一些从不吸烟的人为何也会患肺癌？美国和日本的科研人员在*新研究中发现，这可能与一种被称为miR-21的微RNA（核糖核酸）分子有关。 微RNA分子是能调节基因表达的一种小分子，目前已发现超过250种，其中多种与癌症有关，miR-21正是其中一种。新研究认为，miR-21可能导致从不吸烟者罹患肺腺癌。
科研人员在新一期美国《国家科学院院刊》（PNAS）上说，他们从28名从不吸烟的肺腺癌患者提取肺组织样本，与因吸烟而患肺腺癌者的肺组织样本进行比较，结果发现，miR-21分子在不吸烟的肺癌患者体内显著增加。
科研人员称，10%以上的肺癌发生在从不吸烟的人身上，在不吸烟肺癌患者体内，miR-21分子的水平很高，特别是当表皮生长因子受体基因突变时，miR-21的水平提高得特别快。此前的研究发现，表皮生长因子受体基因突变是造成吸烟和不吸烟的人患肺癌的主要原因之一。
如果科研人员在离体肺癌细胞中阻断miR-21，这些癌细胞便难以存活。科研人员因此认为，遏制miR-21分子可能是未来肺癌**的一个有效方法。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS July 13, 2009, doi: 10.1073/pnas.
MiR-21 is an EGFR-regulatedanti-apoptotic factor in lung cancer in never-smokers
Masahiro Seikea,b, Akiteru Gotoa, TetsuyaOkanoa,b, Elise D. Bowmana, Aaron J. Schettera, Izumi Horikawaa,Ewy A. Mathea, Jin Jenc, Ping Yangd, Haruhiko Sugimurae, AkihikoGemmab, Shoji Kudohb, Carlo M. Crocef,1 and Curtis C. Harrisa,1
Fifteen percent of lung cancer cases occur in never-smokers andshow characteristics that are molecularly and clinically distinctfrom those in smokers. Epidermal growth factor receptor (EGFR) genemutations, which are correlated with sensitivity to EGFR-tyrosinekinase inhibitors (EGFR-TKIs), are more frequent in never-smokerlung cancers. In this study, microRNA (miRNA) expression profiling of 28 cases of never-smoker lung cancer identified aberrantly expressed miRNAs, which were much fewer than in lung cancers of smokers and included miRNAs previously identified (e.g., up-regulated miR-21) and unidentified (e.g., down-regulated miR-138) in those smoker cases. The changes in expression of some of these miRNAs, including miR-21, were more remarkable in cases with EGFR mutations than in those without these mutations. A significant correlation between phosphorylated-EGFR (p-EGFR) and miR-21 levels in lung carcinoma cell lines and the suppression of miR-21 by an EGFR-TKI, AG1478, suggest that the EGFR signaling is a pathway positively regulating miR-21 expression. In the never-smoker–derived lung adenocarcinoma cell line H3255 with mutant EGFR and high levels of p-EGFR and miR-21, antisense inhibition of miR-21 enhanced AG1478-induced apoptosis. In a never-smoker–derived adenocarcinoma cell line H441 with wild-type EGFR, the antisense miR-21 not only showed the additive effect with AG1478 but also induced apoptosis by itself. These results suggest that aberrantly increased expression of miR-21, which is enhanced further by the activated EGFR signaling pathway, plays a significant role in lung carcinogenesis in never-smokers, as well as in smokers, and is a potential therapeutic target in both EGFR-mutant and wild-type cases.