C-terminal binding protein-2 (CtBP2) enhances cancer proliferation and metastasis

C-terminal binding protein-2 (CtBP2) enhances cancer proliferation and metastasis. and 0.047, respectively). The overall survival rate was lower in patients with increased CtBP2 expression and lower p16INK4A expression. Knockdown of CtBP2 resulted in the activation of p16INK4A and downCregulation of cell cycle regulators cyclin D, cyclin E and cyclin-dependent kinase 2 and 4. This down-regulation also led to a decreased transition of the G1-S phase in breast cancer cells. Moreover, gain-of-function experiments showed that CtBP2 suppressed p16INK4A and matrix metalloproteinase-2, subsequently enhancing the migration in breast cancer. However, the silence of CtBP2 abrogated this effect. Collectively, these findings provide insight into the role CtBP2 plays in promoting proliferation and migration in breast cancer by the inhibition of p16INK4A. 0.05 is considered significant. The expression of CtBP2 was positively related to Ki-67 in breast cancer specimens (Physique ?(Figure2).2). In addition, the proportion of p16INK4A-positive tumor cells was negatively correlated with the proportion of CtBP2-positive and N-Dodecyl-β-D-maltoside Ki-67-positive tumor cells (Physique ?(Figure22). Open in a separate window Physique 2 Graphic representation of relationship between CtBP2, p16INK4A and Ki-67 expression in breast cancer(A) The relationship between CtBP2 and p16INK4A. (B) The relationship between CtBP2 and Ki-67. C The relationship between p16INK4A and Ki-67. Correlation between CtBP2, p16INK4A expression and clinicopathological variables in breast cancer As shown in Table ?Table1,1, the level of CtBP2 was positively correlated with the histologic grade ( 0.001), metastasis (= 0.046) and tumor size (= 0.011). However, CtBP2 expression was not associated with this, histology, estrogen receptors (ER), progesterone N-Dodecyl-β-D-maltoside receptors (PR) or HER2 position in sufferers with breasts cancer. On the other hand, the amount of p16INK4A appearance was inversely correlated with histologic quality (= N-Dodecyl-β-D-maltoside 0.004), metastasis (= 0.047) and tumor size (= 0.043), no significant relationship was found between p16INK4A appearance as well as other factors. The appearance of CtBP2 and p16INK4A with regards to prognosis in sufferers with breasts cancer By the end of scientific follow-up, success information was N-Dodecyl-β-D-maltoside designed for a complete of 80 sufferers. The success rate of sufferers with a higher degree of CtBP2 was considerably less than that of sufferers with a minimal degree of CtBP2 (31.2%, (18/57) and 78.3% (18/23), respectively), seeing that shown in Desk ?Desk2.2. Univariable analysis was performed to study the expression of CtBP2 and p16INK4A in relation to survival status (Table ?(Table2).2). KaplanCMeier analysis showed that increased expression of CtBP2 was significantly associated with shorter overall survival (= 0.042, Physique ?Physique3A),3A), whereas a high level of p16INK4A was associated with longer overall survival ( 0.001, Figure ?Physique3B).3B). Patients with a high expression of CtBP2 and low expression of p16INK4A had a poorer overall survival rate when compared to the other patients ( 0.001, Figure ?Physique3C).3C). The Cox’s proportional hazards regression model exhibited that expression level of CtBP2 and p16INK4A, histological grade, tumor size and metastases were independently predictive factors for an adverse prognosis in patients with breast cancer (Table ?(Table33). Table 2 Survival status and clinicopathological parameters in 80 breast carcinomas specimens 0.05 is considered significant. Open in a separate BII window Physique 3 The relationship between CtBP2, p16INK4A and patient survival(A) Based on mean CtBP2 percentages, patients were divided into high CtBP2 expressers ( 61.36%) and low CtBP2 expressers ( 61.36%). Patients in the high-expression CtBP2 group had significantly shorter overall survival. (B) Patients were also divided into two groups according to p16INK4A expression both high expressers ( 37.14%) and low expressers ( 37.14%). Patients in the low-expression p16INK4A group had significantly shorter overall survival. (C) Patients with CtBP2 (+)/p16INK4A (?) phenotype (CtBP2 61.36% and p16INK4A 37.14%) had the worst cumulative survival. Table 3 Contribution of various potential prognostic.