|Table of Contents|

ANewKindofImidazolesInducesTumorCellAutophagyviaAMPK/mTORPathway(PDF)

《南京师大学报（自然科学版）》[ISSN:1001-4616/CN:32-1239/N]

Issue:
2020年01期
Page:
115-121
Research Field:
·生物学·
Publishing date:

Info

Title:
ANewKindofImidazolesInducesTumorCellAutophagyviaAMPK/mTORPathway
Author(s):
MaMengjiao; JinDong; ZhangGuangqin; YuXiaolu; WenChuanjun
SchoolofLifeSciences,NanjingNormalUniversity,InstituteofMolecularandCellBiology,Nanjing210023,China
Keywords:
NO.143; autophagy; tumor; LC3B; AMPK/mTOR
PACS:
Q291
DOI:
10.3969/j.issn.1001-4616.2020.01.017
Abstract:
Autophagyiscloselyrelatedtothetumoroccurrence.Bypreventingtheaccumulationoftoxicitiesindamagedproteinsandorganelles,autophagylimitsoxidativestress,chronictissuedamageandoncogenicsignaling,inhibitingthedevelopmentofcancer.Thisindicatestheroleofautophagyactivationincancerpreventionandtreatment.ItwasfoundanewimidazolenamedNO.143.PANC-1wasusedasamodeltodetecttheeffectofdifferentconcentrationsofNO.143oncellviabilitybyMTS.Theautophagyfluorescencespotswereobservedbyconfocalmicroscopy.Westernblotwasusedtodetecttheexpressionofautophagy-relatedproteinsLC3B,ATG13,p62andtheexpressionofAMPK/mTORsignalingpathway-relatedproteins.TheresultsshowedthatNO.143showedaconcentration-dependentinhibitionoftumorcellproliferation.NO.143cansignificantlyincreaseautophagicfluorescentspotsincells,increaseLC3Bexpression,ATG13contentandp62degradation.TheseresultsshowthatNO.143cansignificantlyup-regulateautophagyintumorcells.FurtherstudiesshowedthatNO.143wasabletoincreasethephosphorylationlevelofAMPKαandreducethephosphorylationlevelsofmammalianrapamycintargetprotein(mTOR)andS6.Conversely,thisphenomenonreversesafterinhibitingAMPKαactivity.TheseresultsmayindicatethatNO.143inducestumorautophagythroughtheAMPK/mTORsignalingpathwayandinhibitstumorcellproliferation.

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Last Update: 2020-03-15