最近，研究人員發(fā)現(xiàn)一種有用蛋白質(zhì),，該蛋白質(zhì)可以預(yù)測(cè)乳腺癌患者發(fā)生肺轉(zhuǎn)移的風(fēng)險(xiǎn)
過氧化物酶2保護(hù)腫瘤細(xì)胞免受氧化應(yīng)激，并促進(jìn)腫瘤細(xì)胞在肺部的生長(zhǎng)和增殖,。
來自Bellvitge生物醫(yī)學(xué)研究所（IDIBELL）的研究表明：轉(zhuǎn)移到肺的乳腺癌細(xì)胞能表達(dá)較高水平的過氧化物酶2（PRDX2）蛋白,。這項(xiàng)研究證實(shí)調(diào)控這種蛋白質(zhì)的水平可能是一個(gè)新的治療腫瘤，以防止肺轉(zhuǎn)移的策略,。研究結(jié)果發(fā)表在Oncogene雜志上,。
PRDX2是一個(gè)氧化還原酶，能保護(hù)細(xì)胞免受自由基和氧化應(yīng)激的損傷,。PRDX2對(duì)肺部腫瘤細(xì)胞能生活在充足氧氣的環(huán)境中至關(guān)重要,。在乳腺癌細(xì)胞中，過度表達(dá)的PRDX2可防止氧化應(yīng)激的損傷,，促進(jìn)肺部腫瘤的生長(zhǎng),、增殖和轉(zhuǎn)移。
Sierra等研究者用細(xì)胞實(shí)驗(yàn)以及小鼠動(dòng)物模型證實(shí)了低表達(dá)水平的PRDX2足以阻止轉(zhuǎn)移性腫瘤細(xì)胞轉(zhuǎn)移至肺,。
Sierra說：“這些研究結(jié)果表明修改的PRDX2表達(dá)可能會(huì)產(chǎn)生一種新的治療方法,，以防止腫瘤細(xì)胞肺轉(zhuǎn)移,，一些抑制該蛋白的藥物的有效性已經(jīng)在其他疾病中得到測(cè)試。
下一步研究工作就是能得到足夠數(shù)量的高表達(dá)這種蛋白的患者,，驗(yàn)證PRDX2能否作為乳腺癌肺轉(zhuǎn)移風(fēng)險(xiǎn)的生物標(biāo)志物,。（生物谷：Bioon）
doi:10.1038/onc.2012.93
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PMID:
Peroxiredoxin 2 specifically regulates the oxidative and metabolic stress response of human metastatic breast cancer cells in lungs.
Stresing V, Baltziskueta E, Rubio N, Blanco J, Arriba M, Valls J, Janier M, Clézardin P, Sanz-Pamplona R, Nieva C, Marro M, Dmitri P, Sierra A.
Little is known about metastatic pathways that are specific to the lung rather than other organs. We previously showed that antioxidant proteins such as peroxiredoxins were specifically upregulated in lung metastatic breast cancer cells. We hypothesize that cancer cells that live under aerobic conditions, as might be the case in lungs, protect themselves against the damage caused by reactive oxygen species (ROS). To examine this hypothesis, we studied the role of peroxiredoxin-2 (PRDX2) in lung vs bone metastasis formation. A metastatic variant of MDA-MB-435 breast cancer cells that specifically metastasize to lungs (435-L3) was transduced with short hairpin RNAs to specifically silence PRDX2. Conversely, a bone metastatic variant of MDA-MB-231 cells (BO2) was stably transfected to overexpress PRDX2. The 435-L3 cells silenced for PRDX2 were significantly more sensitive to H(2)O(2)-induced oxidative stress than the parental and scrambled transfected cells. BO2/PRDX2 cells produced less ROS than BO2/green fluorescent protein control cells under oxidative stress. Moreover, PRDX2 knockdown inhibited the growth of 435-L3 cells in the lungs, whereas lymph node metastasis remained unaffected. In contrast, PRDX2 overexpression in bone metastatic BO2 breast cancer cells led to drastic inhibition of the skeletal tumor burden and reduction of bone destruction. Furthermore, PRDX2 expression in breast cancer cells was associated with a glucose-dependent phenotype, different from bone metastatic cells. Overall, our results strongly suggest that PRDX2 is a targetable 'metabolic adaptor' driver protein implicated in the selective growth of metastatic cells in the lungs by protecting them against oxidative stress.
