Notch 2 signaling contributes to cell growth, anti-apoptosis and metastasis in laryngeal squamous cell carcinoma

Notch 2 信号促进喉鳞状细胞癌细胞生长、抗凋亡和转移

阅读:8
作者:You Zou, Fang Fang, Yong-Jun Ding, Meng-Yuan Dai, Xing Yi, Chen Chen, Ze-Zhang Tao, Shi-Ming Chen

Abstract

Notch signaling is important during the development of a variety of human tumors. Depending on the context, Notch signaling can be either oncogenic or anti‑proliferative, and therefore, its effects in cancer are unpredictable. The aim of the present study was to identify the importance of Notch 2 in the cell growth and metastasis of laryngeal squamous cell carcinoma (LSCC). The current study performed quantum dots‑based immunofluorescence histochemistry to determine expression of Notch 2 in 72 LSCC samples without lymph node metastasis, 23 LSCC samples with lymph node metastasis and 31 samples from vocal cord polyps. It was observed that Notch 2 was upregulated in LSCC tissue compared with normal vocal cord polyps. This upregulation was further enhanced in LSCC tissues with lymph node metastasis compared with LSCC tissues without lymph node metastasis. Following knockdown of NOTCH2 expression in LSCC cells, the in vitro tumorigenicity of Hep‑2 cells was inhibited, with growth, migration, invasion and proliferation reduced, and apoptosis induced. Additionally, following downregulation of Notch 2 protein expression, the protein expression levels of phospho‑mitogen‑activated protein kinase 1 (p‑ERK), v‑myc avian myelocytomatosis viral oncogene homolog and B‑cell CLL/lymphoma 2 (Bcl2) were also downregulated, whereas, Bcl2‑associated X protein expression was upregulated. There were no changes detected in the protein expression levels of total‑ERK, phospho‑v‑akt murine thymoma viral oncogene homolog 1 (p‑Akt) and total‑Akt. The results of the present study suggest that Notch 2 is important for the cell growth, anti‑apoptosis and metastasis of LSCC. Therefore, Notch 2 inhibitors may have therapeutic potential for the treatment of patients with LSCC via the inhibition of cancer cell growth and metastasis.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。