Overexpression of Contactin 1 promotes growth, migration and invasion in Hs578T breast cancer cells.

BACKGROUND: Contactin1 (CNTN1) has been shown to play an important role in the invasion and metastasis of several tumors; however, the role of CNTN1 in breast cancer has not been fully studied. The purpose of this study is to investigate the role of CNTN1 in regulating tumor growth, migration and invasion in breast cancer. RESULTS: To investigate its function, CNTN1 was expressed in Hs578T cells. CNTN1 expression was confirmed by western blot, immunohistochemistry and real-time RT-PCR. The effect of CNTN1 overexpression on proliferation, migration and invasion of Hs578T breast cancer cells was assessed in vitro and in vivo. Our results showed that CNTN1 overexpression promoted Hs578T cell proliferation, cell cycle progression, colony formation, invasion and migration. Notably, overexpression of CNTN1 in Hs578T cells enhanced the growth of mouse xenograft tumors. CONCLUSIONS: CNTN1 promotes growth, metastasis and invasion of Hs578T breast cancer cell line. Thus, therapies targeting CNTN1 may prove efficacious for breast cancer. However, further investigation is required to understand the mechanism by which CNTN1 influences proliferation, metastasis and invasion in breast cancer.

[Upregulation of survivin in non-small cell lung cancer and its clinicopathological correlation with p53 and Bcl-2].

AIM: To retrospectively analyze the clinicopathological data of 87 non-small cell lung cancer (NSCLC) specimens and explore the clinicopathological correlation of survivin with p53 and Bcl-2 and the applicability of combined detection for NSCLC prognosis. METHODS: Survivin, p53 and bcl-2 expression levels were examined in 87 NSCLC specimens using streptavidin-peroxidase (SP) immunohistochemistry. The correlation with NSCLC was analyzed with Spearman rank correlation test. RESULTS: Survivin was positive in 55.2% (48/87) of NSCLC specimens, which was mainly located in cytoplasms and cell-specific. NSCLC at various stages showed significant difference in the positivity of survivin: at stage III and IV (mid and late stage) was 71.1% (32/45) while at stage I and II (early and mid stage) was 38.1% (16/42, P<0.01). Primary tumor with various staging showed no differential expressions of survivin; expression of survivin was significantly correlated with N staging whereby the positivity of specimens without lymph nodal involvement (N0) was 43.5% (27/62) and that for those with lymph nodal involvement (N1-2) was 84.0% (21/25, P<0.01). Survivin was detected in 76.0% (38/50) squamous cell carcinoma and 27.0% (10/37) of adenocarcinoma in a significantly different manner (P<0.01). p53 was positive in 64.6% (56/87) of NSCLC specimens, which was mainly located in cytoplasms and cell-specific. The positivity of specimens with lymph nodal involvement (N1-2) (84.0%, 21/25) was significantly higher than that for those without lymph nodal involvement (N0) (54.8%) (34/62, P<0.01). Moreover, p53 expression was tissue-specific whereby the positivity with squamous cell carcinoma (76.0%, 38/50) was significantly higher than that with adenocarcinoma (27.0%), (10/37, P<0.01). Bcl-2 was positive in 56.3% (49/87) of NSCLC specimens, which was mainly located in cytoplasms and nuclei and cell-specific. The positivity of specimens with lymph nodal involvement (N1-2) (48.0%, 12/25) was significantly higher than that for those without lymph nodal involvement (N0) (22.6%) (14/62, P<0.01). CONCLUSION: Upregulation of survivin represented its clinico-pathological association with NSCLC and meanwhile substantial correlation is confirmed between survivin, p53 and bcl-2.