Abstract
Here, BTG1 overexpression inhibited proliferation, induced differentiation, autophagy, and apoptosis in colorectal cancer cells (p2 arrest might be related to Cyclin B1 and Cdc25B hypoexpression in HCT-15 transfectants, while G1 arrest in HCT-116 transfectants overexpressing p21 and p27. BTG1 overexpression decreased the expression of Bcl-2, Bcl-xL, XIAP, Akt1 or survivin and increased the expression of Bax or p53 in colorectal cancer cells. BTG1-induced autophagy was dependent on Beclin-1 expression. BTG1 overexpression might weaken β-catenin pathway in colorectal cancer cells. The chemosensitivity of BTG1 transfectants to paclitaxel, cisplatin, MG132 or SAHA was positively correlated with its apoptotic induction. There was a lower expression level of BTG1 in cancer than matched non-neoplastic mucosa by RT-PCR (p
Highlights
Colorectal cancer is the third most common cancer in both men and women, accounting for nearly 10% of new cases in all cancers
At the protein level (Figure 1F), BTG1 overexpression decreased the expression of Cyclin B1, Cyclin D1, Cdc2, Cyclin E, Cdk4 and Cdc25B in HCT-15 cells (p
BTG1 overexpression down-regulated the expression of Cdc2 and Cdc25B (p
Summary
Colorectal cancer is the third most common cancer in both men and women, accounting for nearly 10% of new cases in all cancers. Incidence rates have been decreasing for most of the past two decades, which has been attributed to the alteration in risk factors and the selection of colorectal cancer among adults 50 years and older [1, 2]. The N-terminal domain of BTG1 bears an LxxLL motif favoring nuclear accumulation, and another region encompassing Box A inhibiting nuclear localization [7]. C-terminal region of BTG1 interacts with the nuclear receptor TRα and the myogenic factor MyoD [8]. BTG1 binds to protein arginine www.impactjournals.com/oncotarget methyltransferase 1 via Box C region [9]. Human carbon catabolite repressor protein-associative factor 1 can interact with BTG1, which depends on the phosphorylation of p34cdc2/Cyclin E and p34CDK2/Cyclin A kinase site on BTG1 ser-159 [10]
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