目的运用文献计量学的方法分析中、英文数据库中瘢痕疙瘩的研究现状,探索其当前研究热点和未来研究方向。方法采用中国知网(CNKI)数据库和Web of Science Core Collection进行中、英文文献的检索。以“瘢痕疙瘩”为检索词,检索日期自建...目的运用文献计量学的方法分析中、英文数据库中瘢痕疙瘩的研究现状,探索其当前研究热点和未来研究方向。方法采用中国知网(CNKI)数据库和Web of Science Core Collection进行中、英文文献的检索。以“瘢痕疙瘩”为检索词,检索日期自建库至2022-12-31,纳入已发表瘢痕疙瘩的相关文献,采用VOSviewer 1.6.19软件和Citespace6.2.R3软件对纳入文献的国家、机构及作者等分布、关键词的聚类及其时序分析,绘制对应的循证可视化图谱。结果分别纳入2931篇和2842篇的中、英文文献。结果显示中、英文文献的年发文量均逐年递增;关键词聚类方面,中文文献的结果提示未来潜在的研究热点为瘢痕疙瘩的形成原因及发病机制方面,英文文献未来研究的热点为瘢痕疙瘩的统筹管理。结论目前关于瘢痕疙瘩的研究兴趣呈现出上升趋势,国内和国际上研究人员都在积极探索。展开更多
Background:In vivo experiments were conducted to examine the effects of the targeted drug anlotinib on the stemness of hepatocellular carcinoma(HCC)cells and lenvatinib-resistant liver cancer cells and to explore the ...Background:In vivo experiments were conducted to examine the effects of the targeted drug anlotinib on the stemness of hepatocellular carcinoma(HCC)cells and lenvatinib-resistant liver cancer cells and to explore the underlying molecular mechanisms.Methods:A subcutaneous xenograft model of Hep3B-derived HCC was established in nude mice,which were randomly divided into 2 groups(n=5 males per group):(1)intragastric administration of anlotinib(0.4 mg/kg)and(2)intragastric administration of normal saline.We constructed lenvatinib-resistant cell lines and randomly divided the mice into 3 groups(n=5 males per group):(1)intragastric administration of anlotinib,(2)intragastric administration of lenvatinib,and(3)intragastric administration of normal saline.After 2 weeks of treatment,tumor tissues were harvested,and mRNA and proteins were isolated from the tissues.Changes in the expression of cancer stemness markers(epithelial cell adhesion molecule[EpCAM],CD13,CD90,aldehyde dehydrogenase 1[ALDH1],CD44,and CD45),totipotency factors(sex-determining region Y-box 2[Sox2],Nanog,octamer-binding transcription factor 4[Oct4]),and genes related to the Notch signaling pathway were examined.Results:Compared with that in the control group,tumor size and weight were reduced in nude mice treated with anlotinib.These differences were statistically significant in both the types of nude mice.Anlotinib affected stemness markers and totipotency factors by downregulating the expression of CD133,CD90,and G-protein–coupled receptor 5(LGR5)and upregulating the expression of intercellular adhesion molecule 1(ICAM-1)and Sox2.In addition,lenvatinib-resistant cell lines increased Notch signaling pathway,whereas anlotinib inhibited Notch signaling pathway.Conclusions:The antitumor effect of anlotinib on HCC and lenvatinib-resistant HCC cellsmay occur through inhibition of the Notch signaling pathway.Anlotinib may be the drug of choice for sequential therapy in lenvatinib-resistant liver cancer.展开更多
基金supported by the Natural Science Foundation of the Hubei Province(no.2023 AFB894)Open for the Key Laboratory of Biological Targeted Therapy in 2021(no.2021swbx019).
文摘Background:In vivo experiments were conducted to examine the effects of the targeted drug anlotinib on the stemness of hepatocellular carcinoma(HCC)cells and lenvatinib-resistant liver cancer cells and to explore the underlying molecular mechanisms.Methods:A subcutaneous xenograft model of Hep3B-derived HCC was established in nude mice,which were randomly divided into 2 groups(n=5 males per group):(1)intragastric administration of anlotinib(0.4 mg/kg)and(2)intragastric administration of normal saline.We constructed lenvatinib-resistant cell lines and randomly divided the mice into 3 groups(n=5 males per group):(1)intragastric administration of anlotinib,(2)intragastric administration of lenvatinib,and(3)intragastric administration of normal saline.After 2 weeks of treatment,tumor tissues were harvested,and mRNA and proteins were isolated from the tissues.Changes in the expression of cancer stemness markers(epithelial cell adhesion molecule[EpCAM],CD13,CD90,aldehyde dehydrogenase 1[ALDH1],CD44,and CD45),totipotency factors(sex-determining region Y-box 2[Sox2],Nanog,octamer-binding transcription factor 4[Oct4]),and genes related to the Notch signaling pathway were examined.Results:Compared with that in the control group,tumor size and weight were reduced in nude mice treated with anlotinib.These differences were statistically significant in both the types of nude mice.Anlotinib affected stemness markers and totipotency factors by downregulating the expression of CD133,CD90,and G-protein–coupled receptor 5(LGR5)and upregulating the expression of intercellular adhesion molecule 1(ICAM-1)and Sox2.In addition,lenvatinib-resistant cell lines increased Notch signaling pathway,whereas anlotinib inhibited Notch signaling pathway.Conclusions:The antitumor effect of anlotinib on HCC and lenvatinib-resistant HCC cellsmay occur through inhibition of the Notch signaling pathway.Anlotinib may be the drug of choice for sequential therapy in lenvatinib-resistant liver cancer.
