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. 2020 May 30;40(5):698-702.
doi: 10.12122/j.issn.1673-4254.2020.05.13.

[Long-chain non-coding RNA MALAT1 regulates paclitaxel resistance of breast cancer cells by targeting miR-485-3p]

[Article in Chinese]
Shatar Aini  1 , Huanying Yan  2 , Wei Ding  1 , Lijiang Adi  1 , Pengcheng Su  1
Affiliations

[Long-chain non-coding RNA MALAT1 regulates paclitaxel resistance of breast cancer cells by targeting miR-485-3p]

[Article in Chinese]
Shatar Aini et al. Nan Fang Yi Ke Da Xue Xue Bao. .

Abstract
in English, Chinese

Objective: To investigate the role of long-chain non-coding RNA MALAT1 in modulating paclitaxel resistance in breast cancer cells.

Methods: Breast cancer SK-BR-3 cells were treated with gradient concentrations of paclitaxel to induce paclitaxel resistance of the cells. The resistant cells were transfected with si-NC, si-MALAT1, pcDNA, pcDNA-MALAT1, miRNC, miR-485-3p mimics, si-MALAT1+anti-miR-NC, or si-MALAT1+anti-miR-485-3p via liposomes. Following the transfections, the cells were examined for changes in IC50 of paclitaxel using MTT assay; the protein expression of P-gp, Bcl-2 and Bax were detected with Western blotting, and a dual luciferase reporter assay was used to detect the binding of MALAT1 to miR-485-3p.

Results: Compared with paclitaxel-sensitive SK-BR-3 cells, paclitaxel-resistant SK-BR-3 cells showed significantly increased the IC50 of paclitaxel with up-regulated MALAT1 expression and down-regulated miR-485-3p expression (P < 0.05). Silencing MALAT1 or overexpressing miR-485-3p obviously lowered the IC50 of paclitaxel and the expression of P-gp and Bcl-2 and increased the expression of Bax in SK-BR-3/PR cells (P < 0.05). miR-485-3p was identified as the target of MALAT1, and inhibiting miR-485-3p significantly reverse the effect of MALAT1 silencing on IC50 of paclitaxel and the expressions of P-gp, Bcl-2 and Bax in SK-BR-3/PR cells (P < 0.05).

Conclusions: MALAT1 can modulate paclitaxel resistance in breast cancer cells possibly by targeting miR-485-3p to down-regulate P-gp and Bcl-2 and up-regulate Bax.

目的: 研究长链非编码RNA MALAT1对乳腺癌细胞紫杉醇耐药性的影响机制。

方法: 运用紫杉醇浓度梯度诱导法检测紫杉醇耐药乳腺癌细胞SK-BR-3;将si-NC组(转染si-NC)、si-MALAT1组(转染si-MALAT1)、pc DNA组(转染pc DNA)、pc DNAMALAT1组(转染pc DNA-MALAT1)、miR-NC组(转染miR-NC)、miR-485-3p组(转染miR-485-3p mimics)、si-MALAT1+antimiR-NC组(共转染si-MALAT1和anti-miR-NC)、si-MALAT1+anti-miR-485-3p组(共转染si-MALAT1和anti-miR-485-3p), 均用脂质体法转染SK-BR-3/PR细胞; MTT法检测细胞IC50; Western blot检测细胞中P-gp、Bax、Bcl-2的蛋白表达; 双荧光素酶报告基因检测实验检测细胞中MALAT1与miR-485-3p的结合力。

结果: 与紫杉醇敏感SK-BR-3细胞相比, SK-BR-3/PR细胞的IC50、MALAT1均上调, miR-485-3p下调, 差异具有统计学意义(P < 0.05)。沉默MALAT1或过表达miR-485-3p均可下调SK-BR-3/PR细胞的IC50, 下调P-gp和Bcl-2表达, 上调Bax表达, 差异具有统计学意义(P < 0.05)。miR-485-3p是MALAT1的靶标。抑制miR-485-3p可逆转沉默MALAT1对SK-BR-3/PR细胞的IC50、P-gp、Bcl-2和Bax表达的影响, 差异具有统计学意义(P < 0.05)。

结论: 长链非编码RNA MALAT1可调控乳腺癌细胞对紫杉醇的耐药性, 其机制可能与靶向miR-485-3p下调P-gp、Bcl-2, 上调Bax有关。

Keywords: MALAT1; breast cancer; miR-485-3p; paclitaxel resistance.

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Figures

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1
沉默MALAT1对耐药相关蛋白表达的影响 Effect of silencing MALAT1 on the expression of drug resistance-related proteins.
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2
靶向结合位点 Target binding sites.
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过表达miR-485-3p对SK-BR-3/PR耐药相关蛋白表达的影响 Effects of overexpression of miR-485-3p on expression of drug resistance-related proteins in SK-BR-3/PR cells.
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抑制miR-485-3p对SK-BR-3/PR耐药相关蛋白表达的影响 Effects of inhibition of miR-485-3p on expression of resistance-related proteins in SK-BR-3/PR cells.
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