4-Propargyl-substituted 1H-pyrroles induce apoptosis and autophagy via extracellular signal-regulated signaling pathway in breast cancer

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dc.contributor.authorAtmaca H.
dc.contributor.authorIlhan S.
dc.contributor.authorYilmaz E.S.
dc.contributor.authorZora M.
dc.date.accessioned2024-07-22T08:05:36Z
dc.date.available2024-07-22T08:05:36Z
dc.date.issued2021
dc.description.abstractNovel pyrrole derivatives (PDs) with propargyl units (1–7) were investigated for their anticancer activity on breast cancer cells. The MTT assay was used to assess the cell viability. Morphological changes in human breast cancer cells were visualized under a phase-contrast microscope. Apoptosis and autophagy were detected using the DNA fragmentation assay and staining by autophagic vacuoles, respectively. The levels of apoptosis- and autophagy-related proteins such as cytochrome c, Bcl-2, LC3-I/II were investigated by Western blot analysis. The effect of PDs on the ERK1/2 signaling pathway was investigated using specific inhibitors. All the tested PDs were found to be active in the range of 36.7 ± 0.2 to 459.7 ± 4.2 µM. Compounds 3 and 4 showed cytotoxic activity in breast cancer cells, but were found to be safer with lower cytotoxicity on human nontumorigenic epithelial breast cells. Compound 4 induced apoptosis, whereas compound 3 induced autophagy. Both compounds inhibited the ERK signaling pathway in breast cancer cells. The present study revealed that both synthesized PDs induced different programmed cell death types by inhibiting the ERK signaling pathway in two genotypically different breast cancer cells. Therefore, novel PDs might be promising anticancer agents for breast cancer therapy and further structural modifications of PDs may yield promising anticancer agents. © 2021 Deutsche Pharmazeutische Gesellschaft
dc.identifier.DOI-ID10.1002/ardp.202100170
dc.identifier.issn03656233
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/13172
dc.language.isoEnglish
dc.publisherJohn Wiley and Sons Inc
dc.subjectAntineoplastic Agents
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectBreast Neoplasms
dc.subjectCell Line
dc.subjectCell Line, Tumor
dc.subjectCell Survival
dc.subjectEpithelial Cells
dc.subjectFemale
dc.subjectHumans
dc.subjectMAP Kinase Signaling System
dc.subjectPyrroles
dc.subjectSignal Transduction
dc.subjectStructure-Activity Relationship
dc.subjectantineoplastic agent
dc.subjectcaspase 9
dc.subjectcytochrome c
dc.subjectDNA
dc.subjectfluorouracil
dc.subjectlight chain 3 i
dc.subjectlight chain 3 ii
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjectprotein bcl 2
dc.subjectpyrrole derivative
dc.subjectunclassified drug
dc.subjectantineoplastic agent
dc.subjectpyrrole derivative
dc.subjectantineoplastic activity
dc.subjectapoptosis
dc.subjectArticle
dc.subjectautophagic cell death
dc.subjectautophagy (cellular)
dc.subjectbreast cancer
dc.subjectcell structure
dc.subjectcell survival
dc.subjectcell vacuole
dc.subjectcell viability
dc.subjectcontrolled study
dc.subjectcytotoxicity
dc.subjectDNA fragmentation
dc.subjectDNA fragmentation assay
dc.subjectdrug design
dc.subjectdrug synthesis
dc.subjectextracellular signaling
dc.subjecthuman
dc.subjecthuman cell
dc.subjectIC50
dc.subjectMCF-10A cell line
dc.subjectMCF-7 cell line
dc.subjectMDA-MB-231 cell line
dc.subjectMTT assay
dc.subjectphase contrast microscopy
dc.subjectWestern blotting
dc.subjectapoptosis
dc.subjectautophagy
dc.subjectbreast tumor
dc.subjectcell line
dc.subjectchemistry
dc.subjectdrug effect
dc.subjectepithelium cell
dc.subjectfemale
dc.subjectMAPK signaling
dc.subjectpathology
dc.subjectsignal transduction
dc.subjectstructure activity relation
dc.subjectsynthesis
dc.subjecttumor cell line
dc.title4-Propargyl-substituted 1H-pyrroles induce apoptosis and autophagy via extracellular signal-regulated signaling pathway in breast cancer
dc.typeArticle

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