4.7 Article

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

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 123, Issue -, Pages -

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2019.109616

Keywords

Polyrhachis vicina Rogers; NKILA; EGR1; NF-kappa B; Breast cancer; Cell growth

Funding

  1. National Natural Science Foundation of China [81703769, 81960729, 81560663, 81360653, 81702186]
  2. Guangxi Science and Technology Project [AD18216002, AD17195002, AA17202040, AD16380013]
  3. Natural Science Foundation of Guangxi Province [2018GXNSFDA281046, 2017GXNSFBA198061]
  4. New Centuary Guangxi Ten-hun-dred-thousand Talents Project
  5. Key Laboratory Project of Quality Standards of TCM in Guangxi [201608]
  6. Nanning Science and Technology Project [20193118, 20183109]

Ask authors/readers for more resources

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-kappa B 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-kappa B axis.

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