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GLO 1 and PKCλ Regulate ALDH1-positive Breast Cancer Stem Cell Survival
- Source :
- Anticancer Research. 41:5959-5971
- Publication Year :
- 2021
- Publisher :
- Anticancer Research USA Inc., 2021.
-
Abstract
- BACKGROUND/AIM We examined the inhibitory effects of both glyoxalase 1 (GLO 1) and protein kinase C (PKC)λ in aldehyde dehydrogenase 1 (ALDH1)-positive breast cancer stem cells (CSCs). MATERIALS AND METHODS Breast cancer genomics datasets (TCGA, n=593; METABRIC, n=1904) were downloaded and statistically analyzed. The effects of GLO 1 and PKCλ on trypan blue staining and tumor-sphere formation by ALDH1high cells derived from triple negative breast cancer (TNBC) and basal-like breast cancer were examined. RESULTS GLO 1high, PKCλhigh, and ALDH1A3high tumors were enriched in stage I/II/III/IV samples, associated with the HER2 and TNBC subtypes according to receptor status, and associated with the HER2-enriched and basal-like subtypes according to PAM50. Inhibition of either GLO 1 (TLSC702) or PKCλ (ANF) suppressed tumor-sphere formation and enhanced death in ALDH1high cells. TLSC702 also effectively inhibited tumor-sphere formation and induced death in PKCλ knockout ALDH1high cells. CONCLUSION GLO 1 and PKCλ are important for the survival of ALDH1-positive breast CSCs, and may represent potential therapeutic targets for the treatment of ALDH1-positive breast CSCs.
- Subjects :
- Cancer Research
Receptor Status
Cell Survival
Aldehyde dehydrogenase
Breast Neoplasms
Biology
Aldehyde Dehydrogenase 1 Family
Breast cancer
Cancer stem cell
Cell Line, Tumor
Biomarkers, Tumor
medicine
Humans
skin and connective tissue diseases
Protein Kinase C
Protein kinase C
Triple-negative breast cancer
Neoplasm Staging
Gene Expression Profiling
Breast cancer stem cell
Lactoylglutathione Lyase
General Medicine
Flow Cytometry
medicine.disease
Isoenzymes
Oncology
Neoplastic Stem Cells
Cancer research
biology.protein
Female
Stem cell
Transcriptome
Subjects
Details
- ISSN :
- 17917530 and 02507005
- Volume :
- 41
- Database :
- OpenAIRE
- Journal :
- Anticancer Research
- Accession number :
- edsair.doi.dedup.....3880f2383483738d1449ff26592967bc