目的探讨单磷酸腺苷活化蛋白激酶(AMPK)通过调控能量代谢对肿瘤发挥双重作用的机制,为靶向AMPK治疗肿瘤提供理论基础。方法应用PubMed及中国知网数据库检索系统,以“adenosine 5’-monophosphate-activated protein kinase(AMPK)、tumor...目的探讨单磷酸腺苷活化蛋白激酶(AMPK)通过调控能量代谢对肿瘤发挥双重作用的机制,为靶向AMPK治疗肿瘤提供理论基础。方法应用PubMed及中国知网数据库检索系统,以“adenosine 5’-monophosphate-activated protein kinase(AMPK)、tumor、metabolic regulator、Metformin”为英文关键词,以“单磷酸腺苷酸活化蛋白激酶、肿瘤、能量代谢、二甲双胍”为中文关键词,交叉检索2002年1月-2023年4月的相关文献。纳入标准:(1)AMPK的结构及调控能量代谢的作用;(2)AMPK通路在肿瘤中的调控作用;(3)AMPK在肿瘤治疗中的临床应用。排除标准:与肿瘤相关性较小及质量较低的文章。最终纳入文献61篇。结果AMPK在不同肿瘤类型、分期以及治疗方式中,通过调控糖代谢、脂代谢和蛋白质代谢等,发挥抑癌或促癌的双重作用。结论AMPK可以通过调控肿瘤代谢微环境发挥其促癌或抑癌作用,具有潜在的肿瘤临床治疗价值,但其作用于肿瘤的复杂机制仍需进一步探索。展开更多
Tumors are believed to consist of a heterogeneous population of tumor ceils originating from rare cancer stem cells （CSCs）. However, emerging evidence suggests that tumor may also origi- nate from non-CSCs. To suppo...Tumors are believed to consist of a heterogeneous population of tumor ceils originating from rare cancer stem cells （CSCs）. However, emerging evidence suggests that tumor may also origi- nate from non-CSCs. To support this viewpoint, we are here to present definitive evidence indicating that the number of tumorigenic tumor cells is greater than that of CSCs in tumor, and tumor can also derive from non-CSCs. To achieve this, an idealized mathematical model was employed in the pre- sent study and theoretical calculation revealed that non-CSCs could initiate the occurrence of tumor if their proliferation potential was adequate. Further, experimental studies demonstrated that 17.7%, 38.6% and 5.2% of tumor cells in murine B16 solid melanoma, H22 hepatoma and Lewis lung carci2 noma, respectively, were potentially tumorigenic. Thus, based on the aforementioned findings, we propose that the scarce CSCs, if exist, are not the sole source of a tumor.展开更多
文摘目的探讨单磷酸腺苷活化蛋白激酶(AMPK)通过调控能量代谢对肿瘤发挥双重作用的机制,为靶向AMPK治疗肿瘤提供理论基础。方法应用PubMed及中国知网数据库检索系统,以“adenosine 5’-monophosphate-activated protein kinase(AMPK)、tumor、metabolic regulator、Metformin”为英文关键词,以“单磷酸腺苷酸活化蛋白激酶、肿瘤、能量代谢、二甲双胍”为中文关键词,交叉检索2002年1月-2023年4月的相关文献。纳入标准:(1)AMPK的结构及调控能量代谢的作用;(2)AMPK通路在肿瘤中的调控作用;(3)AMPK在肿瘤治疗中的临床应用。排除标准:与肿瘤相关性较小及质量较低的文章。最终纳入文献61篇。结果AMPK在不同肿瘤类型、分期以及治疗方式中,通过调控糖代谢、脂代谢和蛋白质代谢等,发挥抑癌或促癌的双重作用。结论AMPK可以通过调控肿瘤代谢微环境发挥其促癌或抑癌作用,具有潜在的肿瘤临床治疗价值,但其作用于肿瘤的复杂机制仍需进一步探索。
基金supported by Scientific Research Fund of Shanghai Health Bureau of China(No.2008131)
文摘Tumors are believed to consist of a heterogeneous population of tumor ceils originating from rare cancer stem cells （CSCs）. However, emerging evidence suggests that tumor may also origi- nate from non-CSCs. To support this viewpoint, we are here to present definitive evidence indicating that the number of tumorigenic tumor cells is greater than that of CSCs in tumor, and tumor can also derive from non-CSCs. To achieve this, an idealized mathematical model was employed in the pre- sent study and theoretical calculation revealed that non-CSCs could initiate the occurrence of tumor if their proliferation potential was adequate. Further, experimental studies demonstrated that 17.7%, 38.6% and 5.2% of tumor cells in murine B16 solid melanoma, H22 hepatoma and Lewis lung carci2 noma, respectively, were potentially tumorigenic. Thus, based on the aforementioned findings, we propose that the scarce CSCs, if exist, are not the sole source of a tumor.
