RESUMEN
【Objective】 To investigate the effects of total flavone of oldenlandia diffusa (FOD) on the proliferation and apoptosis of hepatocellular carcinoma (HCC) stem cells sorted from Huh7. 【Methods】 Human HCC cell lines Huh7 was cultured in vitro; CD133 positive (CD133+) stem cells in Huh7 cell line were sorted by flow cytometry, and stem cell markers such as Nanog, Oct4 and Sox2 were tested by Western blotting. CD133+-Huh7 was stimulated by different concentrations (0 μg/mL, 50 μg/mL, 100 μg/mL and 400 μg/mL) of FOD for different time (24 h, 48 h, 72 h and 96 h). CCK8 and plate cell cloning assay were used to detect the effect of FOD on CD133+-Huh7 proliferation while Annexin V-PE/7-AAD was used to detect the effect of FOD on CD133+-Huh7 apoptosis. Western blotting was used to detect the protein expressions of protein 53 (P53), factor associated suicide-Fas-associating protein with a novel death domain (Fas-FADD), B-cell lymphoma-2 (Bcl-2), Cleaved-Caspase3, and Bcl-2 associated X protein (Bax). 【Results】 More than 95% of stem cells were purified for further experiments. Cell proliferation of CD133+-Huh7 was significantly inhibited by FOD, with the significant suppression at the concentration of 100 μg/mL for 72 h compared with negative control group (P<0.05). The apoptosis rate was significantly upregulated than that in the negative control group (P<0.05). The protein expression of Bcl2 decreased while Bax and Cleaved-Caspae3 increased via FAS/FADDD and P53 axis. 【Conclusion】 FOD can significantly inhibit the proliferation and promote the apoptosis of CD133+-Huh7.
RESUMEN
【Objective】 To investigate the effect of total flavone of oldenlandia diffusa(FOD) on the stemness, proliferation and apoptosis of breast cancer(BC) stem cells sorted from MDA-MB-231. 【Methods】 Human BC cell lines MDA-MB-231 was cultured in vitro; MDA-MB-231 was stimulated by different concentrations(0 μg/mL, 100 μg/mL, 200 μg/mL and 400 μg/mL) of FOD for different time (24 h, 48 h and 72 h). CCK8 and plate cell cloning assay were used to detect the effect of FOD on MDA-MB-231 proliferation; CD44+/CD24-MDA-MB-231 cell line were tested by flow cytometry and stem cell markers such as Nanog, Oct4 and Sox2 were tested by Western blotting; Annexin V-PE/7-AAD was used to detect the effect of FOD on MDA-MB-231 apoptosis and Bcl2, cleaved-caspase3 and Bax were tested by Western blotting. 【Results】 Cell proliferation of MDA-MB-231 was significantly inhibited by FOD, with the significant suppression at concentrations of 400 μg/mL for 72 h compared with negative control group(P<0.05). The apoptosis rate was significantly upregulated than the negative control group (P<0.05). The protein expression of Bcl2 decreased while Bax and cleaved-caspae3 increased, and stemness markers such as Nanog, Sox2 and Oct4 decreased in FOD-treated cells. Moverover, Akt-GSK3β-β-catenin axis was inhibited in FOD-treated cells. 【Conclusion】 FOD could significantly inhibit the stemness and proliferation and promote the apoptosis of MDA-MB-231.
RESUMEN
Conversion therapy has become the core in the treatment of borderline resectable or unresectable liver cancer, which provides resectable opportunities for more advanced liver cancer patients. In accordance with the first-choice treatment regimen recommended by the guidelines, the authors reported a successful case of Atezolizumab and Bevacizumab (T+A regimen) conversion therapy. The patient with initially borderline resectable advanced liver cancer was performed liver segment resection sucessfully after conversion therapy, and non-tumor recurrence was observed at postoperative 9 months. Postoperative pathological examination showed combined hepatocellular-cholangiocarcinoma, which also indicated the important value of T+A regimen in the conversion therapy of combined hepatocellular-cholangiocarcinoma.
RESUMEN
Interactions between hepatocellular carcinoma (HCC) cells and the tumor stromal microenvironment have profound effects on tumor growth,epithelial-mesenchymal transition (EMT),invasion and metastasis.Activated hepatic stellate cells (HSCs) are the major subtype of stromal cells in the liver tumor microenvironment.HCC cells can induce the activation of HSCs during carcinogenesis,while activated HSCs promote HCC cells growth and migration through secreting growth factors,inducing angiogenesis and immune suppression.Bidirectional interactions between HCC cells and HSCs may function as an ＂amplification loop＂ to further enhance metastatic growth in the liver.In this review,we summarized the most recent data from the research on HSCs and its relationship with HCC.
RESUMEN
Objective:To investigate the ability of fluoride toothpaste and fluoride varnish on enamel remineralization and acid resist-ance.Methods:Enamel specimens were prepared from bovine incisors,and were randomly divided into 4 groups(n=3)after acid-etching by 37%phosphoric acid.Specimens in group A(control)was processed daily with normal saline;those in group B and C were treated once with Duraphat varnish and Fluor Protector varnish respectively;in group D was daily processed with fluoride toothpaste. All specimens were incubated in artificial saliva for 2 weeks.Then all specimens received acid-etching again.Micro-hardness test, SEM observation and image analysis were performed before and after each step.Results:After 2 weeks of processing,no remineraliza-tion was found in group A.Varnish layers were observed on the surface of specimens in group B and C.In group D remineralization was detected on the enamel surface.After re-etching,micro-hardness decreased in group A and D.Fluoride varnish layers in group B and C showed strong resistance to acid-etching.After re-etching,area of micro-holes in group A and D increased(P<0.05 ),but that in group D was smaller than in the control(P<0.05).No micro-hole was observed in group B and group C.Conclusion:Protec-tive layer formed on the enamel surface by fluoride varnish is resistant to acid-etching and promotes enamel remineralization.Fluoride toothpaste application can promote enamel remineralization,but with less resistance to acid.