Abstract
Here, we found that down-regulated expression of BTG3 might be positively correlated with colorectal carcinogenesis and its overexpression suppressed proliferation, glycolysis, mitochondrial respiration, cell cycle progression, migration, and invasion, and induced apoptosis, senescence and differentiation in SW480 and SW620 cells. After treated with cisplatin, MG132, paclitaxel and SAHA, BTG3 transfectants exhibited lower viability and higher apoptosis than the control in both time- and dose-dependent manners. BTG3 overexpression up- regulated the protein expression of Cyclin E, p16, p27, NF-κB, p38α/β, XIAP, Bcl-2, ATG14 and p53, but down-regulated the mRNA expression of MRP1, BCRP, and mTOR in SW480 and SW620 cells. BTG3 overexpression inhibited tumor growth of SW620 cells by suppressing proliferation and inducing apoptosis. It was suggested that down-regulated BTG3 expression might be considered as a marker for colorectal carcinogenesis. BTG3 overexpression might reverse the aggressive phenotypes and be employed as a potential target for gene therapy of colorectal cancer.
Highlights
Colorectal cancer (CRC) is one of the most common cancers in the world and accounts for nearly one-tenth of new cases of all cancers
BTG3 overexpression inhibited www.impactjournals.com/oncotarget www.impactjournals.com/oncotarget the migration and invasion of CRC cells according to wound healing (Figure 2E, p
In line with the results of oncomine analysis, we found that BTG3 expression was decreased in CRC, compared with adjacent NNM by Western blot and realtime RT-PCR, even followed by laser capture microdissection (LCM)
Summary
Colorectal cancer (CRC) is one of the most common cancers in the world and accounts for nearly one-tenth of new cases of all cancers. BTG3 interacts with Smad receptor- regulated Smad transcription factor [6], and with src to suppress Ras/MAP kinase signaling [7]. BTG3 can be phosphorylated and activated via the interaction with checkpoint kinase 1 (CHK1). The down-regulated BTG3 expression was attributable to its promoter methylation in breast, lung, prostate or renal, hepatocellular, and gastric cancer tissues or cells [10,11,12,13,14,15]. The down- regulated BTG3 expression was found during ovarian carcinogenesis, and positively correlated with the dedifferentiation, FIGO staging, and adverse prognosis of cancers [16]. Our group demonstrated that BTG3 overexpression inhibited proliferation, migration, invasion and tumor growth, induced S/G2 arrest, differentiation, autophagy, apoptosis and chemosensitivity of gastric cancer cells [18]
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