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BMP2 promotes proliferation and invasion of nasopharyngeal carcinoma cells via mTORC1 pathway

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机构: [1]State Key Lab Oncol South China, Guangzhou 510060, Guangdong, Peoples R China; [2]Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Guangzhou 510060, Guangdong, Peoples R China; [3]Zhoukou Hosp Tradit Chinese Med, Zhoukou, Peoples R China; [4]Guangzhou Med Univ, Canc Ctr, Guangzhou, Guangdong, Peoples R China; [5]Rutgers State Univ, Rutgers Canc Inst New Jersey, New Brunswick, NJ 08901 USA
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关键词: nasopharyngeal carcinoma BMP2 metastasis mTORC1

摘要:
Bone morphogenetic protein-2 (BMP2) is a secreted protein that highly expressed in a variety of cancers and contributes to cell proliferation, migration, invasiveness, mobility, metastasis and EMT. However, its clinical significance and biological function in nasopharyngeal carcinoma (NPC) remain unknown up to now. Upregulation of BMP2 was first observed in NPC cell lines by a genome-wide transcriptome analysis in our previous study. In this study, BMP2 mRNA was detected by qRT-PCR and data showed that it was upregulated in NPC compared with non-cancerous nasopharynx samples. Immunohistochemistry (IHC) analysis in NPC specimens revealed that high BMP2 expression was significantly associated with clinical stage, distant metastasis and shorter survival of NPC patients. Moreover, overexpression of BMP2 in NPC cells promoted cell proliferation, migration, invasiveness and epithelial-mesenchymal transition (EMT). Mechanistically, BMP2 overexpression increase phosphorylated protein level of mTOR, S6K and 4EBP1. Correspondingly, mTORC1 inhibitor rapamycin blocked the effect of BMP2 on NPC cell proliferation and invasion. In conclusion, our results suggest that BMP2 overexpression in NPC enhances proliferation, invasion and EMT of tumor cells through the mTORC1 signaling pathway.

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出版当年[2017]版:
大类 | 2 区 生物
小类 | 3 区 细胞生物学
最新[2023]版:
大类 | 3 区 医学
小类 | 3 区 细胞生物学 3 区 老年医学
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第一作者机构: [1]State Key Lab Oncol South China, Guangzhou 510060, Guangdong, Peoples R China; [2]Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Guangzhou 510060, Guangdong, Peoples R China;
通讯作者:
通讯机构: [1]State Key Lab Oncol South China, Guangzhou 510060, Guangdong, Peoples R China; [2]Sun Yat Sen Univ, Canc Ctr, Collaborat Innovat Ctr Canc Med, Guangzhou 510060, Guangdong, Peoples R China; [5]Rutgers State Univ, Rutgers Canc Inst New Jersey, New Brunswick, NJ 08901 USA
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