Luteolin Isolated from Cuscuta Chinensis Lam Inhibits Lung Cancer Cell Viability and Migration via Co-Treatment with Mithramycin A.
1/5 보강
[INTRODUCTION] As a common herbal medicine, Cuscuta chinensis Lam is widely used for cancer treatment in China.
APA
Maimaiti T, Ablise M, Maimaiti A (2026). Luteolin Isolated from Cuscuta Chinensis Lam Inhibits Lung Cancer Cell Viability and Migration via Co-Treatment with Mithramycin A.. Current cancer drug targets. https://doi.org/10.2174/0115680096433191251202075137
MLA
Maimaiti T, et al.. "Luteolin Isolated from Cuscuta Chinensis Lam Inhibits Lung Cancer Cell Viability and Migration via Co-Treatment with Mithramycin A.." Current cancer drug targets, 2026.
PMID
41540539
Abstract
[INTRODUCTION] As a common herbal medicine, Cuscuta chinensis Lam is widely used for cancer treatment in China. However, the anti-lung cancer effect of the bioactive constituents in C. chinensis and, the potential molecular mechanisms of action have yet to be elucidated.
[MATERIALS AND METHODS] Bioassay-guided fractionation was used to isolate luteolin from the water extract of C. chinensis (CLW). The structure of luteolin was determined by spectroscopic analysis. The viability of A549 and H1650 lung cancer cells was determined using the MTT assay. Annexin V-FITC staining assay and cell cycle analysis were performed to explore the apoptosis and cell cycle phase distribution of lung cancer cells, respectively. Transwell invasion, wound healing, transwell migration, and adhesion assays were conducted to observe the lung cancer cell invasion, migration, and adhesion. Protein expression was determined via Western blot analysis.
[RESULTS AND DISCUSSION] Luteolin was isolated from CLW by bioassay-guided fractionation, and its structure was determined by HR-ESI-MS and NMR. Luteolin inhibited the viability of A549 and H1650 lung cancer cells in a dose and time-dependent manner. Luteolin also dose-dependently induced apoptosis, and arrested the cell cycle at the G0/G1 phase in both cell types. Treatment with luteolin dose-dependently inhibited the invasion, migration, and adhesion of these cells. Luteolin consistently up-regulated FOSB, FGFBP1, and NPTX1 protein expression levels, and down-regulated H3K9me3, SETDB1, and MAP2K6 protein expression levels in A549 and H1650 cells. Co-treatment of luteolin and mithramycin A on A549 and H1650 lung cancer cells exhibited stronger up-regulation of FOSB and NPTX1 protein expression levels, and stronger down-regulation of SETDB1, H3K9me3, and MAP2K6 protein expression levels than luteolin or mithramycin A treatment alone. Co-treatment of luteolin and mithramycin A synergistically inhibited A549 and H1650 cell viability; induced apoptosis; delayed cell cycle at the G0/G1 phase; and inhibited the invasion, migration, and adhesion of A549 and H1650 cells compared with the treatment of luteolin or mithramycin A alone.
[CONCLUSION] Luteolin may suppresses the viability, invasion, migration, and adhesion of lung cancer cells via co-treatment with mithramycin A.
[MATERIALS AND METHODS] Bioassay-guided fractionation was used to isolate luteolin from the water extract of C. chinensis (CLW). The structure of luteolin was determined by spectroscopic analysis. The viability of A549 and H1650 lung cancer cells was determined using the MTT assay. Annexin V-FITC staining assay and cell cycle analysis were performed to explore the apoptosis and cell cycle phase distribution of lung cancer cells, respectively. Transwell invasion, wound healing, transwell migration, and adhesion assays were conducted to observe the lung cancer cell invasion, migration, and adhesion. Protein expression was determined via Western blot analysis.
[RESULTS AND DISCUSSION] Luteolin was isolated from CLW by bioassay-guided fractionation, and its structure was determined by HR-ESI-MS and NMR. Luteolin inhibited the viability of A549 and H1650 lung cancer cells in a dose and time-dependent manner. Luteolin also dose-dependently induced apoptosis, and arrested the cell cycle at the G0/G1 phase in both cell types. Treatment with luteolin dose-dependently inhibited the invasion, migration, and adhesion of these cells. Luteolin consistently up-regulated FOSB, FGFBP1, and NPTX1 protein expression levels, and down-regulated H3K9me3, SETDB1, and MAP2K6 protein expression levels in A549 and H1650 cells. Co-treatment of luteolin and mithramycin A on A549 and H1650 lung cancer cells exhibited stronger up-regulation of FOSB and NPTX1 protein expression levels, and stronger down-regulation of SETDB1, H3K9me3, and MAP2K6 protein expression levels than luteolin or mithramycin A treatment alone. Co-treatment of luteolin and mithramycin A synergistically inhibited A549 and H1650 cell viability; induced apoptosis; delayed cell cycle at the G0/G1 phase; and inhibited the invasion, migration, and adhesion of A549 and H1650 cells compared with the treatment of luteolin or mithramycin A alone.
[CONCLUSION] Luteolin may suppresses the viability, invasion, migration, and adhesion of lung cancer cells via co-treatment with mithramycin A.