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AIM2 regulates viability and apoptosis in human colorectal cancer cells via the PI3K/Akt pathway

Authors Chen JJ, Wang ZJ, Yu SS

Received 18 October 2016

Accepted for publication 16 January 2017

Published 13 February 2017 Volume 2017:10 Pages 811—817


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ashok Kumar Pandurangan

Peer reviewer comments 4

Editor who approved publication: Dr Samir Farghaly

Jianjun Chen, Zhenjun Wang, Sanshui Yu

Department of General Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing, People’s Republic of China

Abstract: Absent in melanoma 2 (AIM2) plays an important role in innate immunity as a DNA sensor in the cytoplasm by triggering the assembly of an AIM2 inflammasome that results in caspase-1-mediated inflammatory responses and cell death. In recent years, studies have indicated that AIM2 can suppress cancer cell proliferation, and mutations in the gene encoding AIM2 are frequently identified in patients with colorectal cancer (CRC). However, the mechanism by which AIM2 restricts tumor growth remains unclear. We reconstructed AIM2 expression in HCT116 CRC cells by lentivirus transfection. Using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, we demonstrated that expression of AIM2 inhibited the viability and increased the apoptosis rate of CRC cells, and cell cycle analysis suggested that AIM2 blocked cell cycle transition from G1 to S phase. Western blot analysis showed that AIM2 promoted apoptosis in CRC cells by suppressing the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway. Our data suggest that AIM2 plays a critical role as a tumor suppressor and might serve as a potential therapeutic target in CRC.

Keywords: AIM2, colorectal cancer, PI3K/Akt pathway, apoptosis

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