The effect of "NutramilTM Complex," food for special medical purpose, on breast and prostate carcinoma cells

PLoS One. 2018 Feb 14;13(2):e0192860. doi: 10.1371/journal.pone.0192860. eCollection 2018.

Abstract

NutramilTM Complex is a multicomponent food product that meets the requirements of a food for special medical purpose. As a complete, high-energy diet it consists of properly balanced nutrients, vitamins and minerals. The aim of this study was to assess the effect of NutramilTM Complex on breast and prostate carcinoma cells. Our results showed that NutramilTM Complex reduced the viability and proliferation of breast and prostate cancer cells and that this process was associated with the induction of apoptosis via activation of caspase signalling. Data showed elevated levels of p53 tumour suppressor, up-regulation of p38 MAPK and SAPK / JNK proteins and downregulation of anti-apoptotic ERK1/2, AKT1 and HSP27. Treatment with NutramilTM Complex also affected the expression of the BCL2 family genes. Results also showed down-regulation of anti-apoptotic BCL-2 and up-regulation of pro-apoptotic members such as BAX, BAD, BID. In addition, we also observed regulation of many other genes, including Iκβα, Chk1 and Chk2, associated with apoptotic events. Taken together, our results suggest activation of the mitochondrial apoptotic pathway as most likely mechanism of anti-carcinogenic activity of NutramilTM Complex.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anticarcinogenic Agents / pharmacology
  • Apoptosis / genetics
  • Breast Neoplasms / diet therapy*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Survival
  • Female
  • Food, Fortified / analysis
  • Foods, Specialized* / analysis
  • Gene Expression
  • Genes, cdc
  • Humans
  • MCF-7 Cells
  • Male
  • Prostatic Neoplasms / diet therapy*
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Signal Transduction
  • Stress, Physiological

Substances

  • Anticarcinogenic Agents
  • RNA, Messenger

Grants and funding

This work was supported by the Polish Ministry of Science and Higher Education DS 3710/KŻCz/2017. The funder provided support in the form of salaries for authors [AAK, TL, MD, EPS, DD], but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the 'author contributions' section.