and NSCLC. (B) Transcription factors among the intersecting genes were analyzed to identify key node genes. Reverse-transcription-quantitative PCR analysis revealed that Sch A increased the mRNA expression levels of YAP1 in (C) A549 and (D) HCC827 cells. Western blot analysis revealed that Sch A increased the expression levels of TfR, ACSL4 and YAP in (E) A549 and (F) HCC827 cells. *P<0.05 and **P<0.01 vs. Con. Con, control; YAP, yes-associated protein; Sch A, Schisantherin A; TfR, transferrin receptor; ACSL4, acyl-CoA synthase long-chain family member 4; NSCLC, non-small cell lung cancer.

Article Snippet: Procell Life Science & Technology Co., Ltd. provided the EGFR-mutant HCC827 cell line (human lung adenocarcinoma origin, harboring the classic EGFR Exon19del E746-A750 deletion mutation; cat. no. CL-0094) and the EGFR wild-type A549 cell line (cat. no. CL-0016).

Techniques: Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Control

Silencing of YAP reverses Sch A-induced ferroptosis. Western blot analysis showed that the expression of YAP was decreased in (A) A549 and (B) HCC827 cells. In (C) A549 and (D) HCC827 cells, si-YAP decreased the expression of YAP and downstream signaling molecules. Fe 2+ accumulation was induced by Sch A in (E) A549 and (F) HCC827 cells, and the increase in Fe 2+ was reversed by YAP silencing, as demonstrated by FerroOrange staining (scale bar, 10 µm). After silencing YAP, the Sch A-induced increase in Fe 2+ and MDA in (G) A549 and (H) HCC827 cells was reduced. *P<0.05, **P<0.01 and ***P<0.001 vs. NC; ### P<0.001 vs. Sch A. NC, negative control; YAP, yes-associated protein; Sch A, Schisantherin A; si, small interfering RNA; MDA, malondialdehyde; ACSL4, acyl-CoA synthase long-chain family member 4; TfR, transferrin receptor.

Journal: Molecular Medicine Reports

Article Title: Schisantherin A induces ferroptosis in non-small cell lung cancer through activation of the YAP/ACSL4/TfR signaling pathway

doi: 10.3892/mmr.2025.13734

Figure Lengend Snippet: Silencing of YAP reverses Sch A-induced ferroptosis. Western blot analysis showed that the expression of YAP was decreased in (A) A549 and (B) HCC827 cells. In (C) A549 and (D) HCC827 cells, si-YAP decreased the expression of YAP and downstream signaling molecules. Fe 2+ accumulation was induced by Sch A in (E) A549 and (F) HCC827 cells, and the increase in Fe 2+ was reversed by YAP silencing, as demonstrated by FerroOrange staining (scale bar, 10 µm). After silencing YAP, the Sch A-induced increase in Fe 2+ and MDA in (G) A549 and (H) HCC827 cells was reduced. *P<0.05, **P<0.01 and ***P<0.001 vs. NC; ### P<0.001 vs. Sch A. NC, negative control; YAP, yes-associated protein; Sch A, Schisantherin A; si, small interfering RNA; MDA, malondialdehyde; ACSL4, acyl-CoA synthase long-chain family member 4; TfR, transferrin receptor.

Article Snippet: Procell Life Science & Technology Co., Ltd. provided the EGFR-mutant HCC827 cell line (human lung adenocarcinoma origin, harboring the classic EGFR Exon19del E746-A750 deletion mutation; cat. no. CL-0094) and the EGFR wild-type A549 cell line (cat. no. CL-0016).

Techniques: Western Blot, Expressing, Staining, Negative Control, Small Interfering RNA