PMID- 27572051 OWN - NLM STAT- MEDLINE DCOM- 20170413 LR - 20181113 IS - 1791-3004 (Electronic) IS - 1791-2997 (Print) IS - 1791-2997 (Linking) VI - 14 IP - 4 DP - 2016 Oct TI - Notch 2 signaling contributes to cell growth, anti-apoptosis and metastasis in laryngeal squamous cell carcinoma. PG - 3517-24 LID - 10.3892/mmr.2016.5688 [doi] AB - 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. FAU - Zou, You AU - Zou Y AD - Department of Otolaryngology Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. FAU - Fang, Fang AU - Fang F AD - Department of Medical Market, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. FAU - Ding, Yong-Jun AU - Ding YJ AD - Department of Otolaryngology Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. FAU - Dai, Meng-Yuan AU - Dai MY AD - Department of Otolaryngology Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. FAU - Yi, Xing AU - Yi X AD - Department of Otolaryngology Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. FAU - Chen, Chen AU - Chen C AD - Department of Otolaryngology Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. FAU - Tao, Ze-Zhang AU - Tao ZZ AD - Department of Otolaryngology Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. FAU - Chen, Shi-Ming AU - Chen SM AD - Department of Otolaryngology Head and Neck Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China. LA - eng PT - Journal Article DEP - 20160829 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (NOTCH2 protein, human) RN - 0 (Receptor, Notch2) SB - IM MH - *Apoptosis MH - Carcinoma, Squamous Cell/genetics/metabolism/*pathology MH - Cell Line, Tumor MH - Cell Movement MH - *Cell Proliferation MH - Gene Expression Regulation, Neoplastic MH - Humans MH - Laryngeal Neoplasms/genetics/metabolism/*pathology MH - Larynx/metabolism/*pathology MH - Neoplasm Invasiveness/genetics/pathology MH - Neoplasm Metastasis/genetics/pathology MH - RNA Interference MH - Receptor, Notch2/genetics/*metabolism MH - *Signal Transduction PMC - PMC5042778 EDAT- 2016/08/31 06:00 MHDA- 2017/04/14 06:00 PMCR- 2016/08/29 CRDT- 2016/08/31 06:00 PHST- 2015/06/18 00:00 [received] PHST- 2016/05/31 00:00 [accepted] PHST- 2016/08/31 06:00 [entrez] PHST- 2016/08/31 06:00 [pubmed] PHST- 2017/04/14 06:00 [medline] PHST- 2016/08/29 00:00 [pmc-release] AID - mmr-14-04-3517 [pii] AID - 10.3892/mmr.2016.5688 [doi] PST - ppublish SO - Mol Med Rep. 2016 Oct;14(4):3517-24. doi: 10.3892/mmr.2016.5688. Epub 2016 Aug 29.