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Skullcapflavone I has a potent anti‐pancreatic cancer activity by targeting miR‐23a
Author(s) -
Cui Jing,
Li Hao,
Wang Ying,
Tian Tian,
Liu Chao,
Wang Yanan,
Sun Shukai,
Feng Baisui
Publication year - 2020
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1621
Subject(s) - apoptosis , pancreatic cancer , cell growth , cancer research , mapk/erk pathway , transfection , cancer cell , bromodeoxyuridine , western blot , downregulation and upregulation , cell cycle , chemistry , biology , signal transduction , cancer , microbiology and biotechnology , cell culture , biochemistry , gene , genetics
Baicalein has been widely studied and showed a potent activity against pancreatic cancer in both in vivo and in vitro studies. Little is known regarding the effects of Skullcapflavone I (SFI), despite they have similar structures. So, this study was to explore the function of SFI on human pancreatic cancer. Panc‐1 cells were transfected with miR‐23a precursor, miR‐23a inhibitor or the negative controls, and subsequently treated by SFI. Cell viability, Bromodeoxyuridine (BrdU)‐positive cell rate, apoptosis, migration, invasion, and related protein expression were assessed by utilizing Cell Counting Kit‐8 (CCK‐8), BrdU staining, apoptosis assessment, transwell assay, and western blot. SFI significantly reduced the proliferation, migration, and invasion, as well as induced apoptosis of Panc‐1 cells. MiR‐23a, miR‐21, and miR‐155 were lowly expressed while miR‐145 and miR‐146a were highly expressed in SFI‐treated cell. Of note, the antitumor effects of SFI were promoted by miR‐23a suppression whereas attenuated by miR‐23a overexpression. JAK/STAT and MAPK pathways were inhibited by SFI. Also, the pathway inhibition in SFI‐treated cells was reversed by miR‐23a overexpression. SFI might be a promising anti‐pancreatic cancer agent by inhibiting cancer cells growth and motility. The anticancer activities of SFI might be through downregulation of miR‐23a, as well as inhibition of JAK/STAT and MAPK pathways.