Ibrahim, Sherif; Gadalla, Ramy; El-Ghonaimy, Eslam A.; Samir, Omnia; Mohamed, Hossam Taha; Hassan, Hebatallah; Eshmawy, Hebatallah; Greve, Burkhard; El-Shinawi, Mohamed; Mohamed, Mona Mostafa; Götte, Martin: Syndecan-1 is a novel molecular marker for triple negative inflammatory breast cancer and modulates the cancer stem cell phenotype via the IL-6/STAT3, [...]
Inhalt
- Conclusions
- Background
- Methods
- Antibodies and reagents
- Cell culture
- Patient’s samples
- Immunohistochemical staining of CD44 and Syndecan-1
- siRNA-mediated knockdown of Syndecan-1 expression
- Flow cytometry
- Quantitative real-time PCR
- Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting
- Three dimensional (3D) spheroids and colony formation assays
- Secretome profiling of conditioned media of SUM-149 cells grown in 3D spheroids
- Statistical analysis
- Results
- Clinical and pathological characteristics of patients
- Higher expression with a positive correlation of Syndecan-1 with CD44 in carcinoma tissues of triple-negative IBC vs non-IBC patients
- Syndecan-1 silencing significantly reduces the CD44(+)CD24(-/low) pool and ALDH1 activity in SUM-149 and SKBR3 cells
- Syndecan-1 knockdown perturbs the formation of colonies and spheroids growing in 3D
- Syndecan-1 silencing downregulates a myriad of cancer stem cell-related genes in SUM-149 and SKBR3 cells
- Syndecan-1 siRNA knockdown reduces the secretome profile of SUM-149 cells
- Syndecan-1 silencing downregulates gp130 and attenuates the constitutive activity of STAT3 and NFκB in SUM-149 and SKBR3 cells
- Notch-1 and -3 are positively correlated with Syndecan-1 mRNA expression in tissues of triple negative IBC vs non-IBC
- Syndecan-1 orchestrates colony formation and expression of inflammatory cytokines via Notch signaling in SUM-149 cells
- Syndecan-1 regulates EGFR expression via Notch signaling and promotes EGF-induced colony formation in IBC
- Discussion
- Conclusions
- Additional files
- Abbreviations
- Acknowledgements
- Funding
- Availability of data and materials
- Authors’ contributions
- Competing interests
- Consent for publication
- Ethics approval and consent to participate
- Author details
- References