Open AccessRetracted: Hispidulin suppresses cell growth and metastasis by targeting PIM 1 through JAK 2/ STAT 3 signaling in colorectal cancer
Author(s) -
Liu Kaili,
Gao Hui,
Wang Qiaoyun,
Wang Longyuan,
Zhang Bin,
Han Zhiwu,
Chen Xuehong,
Han Mei,
Gao Mingquan
Publication year - 2018
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13575
Subject(s) - cancer research , colorectal cancer , metastasis , oncogene , cell growth , gene knockdown , downregulation and upregulation , cancer , apoptosis , chemistry , pharmacology , medicine , cell cycle , biochemistry , gene
Colorectal cancer ( CRC ) accounts for over 600 000 deaths annually worldwide. The current study aims to evaluate the value of proto‐oncogene PIM 1 as a therapeutic target in CRC and investigate the anticancer activity of hispidulin, a naturally occurring phenolic flavonoid compound, against CRC . Immunohistochemistry analysis showed that PIM 1 was upregulated in CRC tissue. The role of PIM 1 as an oncogene was evidenced by the fact that PIM 1 knockdown inhibits cell growth, induces apoptosis, and suppresses invasion. Our results showed that hispidulin exerts antitumor activity in CRC through inhibiting the expression of PIM 1 . Moreover, our findings revealed that hispidulin downregulated the expression of PIM 1 by inhibiting JAK 2/ STAT 3 signaling by generating reactive oxygen species. Furthermore, our in vivo studies showed that hispidulin can significantly inhibit tumor growth and metastasis in CRC . Collectively, our results provide an experimental basis for trialing hispidulin in CRC treatment. PIM 1 can be considered a potential therapeutic target in CRC .