清道夫受體（scavenger receptor）是吞噬細胞表面的一組異質性分子,，至少以6種不同的分子形式存在,。此類受體多見于巨噬細胞表面,，它們以化學修飾的蛋白質,、多核苷酸,、多糖和磷脂等為配體并可促進其胞吞作用,，起著清除體內有毒物質和衰老、凋亡或壞死細胞的作用,。
清道夫受體成員5（SCARA5）是一類清道夫受體新成員,，在人類肝細胞癌（HCC）中是一種新的候選腫瘤抑制基因。
近日刊登在Cancer Sci雜志上的一則研究發(fā)現各種癌癥細胞系和腫瘤樣本中,，SCARA5表達都出現經常性地下調,。此外，研究結果表明,，在人類癌癥細胞株SCARA5中,，該受體上調導致腫瘤細胞的增殖、克隆形成能力急劇減少,，遷移和體外侵襲能力也減弱,。
此外，研究人員將荷瘤小鼠給予SCARA5-陽離子脂質體后,，皮下人腦膠質瘤腫瘤的生長被抑制,，同時自發(fā)性肺轉移也被抑制。
而在另一個A549肺癌小鼠實驗中,，小鼠給予SCARA5-陽離子脂質體后A549肺轉移也減少,。與對照組相比，SCARA5治療的U251老鼠自發(fā)性肺轉移率減少77.3％,，A549肺轉移率減少70.2％,。
為了探索的分子機制，研究者采用免疫印跡方法,，結果表明SCARA5能與FAK相互作用發(fā)揮作用,。有趣的是SCARA5的上調對STAT3以及一些下游信號包括cyclinB1、cyclinD1,、AKT,、MMP-9和VEGF-A的失活是必須的?？偟膩碚f,，這些研究結果首次證實了SCARA5可能是一個有前途的抗腫瘤轉移的癌基因治療新靶標。（生物谷：Bioon.com）
doi:10.1111/j.1349-7006.2012.02350.x
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Therapeutic upregulation of SCARA5 inhibits tumor growth and metastasis.
Yan N, Zhang S, Yang Y, Cheng L, Li C, Dai L, Dai L, Zhang X, Fan P, Tian H, Wang R, Chen X, Su X, Li Y, Zhang J, Du T, Wei Y, Deng H.
Class A scavenger receptor member 5 (SCARA5) is a new member of class A scavenger receptor, which serves as a novel candidate tumor suppressor gene in human hepatocellular carcinoma (HCC) in recent report. Here, we found that SCARA5 expression was frequently downregulated in various cancer cell lines and tumor samples. Additionally, our results showed that upexpression SCARA5 in human cancer cell line led to dramatically decreased cell proliferation, clone formation, migration and invasion in vitro. Furthermore, our study showed that systemic treatment of tumor-bearing mice with SCARA5-Cationic Liposome Complex not only reduced the subcutaneous human glioma tumor growth but also markedly suppressed formation of spontaneous lung metastases. We found similar results in another experiment using mice bearing experimental A549 lung metastasis. Compared with the untreated control group, the mice treated with SCARA5 exhibited a reduction U251 spontaneous lung metastasis rate of 77.3% and experimental A549 lung metastasis rate of 70.2%, respectively. To explore the molecular mechanisms, western blot was done and the results showed that SCARA5 physically associated with FAK. Interestingly, upregulation of SCARA5 was capable for inactivation of STAT3 and some downstream signaling including cyclinB1, cyclinD1, AKT, surviving, MMP-9 and VEGF-A. Overall, these findings provided the first evidence that SCARA5 might be a promising target for the development of new anti-metastasis reagent for cancer gene therapy.
