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@# Objective To systematically evaluate the expression of programmed cell death receptor 1 (PD-1) and programmed cell death ligand 1 (PD-L1) in esophageal squamous cell carcinoma and its relationship with prognosis. Methods The literature from PubMed, EMbase, The Cochrane Library, Web of Science, CNKI and Wanfang data from inception to February 22, 2020 was searched by computer. Data were extracted and the quality of literature was evaluated using RevMan 5.3 software for meta-analysis. Egger's and Begg's tests were used to evaluate publication bias, and Stata 15.1 software was used for sensitivity analysis. Results A total of 16 articles were included, and there were 3 378 patients with esophageal squamous cell carcinoma. The methodological index for nonrandomized studies (MINORS) scores were all 12 points and above. The meta-analysis results showed that the positive expression rates of PD-1 and PD-L1 in tumor cells were 37.8% (190/504) and 41.7% (1 407/3 378), respectively. The positive expression of PD-L1 in tumor immune infiltrating cells was 41.7% (412/987). The overall survival (OS) of the tumor cell with high PD-L1 expression was lower than that with low PD-LI expression (HR=1.30, 95%CI 1.01-1.69, P=0.04). The OS of the tumor immune infiltrating cell with high PD-L1 expression was significantly higher than that with low PD-LI expression (HR=0.65, 95%CI 0.53-0.80, P<0.000 1). Conclusion PD-L1 has a high expression rate in esophageal squamous cell carcinoma and is an important factor for the prognosis of esophageal squamous cell carcinoma.
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Aim To study the apoptosis effect of cucurbitacin Ⅱa on non-small cell lung cancer cell lines NCI-H460 and A549 and its underlying mechanism.Methods Cell viability was assessed by CCK-8 assay.The apoptosis effect and cell cycle arrest were detected by Flow cytometry.Western blot was employed to detect the related protein.Results The proliferation of lung cancer cell lines NCI-H460 and A549 was inhibited by CuⅡa, which showed cytotoxic activity with IC50 values of 224.9 nmol·L-1 and 108.3 nmol·L-1 against NCI-H460 and A549 respectively.CuⅡa induced the cells apoptosis and cell cycle arrest at G2/M phase.The results of Western blot showed CuⅡa inhibited the phosphorylation of STAT3 and Cofilin in a dose-dependent manner.Further, CuⅡa inhibited the phosphorylation of Aurora A, in line with the important characteristics of anti-tumor effect of Aurora A kinase inhibitor with blocking cells in the G2/M phase.Conclusion CuⅡa has obvious anti-tumor effect against non-small cell lung cancer, which suggests its value as a lead compound for lung cell carcinoma.
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Objective To investigate the effect of tamibarotene(Am80)on cerebral ischemia reperfusion injury. Methods Rats were randomly divided into sham operation group(Sham),model group(I/R) and tamibarotene in-tervention group (Am80, intragastric administration of Am80 6 mg/kg). The middle cerebral artery occlusion (MCAO) was established by suture method. At 24 h after reperfusion,the brain was removed. And the neurological behavioral score was assessed by double blind method.The cerebral infarction volume was measured by TTC staining. The proteins of RARα,Bcl-2,Bax and mRNA were examined by Western blot and RT-qPCR,respectively. Results Am80 significantly improved the neurological deficits of MCAO rats and effectively reduced the infarct volume. And upregulated the level of RARα and Bcl-2, decreased the expression of Bax. Conclusions Am80 has a protective effect on cerebral ischemia-reperfusion in rats,and its effect may be related to anti-apoptosis.
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Objective To investigate the effect of tamibarotene(Am80)on cerebral ischemia reperfusion injury. Methods Rats were randomly divided into sham operation group(Sham),model group(I/R) and tamibarotene in-tervention group (Am80, intragastric administration of Am80 6 mg/kg). The middle cerebral artery occlusion (MCAO) was established by suture method. At 24 h after reperfusion,the brain was removed. And the neurological behavioral score was assessed by double blind method.The cerebral infarction volume was measured by TTC staining. The proteins of RARα,Bcl-2,Bax and mRNA were examined by Western blot and RT-qPCR,respectively. Results Am80 significantly improved the neurological deficits of MCAO rats and effectively reduced the infarct volume. And upregulated the level of RARα and Bcl-2, decreased the expression of Bax. Conclusions Am80 has a protective effect on cerebral ischemia-reperfusion in rats,and its effect may be related to anti-apoptosis.