MFAP2 is overexpressed in gastric cancer and promotes motility via the MFAP2/integrin α5β1/FAK/ERK pathway.,Oncogenesis

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MFAP2 is overexpressed in gastric cancer and promotes motility via the MFAP2/integrin α5β1/FAK/ERK pathway.
Oncogenesis ( IF 5.9 ) Pub Date : 2020-02-13 , DOI: 10.1038/s41389-020-0198-z
Li-Wen Yao _{1,

2} , Lian-Lian Wu _{1,

2} , Li-Hui Zhang _{1,

2} , Wei Zhou _{1,

2} , Lu Wu _{1,

2} , Ke He _{3,

4} , Jia-Cai Ren ₅ , Yun-Chao Deng _{1,

2} , Dong-Mei Yang _{1,

2} , Jing Wang _{1,

2} , Gang-Gang Mu _{1,

2} , Ming Xu _{1,

2} , Jie Zhou _{1,

2} , Guo-An Xiang ₃ , Qian-Shan Ding _{1,

2} , Yan-Ning Yang ₆ , Hong-Gang Yu _{1,

2}

Affiliation

Gastric cancer (GC) is one of the most common malignancies and its prognosis is extremely poor. This study identifies a novel oncogene, microfibrillar-associated protein 2 (MFAP2) in GC. With integrative reanalysis of transcriptomic data, we found MFAP2 as a GC prognosis-related gene. And the aberrant expression of MFAP2 was explored in GC samples. Subsequent experiments indicated that silencing and exogenous MFAP2 could affect motility of cancer cells. The inhibition of silencing MFAP2 could be rescued by another FAK activator, fibronectin. This process is probably through affecting the activation of focal adhesion process via modulating ITGB1 and ITGA5. MFAP2 regulated integrin expression through ERK1/2 activation. Silencing MFAP2 by shRNA inhibited tumorigenicity and metastasis in nude mice. We also revealed that MFAP2 is a novel target of microRNA-29, and miR-29/MFAP2/integrin α5β1/FAK/ERK1/2 could be an important oncogenic pathway in GC progression. In conclusion, our data identified MFAP2 as a novel oncogene in GC and revealed that miR-29/MFAP2/integrin α5β1/FAK/ERK1/2 could be an important oncogenic pathway in GC progression.

中文翻译：

MFAP2在胃癌中过表达，并通过MFAP2 /整合素α5β1/ FAK / ERK途径促进运动。

胃癌（GC）是最常见的恶性肿瘤之一，其预后极差。这项研究确定了GC中的一种新的致癌基因，微纤维相关蛋白2（MFAP2）。通过对转录组数据的综合再分析，我们发现MFAP2是与GC预后相关的基因。并在GC样品中探讨了MFAP2的异常表达。随后的实验表明沉默和外源性MFAP2可能影响癌细胞的运动。可以通过另一种FAK激活剂纤连蛋白来挽救对MFAP2沉默的抑制作用。此过程可能是通过调节ITGB1和ITGA5影响粘着斑过程的激活。MFAP2通过ERK1 / 2激活调节整联蛋白表达。shRNA沉默MFAP2可抑制裸鼠的致瘤性和转移。我们还发现MFAP2是microRNA-29的新型靶标，而miR-29 / MFAP2 /整合素α5β1/ FAK / ERK1 / 2可能是GC进展中的重要致癌途径。总之，我们的数据将MFAP2鉴定为GC中的新型致癌基因，并揭示了miR-29 / MFAP2 / integrinα5β1/ FAK / ERK1 / 2可能是GC进展中的重要致癌途径。

更新日期：2020-02-13

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