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8-Bromo-7-methoxychrysin-blocked STAT3/Twist axis inhibits the stemness of cancer stem cell-like cell originated from SMMC-7721 cells

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收录情况: ◇ 统计源期刊 ◇ CSCD-C

机构: [1]Univ South China, Coll Med, Inst Canc, Hengyang 421001, Peoples R China [2]Univ South China, Key Lab Tumor Cellular & Mol Pathol, Hengyang 421001, Peoples R China [3]Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Peoples R China [4]Hunan Normal Univ, Coll Med, Dept Pharmaceut Sci, Changsha 410013, Hunan, Peoples R China [5]Hunan Normal Univ, Lab Mol & Stat Genet, Changsha 410081, Hunan, Peoples R China
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关键词: liver cell carcinoma cancer stem cell 8-bromo-7-methoxychysin STAT3 Twist

摘要:
Signal transducer and activator of transcription 3 (STAT3) is a member of the family of latent cytoplasmic transcriptional factors that could regulate cell proliferation, survival, and development. It has been reported that Twist is a target gene of STAT3, and STAT3/Twist signaling plays an important role in regulating cancer progress. Here, to explore whether 8-bromo-7-methoxychrysin (BrMC) inhibits liver cancer stem-like cell (LCSLC) properties via disrupting STAT3/Twist signaling, we cultured SMMC-7721 cells in vitro, and evaluated the effects of BrMC on the stemness of spheroids by determining the sphere-forming capability and migration. The sphere formation assay results showed a concentration-dependent decrease of sphere-forming capacity in LCSLCs (P < 0.05) treated with different concentrations of BrMC. Wound-healing assays results demonstrated a concentration-dependent decline in cell migration of LCSLCs treated with different concentrations of BrMC. In addition, CD133, CD44, and ALDH1 levels were decreased in LCSLCs treated with BrMC. Treatment with different concentrations of BrMC also reduced the expressions of p-STAT3 and Twist1 proteins. The effect of BrMC was substantially enhanced by co-treatment with JSI-124, a specific inhibitor of STAT3. Ectopic expression of Twist1 attenuated the inhibitory effects of BrMC on sphere formation, migration, and expression of the markers in LCSLCs. However, it had no affect on p-STAT3 expression in LCSLCs. These results demonstrated that BrMC inhibits the stemness of LCSLCs originated from SMMC-7721 cell line by inhibiting STAT3/Twist signal axis.

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出版当年[2017]版:
大类 | 3 区 生物
小类 | 4 区 生化与分子生物学 4 区 生物物理
最新[2023]版:
大类 | 2 区 生物学
小类 | 2 区 生物物理 3 区 生化与分子生物学
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第一作者机构: [1]Univ South China, Coll Med, Inst Canc, Hengyang 421001, Peoples R China [2]Univ South China, Key Lab Tumor Cellular & Mol Pathol, Hengyang 421001, Peoples R China [3]Hunan Prov Cooperat Innovat Ctr Mol Target New Dr, Hengyang 421001, Peoples R China
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通讯机构: [4]Hunan Normal Univ, Coll Med, Dept Pharmaceut Sci, Changsha 410013, Hunan, Peoples R China
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