1.中山大学生命科学学院,广东 广州 510275
2.中山大学附属第七医院,广东 深圳 518107
3.惠州学院生命科学学院,广东 惠州 516007
4.中山大学深圳研究院,广东 深圳 518057
李飞(1992年生),男;研究方向:肿瘤生物学;E-mail:lifei67@mail.sysu.edu.cn
李超怡(1996年生),女;研究方向:肿瘤生物学;E-mail:sjtulichaoyi@sjtu.edu.cn
何越(1994年生),男;研究方向:生物与医药;E-mail:heyue35@mail2.sysu.edu.cn
宋琳(1975年生),女;研究方向:中医药防治痴呆机制;E-mail:drsonglin@163.com
张擎(1966年生),男;研究方向:分子药理学;E-mail:lsszq@mail.sysu.edu.cn (宋琳、张擎为共同通信作者)
纸质出版日期:2024-03-25,
网络出版日期:2023-12-04,
收稿日期:2023-08-31,
录用日期:2023-11-03
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李飞,李超怡,何越等.整合素β3通过激活MAPK/ERK途径促进鼻咽癌细胞转移[J].中山大学学报(自然科学版)(中英文),2024,63(02):139-149.
LI Fei,LI Chaoyi,HE Yue,et al.Integrin β3 promotes metastasis of nasopharyngeal carcinoma cells by activating the MAPK/ERK pathway[J].Acta Scientiarum Naturalium Universitatis Sunyatseni,2024,63(02):139-149.
李飞,李超怡,何越等.整合素β3通过激活MAPK/ERK途径促进鼻咽癌细胞转移[J].中山大学学报(自然科学版)(中英文),2024,63(02):139-149. DOI: 10.13471/j.cnki.acta.snus.2023E045.
LI Fei,LI Chaoyi,HE Yue,et al.Integrin β3 promotes metastasis of nasopharyngeal carcinoma cells by activating the MAPK/ERK pathway[J].Acta Scientiarum Naturalium Universitatis Sunyatseni,2024,63(02):139-149. DOI: 10.13471/j.cnki.acta.snus.2023E045.
鼻咽癌(NPC, nasopharyngeal carcinoma)作为我国南方及东南亚地区高发的一种头颈部恶性肿瘤,远端转移和局部复发是导致其治疗失败的主要原因。本研究通过对不同转移能力的鼻咽癌细胞进行分析,发现整合素β3(ITGB3, integrin β3)在高转移鼻咽癌细胞中的表达明显高于低转移鼻咽癌细胞。随后的研究表明ITGB3的上调表达促进了鼻咽癌细胞迁移、侵袭、克隆形成以及黏附能力,同时促进了鼻咽癌细胞增殖并抑制其凋亡水平。进一步地,本研究发现,ITGB3主要通过激活MAPK/ERK途径,进而促进鼻咽癌细胞迁移、侵袭、克隆形成以及黏附。因此,研究揭示了ITGB3对鼻咽癌细胞转移的调控作用及其分子机制,为鼻咽癌细胞转移防治与治疗提供了新的理论基础。
Nasopharyngeal carcinoma (NPC) is a prevalent head and neck malignancy in South China and Southeast Asia
often leading to treatment failure due to distal metastasis and local recurrence. This study showed a significant increase in the expression of integrin β3 (ITGB3) in highly metastatic NPC cells compared to poorly metastatic NPC cells. This study further elucidates that upregulation of ITGB3 expression not only enhances the migratory
invasive
clonogenic
and adhesive capacities of NPC cells
but also promotes their proliferation and inhibiting apoptosis. Mechanistically
ITGB3 primarily activates the MAPK/ERK pathway
as a result
enhancing the migratory
invasive
clonogenic
and adhesive capabilities of NPC cells. These findings in the study reveal the regulatory effect and molecular mechanism of ITGB3 on NPC cell metastasis
providing a new theoretical basis for the prevention and treatment of NPC cell metastasis.
鼻咽癌整合素β3肿瘤转移MAPK/ERK途径
nasopharyngeal carcinomaintegrin β3tumor metastasisMAPK/ERK pathway
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