3.9 Article

Policosanol suppresses tumor progression in a gastric cancer xenograft model

Journal

TOXICOLOGICAL RESEARCH
Volume 38, Issue 4, Pages 567-575

Publisher

KOREAN SOC TOXICOLOGY
DOI: 10.1007/s43188-022-00139-z

Keywords

Gastric cancer; Policosanol; Xenograft mouse model; Healthy functional food; Extracellular matrix

Categories

Funding

  1. Ministry of Education [2021R1A6A3A01086368]
  2. NRF by Korea [2021R1A2C200453511]
  3. Priority Research Centers Program through the NRF [2016R1A6A1A03007648]

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The study aimed to investigate the anticancer effect of policosanol (PC) on gastric cancer (GC). The results showed that PC significantly inhibited GC cell viability and delayed tumor growth without toxicity. Protein expression analysis revealed that PC decreased the expression levels of Ki-67 and cdc2, while also regulating the expression of extracellular matrix proteins. These findings have important implications for the development of therapeutic strategies for GC.
Gastric cancer (GC) is the most common cancer worldwide and the third leading cause of cancer death, with the fifth highest incidence. The development of effective chemotherapeutic agents is needed to decrease GC mortality. Policosanol (PC) extracted from Cuban sugar cane wax is a healthy functional food ingredient that helps improve blood cholesterol levels and blood pressure. Its various physiological activities, such as antioxidant, anti-inflammatory, and anticancer activities, have been reported recently. Nevertheless, the therapeutic efficacy of PC in gastric xenograft models is unclear. We aimed to investigate the anticancer effect of PC on human GC SNU-16 cells and a xenograft mouse model. PC significantly inhibited GC cell viability and delayed tumor growth without toxicity in the SNU-16-derived xenograft model. Therefore, we investigated protein expression levels in tumor tissues; the expression levels of Ki-67, a proliferation marker, and cdc2 were decreased. In addition, we performed proteomic analysis and found thirteen differentially expressed proteins. Our results suggested that PC inhibited GC progression via cdc2 suppression and extracellular matrix protein regulation. Notably, our findings might contribute to the development of novel and effective therapeutic strategies for GC.

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