Abstract
Lactoferrin (Lf) is an iron-binding glycoprotein protein known to have immune-modulatory role and recently, its anticancerous effect against different cancer cell types was emphasized. In the present investigation, a comparative evaluation of anticancer potential of colostrum-derived lactoferrin from Indian native zebu cow (Sahiwal, SAC), crossbred (Karan Fries, KFC) and commercially available (C-Lf) lactoferrin from exotic cow using cellular models was made. A protocol was standardized successfully to purify Lf protein from colostrum of both breeds using HPLC and purity was confirmed by LC–MS. A standardized dose of 750 µg/mL Lf was used to treat two cell types MDA-MB-231 and MCF-7 with Lf from three different sources; SAC-Lf, KFC-Lf and C-Lf for 48 h and 72 h. Different cellular parameters including cytotoxicity, viability, apoptosis and cell proliferation were determined. Comparatively, Lf from commercial source (C-Lf) had maximum effect in both cell types followed by SAC-Lf and KFC-Lf. Further, transcriptional changes in genes associated with apoptosis (Bax and Bcl-2), tumor progression (p53, p21, CD44 and NF-κβ) and survival (survivin) were evaluated in Lf treatment. The overall results strongly emphasized to the fact that Lf purified from cow colostrum has the capacity to inhibit the in vitro growth of cancerous cell lines albeit to a varied extent.
Highlights
Cow milk is considered as balanced and nutritive food that becomes an integral part of healthy diet
The lactoferrin purified from cow colostrum showed high purity in LC/mass spectrometer (MS) analysis
The concentration of Lf purified from colostrum of Sahiwal (SAC) and Karan Fries (KFC) was 6.0 and 1.0 mg/mL, respectively
Summary
Cow milk is considered as balanced and nutritive food that becomes an integral part of healthy diet. Cow breeds with difference in genetic makeup have a striking effect on milk composition as well as on the nutritional value of the obtained dairy foods [1,2]. Intestinal apical cell membranes are a major site for dietery iron absorption, where it reduced to Fe2+ and subsequently transported to enteroctyes eventually exported into the bloodstream via solute carriers. This efflux of Fe2+ from enterocytes is regulated by liver hormone-hepicidin, which is known to induce by proinflammatory cytokines and subsequently reduced the iron uptake through systemic iron homoeostasis [22,23]. The precise mechanism has not been thoroughly elucidated to date
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