Jiejie Yu’s research while affiliated with Zhejiang Chinese Medical University and other places

What is this page?

This page lists works of an author who doesn't have a ResearchGate profile or hasn't added the works to their profile yet. It is automatically generated from public (personal) data to further our legitimate goal of comprehensive and accurate scientific recordkeeping. If you are this author and want this page removed, please let us know.

Publications (1)

Figure 1. Inhibitory effects of GL-V9 on the viabilities of CRC cells and normal human colon epithelial cells. MTT assays were used to detect cell viability after GL-V9 treatment. (A) CRC cells HCT116, SW620, SW480, LS174T, and normal colon epithelial cells FHC were treated with 0-160 μM GL-V9 for 24 h. ** p<0.001 for all the examined cell lines. (B) CRC cells HCT116 were treated with 0-160 μM GL-V9 for 12, 24, and 48 h. (C) Survival rates of CRC cells HCT116, SW620, SW480, LS174T and normal colon epithelial cells FHC treated with 0, 5, 10, 15, and 20 μM GL-V9 for 24 h. GL-V9 showed marginal cytotoxic effect on FHC cells even at a concentration of 20 μM (inhibition rate < 10%). Each error bar represents the mean ± S.D. of three replicate samples. Symbols on each error bar represent the statistical significance of each cell line. HCT116: ◇ , p<0.05, ◆, p<0.001. SW620: ○, p<0.05; •, p<0.001. SW480: □, p<0.05; ■, p<0.001. LS174T: △, p<0.05; ▲, p<0.001. FHC: ☆, p<0.05; ★, p<0.001.
Figure 2. Effect of GL-V9 on cell migration in vitro. CRC cells HCT116 and SW480 treated with 10 μM and 20 μM GL-V9 for 24 h demonstrated significantly reduced migratory capacities, as indicated by wound healing assay. Normal colon epithelial cells FHC with much lower migration potential also showed reduced migration after GL-V9 treatment. The representative photographs (A) and quantification (B) are shown. Images were taken at 0 and 24 h. Each error bar represents the mean ± S.D. of three replicate samples. * p<0.05, ** p<0.001.
Figure 3. Effect of GL-V9 on CRC cell invasion and adhesion in vitro. (A-B) CRC cells HCT116 and SW480 treated with 10 μM and 20 μM GL-V9 for 24 h demonstrated significantly reduced migration and invasion through extracellular matrix as indicated by the transwell migration assay. Normal colon epithelial cells FHC with much lower invasive potential also showed reduced invasion through the extracellular matrix (ECM) after GL-V9 treatment, but with less reduction degree and statistical significance. The number of cells migrated through the ECM after 24 h was counted in five randomly selected (×200) microscopic fields. (C) GL-V9 treatment for 24 h at a concentration of 20 μM significantly reduced cell adhesion for both CRC cells HCT116 and SW480 and normal cells FHC, as indicated by cell attachment assay. Each error bar represents the mean ± S.D. of three replicate samples. * p<0.05; **, p<0.001.
Figure 4. Changes in the expression and activities of MMP-2 and MMP-9 after GL-V9 treatment. (A) Treatment of 5, 10, and 20 μM GL-V9 for 24 h in HCT116 cells led to decreased MMP-2 and MMP-9 protein expression. Relative intensities of western blot bands were quantified using the ImageJ software. The expression levels were normalized by β-actin expression, which was used as internal control. (B) Treatment of 5, 10, and 20 μM GL-V9 for 24 h in HCT116 cells led to reduced activities of MMP-2 and MMP-9, as indicated by gelatin zymorgraphy. Each error bar represents the mean ± S.D. of three replicate samples. * p < 0.05, ** p < 0.01.
Figure 5. Effects of GL-V9 on the PI3K/Akt and MAPK/ERK signaling pathways. (A) Treatment of 5, 10, and 20 μM GL-V9 for 24 h in HCT116 cells inhibited PI3K/Akt activity in a dose-dependent manner, but did not affect the activity of MAPK/ERK signaling. PI3K expression and phosphorylated form of Akt were significantly reduced in GL-V9-treated cells, but expression of p38 MAPK and ERK1/2 in both the total and phosphorylated forms showed little change after GL-V9 treatment. (B) Quantification of the relative protein expression levels of PI3K, Akt, p-Akt, p38, p-p38, ERK1/2, and p-ERK1/2 in HCT116 cells treated with different concentrations of GL-V9, as compared with the control group. Each error bar represents the mean ± S.D. of three replicate samples. * p < 0.05, ** p < 0.01.

+1

Flavonoid GL-V9 suppresses invasion and migration of human colorectal cancer cells by inhibiting PI3K/Akt and MMP-2/9 signaling
  • Article
  • Full-text available

June 2021

·

178 Reads

·

23 Citations

Journal of Cancer

Ye Gu

·

Jiejie Yu

·

Cong Ding

·

[...]

·

Haitao Huang

Tumor distant metastasis is the primary cause of death in colorectal cancer (CRC) patients. GL-V9 is a newly synthesized flavonoid derivative with several beneficial biological functions including anti-tumor and anti-inflammation. However, the anti-metastatic effect of GL-V9 and related mechanisms in CRC remains unknown. In this study, the anti-invasive and anti-migratory activities of GL-V9 were investigated in CRC cells. Using MTT assay, cell wound healing assay, and transwell migration assay, we showed that GL-V9 suppressed CRC cell viability, migration, and invasion in a concentration-dependent manner. In addition, the protein expression levels as well as activities of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) were significantly reduced after GL-V9 treatment. Further analysis of the underlying mechanism revealed that GL-V9 inhibited PI3K/Akt signaling pathway upstream of MMP-2 and MMP-9. In conclusion, our study demonstrated that GL-V9 could suppress CRC cell invasion and migration through PI3K/Ak and MMP-2/9 axis. Therefore, GL-V9 might be a potential novel therapeutic agent against CRC metastasis.

Download

Citations (1)

... Western blotting was carried out as previously described [6]. The total protein in HCC cells was extracted using Radio immunoprecipitation assay (RIPA) buffer(Beyotime, China). ...

Reference:

Flavonoid GL-V9 suppresses development of human hepatocellular cancer cells by inhibiting Wnt/β-Cantenin signaling pathway
Flavonoid GL-V9 suppresses invasion and migration of human colorectal cancer cells by inhibiting PI3K/Akt and MMP-2/9 signaling

Journal of Cancer

Ye Gu

·

Jiejie Yu

·

Cong Ding

·

[...]

·

Haitao Huang