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[微小RNA-542-3p对抗苯并(a)芘-7,8-二醇-9,10-环氧化物诱导的致癌作用的影响]

[Effect of miR-542-3p on carcinogenesis induced by anti-benzo(a) pyrene-7,8-diol-9,10-epoxide].

作者信息

Zhao Yao, Liu Huan-ying, Li Yuan-qi, Jiang Yi-guo

机构信息

Institute for Chemical Carcinogenesis, State Key Laboratory of Respiratory Diseases, Guangzhou Medical University, Guangzhou 510182, China.

出版信息

Zhonghua Yu Fang Yi Xue Za Zhi. 2011 May;45(5):416-21.

Abstract

OBJECTIVE

To explore the effect of miR-542-3p in malignant transformation of human bronchial epithelial cells (16HBE) induced by anti-benzo(a)pyrene-7,8-diol-9,10-epoxide (anti-BPDE).

METHODS

The relative expression level of mature miR-542-3p in transformed cells (16HBE-T) and untransformed control cells (16HBE-N) was measured by real-time quantitative polymerase chain reaction (qRT-PCR). miRNA mimic was transiently transfected into 16HBE-T to change the expression level of miR-542-3p, and then the influenced changes of cell proliferation, cell cycle, apoptosis, and soft agar colony formation rate and the migration of transfected cells were analyzed.

RESULTS

Before transfection, the expression level of mature miR-542-3p in 16HBE-T was lower (39.08 ± 6.95)% than it in 16HBE-N (t = 15.18, P < 0.05). In comparison with the 16HBE-T group, the expression level of miR-542-3p in miR-542-3p mimic-transfected group was (5.23 ± 0.55) fold (t = 17.37, P < 0.05) after transfection. Cell proliferation of mimic-transfected group was decreased to (62.06 ± 5.61)% (t = -17.28, P < 0.05), percentage of cells in G(0)/G(1) phase up to (74.76 ± 4.86)% (t = 4.53, P < 0.05), rate of colony formation degrade to (5.87 ± 0.67)% (t = -6.66, P < 0.05), coverage areas ratio decreased to (0.31 ± 0.08) (t = -6.78, P < 0.05). There was no change with apoptosis.

CONCLUSION

Our studies showed that miR-542-3p played the role as a tumor suppressor, which led to a significant decrease in the proliferation capacity and degree of malignancy. These findings suggest aberrantly down-regulated miR-542-3p may be one critical factor that contributes to malignant transformation of 16HBE induced by anti-BPDE.

摘要

目的

探讨微小RNA-542-3p(miR-542-3p)在抗苯并[a]芘-7,8-二醇-9,10-环氧化物(anti-BPDE)诱导的人支气管上皮细胞(16HBE)恶性转化中的作用。

方法

采用实时定量聚合酶链反应(qRT-PCR)检测转化细胞(16HBE-T)和未转化对照细胞(16HBE-N)中成熟miR-542-3p的相对表达水平。将miRNA模拟物瞬时转染至16HBE-T中以改变miR-542-3p的表达水平,然后分析转染细胞的增殖、细胞周期、凋亡、软琼脂集落形成率及迁移的变化。

结果

转染前,16HBE-T中成熟miR-542-3p的表达水平低于16HBE-N,为(39.08±6.95)%(t=15.18,P<0.05)。与16HBE-T组相比,miR-542-3p模拟物转染组转染后miR-542-3p的表达水平为(5.23±0.55)倍(t=17.37,P<0.05)。模拟物转染组细胞增殖降至(62.06±5.61)%(t=-17.28,P<0.05),G(0)/G(1)期细胞百分比升至(74.76±4.86)%(t=4.53,P<0.05),集落形成率降至(5.87±0.67)%(t=-6.66,P<0.05),覆盖面积比降至(0.31±0.08)(t=-6.78,P<0.05)。凋亡无变化。

结论

我们的研究表明,miR-542-3p起肿瘤抑制作用,导致增殖能力和恶性程度显著降低。这些发现提示,miR-542-3p异常下调可能是anti-BPDE诱导16HBE恶性转化中的一个关键因素。

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