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Sclerotium rolfsii lectin induces stronger inhibition of proliferation in human breast cancer cells than normal human mammary epithelial cells by induction of cell apoptosis. | LitMetric

AI Article Synopsis

  • Sclerotium rolfsii lectin (SRL) specifically binds to certain cancer-associated sugar molecules (O-linked, TF glycans) found in breast cancer cells.
  • The study found that SRL significantly reduces the growth of breast cancer cells (MCF-7 and ZR-75) by causing cell death (apoptosis), while having minimal effect on normal breast cells (MCF-10A and HMECs).
  • SRL shows potential as an anti-cancer agent due to its ability to selectively target cancer cells while sparing normal cells.

Article Abstract

Sclerotium rolfsii lectin (SRL) isolated from the phytopathogenic fungus Sclerotium rolfsii has exquisite binding specificity towards O-linked, Thomsen-Freidenreich (Galβ1-3GalNAcα1-Ser/Thr, TF) associated glycans. This study investigated the influence of SRL on proliferation of human breast cancer cells (MCF-7 and ZR-75), non-tumorigenic breast epithelial cells (MCF-10A) and normal mammary epithelial cells (HMECs). SRL caused marked, dose-dependent, inhibition of proliferation of MCF-7 and ZR-75 cells but only weak inhibition of proliferation of non-tumorigenic MCF-10A and HMEC cells. The inhibitory effect of SRL on cancer cell proliferation was shown to be a consequence of SRL cell surface binding and subsequent induction of cellular apoptosis, an effect that was largely prevented by the presence of inhibitors against caspases -3, -8, or -9. Lectin histochemistry using biotin-labelled SRL showed little binding of SRL to normal human breast tissue but intense binding to cancerous tissues. In conclusion, SRL inhibits the growth of human breast cancer cells via induction of cell apoptosis but has substantially less effect on normal epithelial cells. As a lectin that binds specifically to a cancer-associated glycan, has potential to be developed as an anti-cancer agent.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4217719PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0110107PLOS

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