Med Sci (Paris)
Volume 34, October 2018Cancer biomarkers
|Page(s)||99 - 104|
|Published online||07 November 2018|
UNBS5162 inhibits colon cancer growth via suppression of PI3K/Akt signaling pathway
Gastrointestinal Surgery Department, the First Affiliated Hospital of Jinan University, 613 Huangpu Avenue West, Guangzhou, 510630 PR China
2 Department 1 of General Surgery, the 5th Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510700, PR China
* Corresponding author: Cun-Chuan Wang, MD email@example.com
Colon cancer is a common cause of cancer-related death worldwide. However, the underlying mechanism of tumor progression of colon cancer remains far from being elucidated. In the present study, we report the role of UNBS5162 in colon cancer. UNBS5162 is a naphthalimide that can intercalate into DNA and suppress the expression level of CXCL chemokines. Here, we investigated its effect on cell proliferation, mobility and apoptosis in HCT116 cells, and explored the underlying mechanism. A CCK8 assay revealed that UNBS5162 can block the proliferation of colon cancer cells. Base on a Transwell assay, we showed that cell migration and invasion ability of HCT116 cells are inhibited by UNBS5162. In addition, Annexin V-FITC/PI assay and Western blot analysis were performed to detect whether UNBS5162 could induce cell apoptosis. The results indicated that UNBS5162 increases the number of apoptotic cells remarkably. Furthermore, Western blot analysis demonstrated that UNBS5162 down-regulates the expression level of Bcl2, and up-regulates that of Bax as well as the level of activated Caspase-3. Moreover, we examined the impact of UNBS5162 on PI3K/Akt signaling pathway. UNBS5162 substantially inhibited the phosphorylation of Akt and its downstream effector mTOR, and reduced the expression of p-70. Taken together, these results suggest that UNBS5162 should be considered as a potent therapeutic anticancer agent that targets the PI3K/AKT signaling pathway.
Key words: apoptosis / invasion / migration / PI3K / proliferation / UNBS5162
© 2018 médecine/sciences – Inserm
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