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Updated: Oct 14, 2025

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells
Published on: January 18, 2017
Upregulation of CD271 transcriptome in breast cancer promotes cell survival via NFκB pathway
Nabiha Bashir1, Mehreen Ishfaq1, Kehkashan Mazhar2
1Department of Biosciences, COMSATS University Islamabad (CUI), Islamabad, Pakistan.
Background:
Biological treatment of many cancers currently targets membrane bound receptors located on a cell surface. We are in a great to need identify novel membrane proteins associated with migration and metastasis of breast cancer cells. CD271, a single transmembrane protein belongs to tumor necrosis factor receptor family acts and play its role in proliferation of cancer cell. The purpose of this study is to investigate the role of CD271 in breast cancer.
Methods And Results:
In this study we analyzed the mRNA expression of CD271 in breast tumor tissue, breast cancer cell line MCF7 and isolated cancer stem cells (MCF7-CSCs) by RT-qPCR. We also measured the protein levels through western blotting in MCF-7 cell line. CD271 was upregulated in breast cancer patients among all age groups. Within the promoter region of CD271, there is a binding site for NF-κB1 which overlaps a putative quadraplex forming sequence. While CD271 also activates NF-κB pathway, down regulation of CD271 through quadraplex targeting resulted in inhibition of NF-κB and its downstream targets Nanog and Sox2.
Conclusion:
In conclusion, our data shows that CD271 and NF-κB are regulated in interdependent manner. Upon CD271 inhibition, the NF-κB expression also reduces which in turn affects the cell proliferation and migration. These results suggest that CD271 is playing a crucial rule in cancer progression by regulating NF-κB and is a good candidate for the therapeutic targeting.
Insights
This study reveals CD271 protein is upregulated in breast cancer, driving cancer progression. Inhibiting CD271 reduces NF-κB pathway activity, impacting cell proliferation and migration, suggesting CD271 as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Targeting cell surface receptors is key in cancer treatment.
- Novel membrane proteins are needed to understand breast cancer metastasis.
- CD271, a TNF receptor family member, influences cancer cell proliferation.
Purpose of the Study:
- Investigate the role of CD271 in breast cancer progression.
- Determine the relationship between CD271 and cancer cell migration/metastasis.
Main Methods:
- Analyzed CD271 mRNA expression using RT-qPCR in tumor tissue, MCF7 cells, and MCF7-CSCs.
- Measured CD271 protein levels via Western blotting in MCF-7 cells.
- Examined CD271 promoter region for NF-κB1 binding sites and quadruplex sequences.
Main Results:
- CD271 mRNA and protein were upregulated in breast cancer samples and cell lines.
- CD271 expression correlated with NF-κB pathway activation.
- Targeting CD271's quadruplex sequence inhibited NF-κB, Nanog, and Sox2 expression.
Conclusions:
- CD271 and NF-κB signaling are interdependent in breast cancer.
- CD271 inhibition reduces NF-κB, affecting cell proliferation and migration.
- CD271 represents a promising therapeutic target for breast cancer treatment.
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