Journal
ONCOTARGET
Volume 7, Issue 6, Pages 7066-7079Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.6883
Keywords
TG2; gastric cancer; ERK1/2; tumor progression
Categories
Funding
- National Natural Science Foundation of China [81272749, 81572798, 91229106, 91529302]
- Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support [20152505]
- Doctoral Innovation Fund Projects from Shanghai Jiao Tong University School of Medicine [BXJ201318]
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Gastric cancer (GC) is one of the most common tumors worldwide and involves extensive local tumor invasion, metastasis, and poor prognosis. Understanding mechanisms regulating progression of GC is necessary for developing effective therapeutic strategies. Tissue transglutaminase-2 (TG2), a multifunctional member of the transglutaminase family, has been shown to be critical for tumor initiation and progression. However, how TG2 promotes the progression of GC is unknown. We report that TG2 was highly expressed in GC tissues and positively associated with depth of tumor invasion and late TNM stage. With gain-and loss-of-function approaches, we observed that TG2 promoted GC cell proliferation, migration, invasion, as well as tumorigenesis and peritoneal metastasis in vivo. These events were associated with the ERK1/2 pathway activation and an ERK1/2 inhibitor (U0126) inhibited cell proliferation, migration, and invasion induced by overexpression of TG2. In summary, TG2 contributes to tumorigenesis and progression of GC by activating the ERK1/2 signaling pathway and is a potential therapeutic target of metastatic gastric cancer.
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