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[Dihydromyricetin mediates epithelial mesenchymal transformation and regulates the proliferation and apoptosis of esophageal squamous cell carcinoma cells].
Tian, Y P; Cui, Y S; Zheng, X; Liu, B L; Zhang, Y P; Wei, K P; Zhang, Z; Hu, W N; Zhang, X M; Sun, G G.
Affiliation
  • Tian YP; School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
  • Cui YS; School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
  • Zheng X; School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
  • Liu BL; School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
  • Zhang YP; School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
  • Wei KP; School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
  • Zhang Z; Department of Oncologic Chemoradiotherapy, Tangshan Workers' Hospital, Tangshan 063001, China.
  • Hu WN; Department of Oncologic Chemoradiotherapy, Tangshan Workers' Hospital, Tangshan 063001, China.
  • Zhang XM; College of Life Science, North China University of Science and Technology, Tangshan 062210, China.
  • Sun GG; School of Public Health, North China University of Science and Technology, Tangshan 063210, China.
Zhonghua Zhong Liu Za Zhi ; 44(4): 326-333, 2022 Apr 23.
Article in Zh | MEDLINE | ID: mdl-35448920
ABSTRACT

Objective:

To study the effects of dihydromyricetin (DMY) on the proliferation, apoptosis and epithelial mesenchymal transition (EMT) of esophageal squamous cell carcinoma (ESCC) cell KYSE150 and KYSE410.

Methods:

KYSE150 and KYSE410 cells were treated with different concentrations of DMY (0, 25, 50, 100, 150, 200 µmol/L) for 24 hours. The median inhibition concentration (IC50) values of KYSE150 and KYSE410 were detected by cell counting kit-8 (CCK-8) method. Then 0.5‰ dimethyl sulfoxide (DMSO) was used as control group, dihydromyricetin (DMY), dihydromyricetin and transforming growth factor-ß1 (DMY+ TGF-ß1), transforming growth factor-ß1 (TGF-ß1) were used as experimental group. Cell proliferation and apoptosis rates were measured by clonal formation and flow cytometry. Transwell invasion and wound healing assay were used to detect cell invasion and migration. The protein expression levels of Caspase-3, Caspase-9, Bcl-2, Bax, Smad2/3, phosphorylation-Smad2/3 (p-Smad2/3) and Vimentin were detected by western blot.

Results:

The IC50 values of DMY on KYSE410 and KYSE150 cells were 100.51 and 101.27 µmol/L. The clone formation numbers of KYSE150 and KYSE410 in DMY group [(0.53±0.03) and (0.31±0.03)] were lower than those in DMSO group [(1.00±0.10) and (1.00±0.05), P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in DMY group [(1.84±0.22)% and (2.80±0.07)%] were higher than those in DMSO group [(1.00±0.18)% and (1.00±0.07)%, P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in DMY group [(0.42±0.03) and (0.29±0.05)] were lower than those in DMSO group [(1.00±0.08) and (1.00±0.05), P<0.05]. The migration rates of KYSE150 and KYSE410 cells in DMY group [(0.65±0.14)% and (0.40±0.17)%] were lower than those in DMSO group [(1.00±0.10)% and (1.00±0.08)%, P<0.05]. The clone formation numbers of KYSE150 and KYSE410 in TGF-ß1 group [(1.01±0.08) and (0.99±0.25)] were higher than those in DMY+ TGF-ß1 group [(0.73±0.10) and (0.58±0.05), P<0.05]. The apoptosis rates of KYSE150 and KYSE410 cells in TGF-ß1 group [(0.81±0.14)% and (1.18±0.10)%] were lower than those in DMY+ TGF-ß1 group [(1.38±0.22)% and (1.85±0.04)%, P<0.05]. The invasion numbers of KYSE150 and KYSE410 cells in TGF-ß1 group [(1.19±0.11) and (1.39±0.11)] were higher than those in DMY+ TGF-ß1 group [(0.93±0.09) and (0.93±0.05), P<0.05]. The migration rates of KYSE150 and KYSE410 cells in TGF-ß1 group [(1.87±0.19)% and (1.32±0.04)%] were higher than those in DMY+ TGF-ß1 group [(0.86±0.16)% and (0.77±0.12)%, P<0.05]. The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY group were higher than those in DMSO group, while the protein expression level of Bcl-2 was lower than that in DMSO group (P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in DMY group were lower than those in DMSO group (P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in TGF-ß1 group were lower than those in DMY+ TGF-ß1 group, and the protein expression level of Bcl-2 was higher than that in DMY+ TGF-ß1 group (P<0.05). The protein expression levels of Bax, Caspase-3 and Caspase-9 in KYSE150 and KYSE410 cells in DMY+ TGF-ß1 group were lower than those in DMY group, and the protein expression level of Bcl-2 was higher than that in DMY group (P<0.05). The protein expression levels of p-Smad2/3, Smad2/3 and Vimentin in KYSE150 and KYSE410 cells in TGF-ß1 group were higher than those in DMY+ TGF-ß1 group (P<0.05).

Conclusion:

DMY can inhibit the proliferation and EMT of ESCC mediated by TGF-ß1 and promote cell apoptosis.
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Full text: 1 Collection: 01-internacional Health context: 6_ODS3_enfermedades_notrasmisibles Database: MEDLINE Main subject: Esophageal Neoplasms / Esophageal Squamous Cell Carcinoma Limits: Humans Language: Zh Journal: Zhonghua Zhong Liu Za Zhi Year: 2022 Document type: Article

Full text: 1 Collection: 01-internacional Health context: 6_ODS3_enfermedades_notrasmisibles Database: MEDLINE Main subject: Esophageal Neoplasms / Esophageal Squamous Cell Carcinoma Limits: Humans Language: Zh Journal: Zhonghua Zhong Liu Za Zhi Year: 2022 Document type: Article