Active fraction of Polyrhachis vicina Rogers (AFPR) suppressed breast cancer growth and progression via regulating EGR1/lncRNA-NKILA/NF-κB axis

Biomed Pharmacother. 2020 Mar:123:109616. doi: 10.1016/j.biopha.2019.109616. Epub 2019 Dec 25.

Abstract

Breast cancer (BC) is a major contributor of cancer-associated mortality in women. It is essential to find new therapeutic targets and drugs. Polyrhachis vicina Rogers is one of the Traditional Chinese Medicine (TCM). Our previous studies have shown an active fraction of Polyrhachis vicina Rogers (AFPR) has significant anti-inflammatory activity, suggesting its anti-cancer effect. Here, we aimed to explore the inhibitory effects of AFPR on BC and reveal its mechanism. The effects of AFPR on BC were examined by cell proliferation assay, wound healing assay, invasion assay and xenograft assay. Microarray sequencing, qRT-PCR, Western blot, chromatin immunoprecipitation assay and luciferase reporter assay were performed to investigate the regulation of AFPR on related genes and underlying mechanisms. As a result, AFPR suppressed BC cell growth, migration and invasion and inhibited tumor growth. LncRNA NKILA was most prominently upregulated in AFPR-treated MCF7 cells. AFPR inactivated NF-κB signaling pathway via regulating NKILA. Furthermore, AFPR regulated the expression of NKILA by inhibiting its transcript suppressor EGR1. This study firstly indicated that AFPR was a potential inhibitor of BC development via regulating EGR1/NKILA/NF-κB axis.

Keywords: Breast cancer; Cell growth; EGR1; NF-κB; NKILA; Polyrhachis vicina Rogers.

MeSH terms

  • Animals
  • Ants / chemistry*
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / metabolism
  • Cell Movement / drug effects
  • Chemical Fractionation
  • Early Growth Response Protein 1 / genetics
  • Early Growth Response Protein 1 / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • MCF-7 Cells
  • Male
  • Medicine, Chinese Traditional
  • Mice, Nude
  • NF-kappa B / genetics
  • NF-kappa B / metabolism*
  • Neoplasm Invasiveness
  • Neoplasms, Experimental
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • Up-Regulation

Substances

  • EGR1 protein, human
  • Early Growth Response Protein 1
  • NF-kappa B
  • RNA, Long Noncoding
  • long noncoding RNA NKILA, human