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Biochem Biophys Res Commun. 2014 Mar 28;446(1):105-12. doi: 10.1016/j.bbrc.2014.02.043. Epub 2014 Feb 28.

Antibiotic drug tigecycline inhibited cell proliferation and induced autophagy in gastric cancer cells.

Author information

1
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, PR China.
2
Division of Scientific Research and Training, General Hospital of PLA Chengdu Military Area Command, Chengdu, Sichuan 610083, PR China.
3
Institute of Urinary Surgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, PR China. Electronic address: zhouzhans@sina.com.
4
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, PR China. Electronic address: hcui@swu.edu.cn.

Abstract

Tigecycline acts as a glycylcycline class bacteriostatic agent, and actively resists a series of bacteria, specifically drug fast bacteria. However, accumulating evidence showed that tetracycline and their derivatives such as doxycycline and minocycline have anti-cancer properties, which are out of their broader antimicrobial activity. We found that tigecycline dramatically inhibited gastric cancer cell proliferation and provided an evidence that tigecycline induced autophagy but not apoptosis in human gastric cancer cells. Further experiments demonstrated that AMPK pathway was activated accompanied with the suppression of its downstream targets including mTOR and p70S6K, and ultimately induced cell autophagy and inhibited cell growth. So our data suggested that tigecycline might act as a candidate agent for pre-clinical evaluation in treatment of patients suffering from gastric cancer.

KEYWORDS:

Autophagy; Gastric cancer; Proliferation inhibition; Tigecycline

PMID:
24582751
DOI:
10.1016/j.bbrc.2014.02.043
[Indexed for MEDLINE]

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