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首页> 外文期刊>Cytoskeleton >Regulation of beta-tubulin isotypes by micro-RNA 100 in MCF7 breast cancer cells.
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Regulation of beta-tubulin isotypes by micro-RNA 100 in MCF7 breast cancer cells.

机译：MCF7乳腺癌细胞中微RNA 100调节β-微管蛋白同种型。

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Antimitotic drugs are key components of combination chemotherapy protocols for hematological and solid tumors. The taxanes (e.g., paclitaxel) bind to the beta subunit of the tubulin heterodimer and reduce microtubule dynamics, leading to cell cycle arrest in G2/M. The effectiveness of combination chemotherapy is limited by tumor resistance to drugs initially or as a cumulative effect after several cycles of treatment. Because changes in the drug receptor may be linked to drug resistance, we investigated changes in beta-tubulin isotypes in response to paclitaxel treatment in MCF7 breast cancer cells. We found that paclitaxel induced a 2-3 fold increase in mRNA for beta-tubulin IIA and III genes, TUBB2A, and TUBB3. beta-Tubulin class III protein increased; however, beta-tubulin class II protein was not detected in these cells. Paclitaxel treatment following pretreatment with actinomycin D showed that the change in beta-tubulin class III was due to increased transcription and linked to G2/M arrest. The increase in beta-tubulin IIA mRNA was due to both enhanced stability and increased transcription, unassociated with G2/M arrest. We used micro-RNA superarrays to look for changes in families of micro-RNAs that might be linked to drug-induced changes in beta-tubulin isotype mRNA and/or protein. We found a significant decrease in the tumor suppressor, miR-100, in MCF7 cells in response to paclitaxel treatment. Transfection of MCF7 cells with miR-100 significantly reduced beta-tubulin I, IIA, IIB and V mRNA and prevented paclitaxel-induced increases in beta-tubulin isotypes. This is the first report of a micro-RNA that regulates these specific beta-tubulin isotype mRNAs.
机译：抗杀菌药是血液学和实体瘤组合化疗方案的关键组分。紫杉烷（例如，紫杉醇）与小管蛋白异二聚体的β亚基结合并减少微管动态，导致G2 / m中的细胞循环停滞。组合化疗的有效性受到肿瘤抗性对药物的限制，或者在几次治疗后作为累积效应。因为药物受体的变化可以与耐药性相关，所以我们在MCF7乳腺癌细胞中对紫杉醇治疗进行紫杉醇治疗的β-微管蛋白同种型的变化。我们发现紫杉醇诱导β-微管蛋白IIA和III基因，Tubb2a和Tubb3的mRNA增加2-3倍。 β-管蛋白III类蛋白质增加;然而，在这些细胞中未检测到β-微管蛋白II类蛋白。用放线菌素D进行预处理后的紫杉醇治疗表明，β-管蛋白III类的变化是由于转录增加并与G2 / M逮捕有关。 β-微管蛋白IIA mRNA的增加是由于增强的稳定性和转录增加，无论是G2 / M的逮捕都是无关的。我们使用微RNA超级阵列来寻找微RNA家族的变化，其可能与β-微管蛋白同种型mRNA和/或蛋白质中的药物诱导的变化相关联。我们发现肿瘤抑制器MiR-100在MCF7细胞中的显着降低，响应于紫杉醇治疗。 MIR-100转染MCF7细胞显着降低了β-微管蛋白I，IIA，IIB和V mRNA，并预防紫杉醇诱导的β-微管蛋白同种型增加。这是调节这些特定β-微管蛋白同种型MRNA的微RNA的第一个报告。

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