Shikonin promotes autophagy in BXPC-3 human pancreatic cancer cells through the PI3K/Akt signaling pathway | Zendy

Shuqing Shi | Zendy; Cao Hai-mei | Zendy

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Shikonin promotes autophagy in BXPC-3 human pancreatic cancer cells through the PI3K/Akt signaling pathway

Author(s) -

Shuqing Shi,

Cao Hai-mei

Publication year - 2014

Publication title -

oncology letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.766

H-Index - 54

eISSN - 1792-1082

pISSN - 1792-1074

DOI - 10.3892/ol.2014.2293

Subject(s) - pi3k/akt/mtor pathway , protein kinase b , autophagy , oncogene , cell cycle , viability assay , pancreatic cancer , cancer research , chemistry , signal transduction , microbiology and biotechnology , cell , biology , apoptosis , cancer , biochemistry , genetics

The present study aimed to investigate the effect of shikonin on autophagy in BXPC-3 human pancreatic cancer cells and its underlying mechanism. Cell viability was assessed using the Cell Counting Kit-8 assay and the expression of light chain (LC) 3, p62, phosphoinositide 3-kinase (PI3K), Akt, phosphorylated (p)-PI3K and p-Akt was analyzed using western blot analysis. Following treatment with 1 μmol/l shikonin for 48 h and 2.5 and 5 μmol/l shikonin for 24 and 48 h, the viability of the BXPC-3 cells was found to be significantly reduced and the protein expression of LC3-II/LC3-I was observed to be increased, while the protein expression of p62, PI3K, Akt, p-PI3K and p-Akt was decreased. These findings suggest that shikonin promotes autophagy in BXPC-3 cells and that the underlying mechanism may be associated with the PI3K/Akt signaling pathway.

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