长链非编码RNA LINC00173在紫杉醇耐药乳腺癌细胞中的作用

目的探讨长链非编码RNA LINC00173对紫杉醇耐药乳腺癌细胞增殖、侵袭及迁移的影响，并探讨其可能的作用机制。方法利用qRT-PCR方法检测LINC00173在乳腺癌细胞株（MCF-7、MDA-MB-231和SKBR-3）和正常乳腺癌上皮细胞系（MCF-10A）的表达水平；构建LINC00173过表达载体和干扰片段，各自转染到乳腺癌细胞株中，利用qRT-PCR方法检测转染后LINC00173的表达水平；采用CCK8实验检测乳腺癌细胞的增殖能力；Transwell侵袭和划痕实验，检测细胞的侵袭和迁移能力；Western blotting方法检测CyclinD1、β-catenin、P-gp蛋白的表达。结果与MCF-10A细胞相比，LINC00173在乳腺癌细胞株中低表达；MCF-7细胞转染干扰片段及MCF-7/PR耐药细胞株转染过表达LINC00173载体后，与阴性对照（si-NC）组相比，si-LINC00173的表达降低；而与LV-NC组相比，过表达LV-LINC00173后的表达增加，且差异有统计学意义（P < 0.01）；干扰LINC00173的表达后，MCF-7细胞的增殖及迁移能力增强（P < 0.01）；过表达LINC00173后，MCF-7/PR细胞的增殖、侵袭及迁移能力减弱（P < 0.01）；干扰LINC00173后，MCF-7细胞CyclinD1、β-catenin、P-gp蛋白的表达水平明显增加（P < 0.01）；过表达LINC00173后，MCF-7/PR的CyclinD1、β-catenin、P-gp蛋白表达水平明显下降（P < 0.01）。结论LINC00173在乳腺癌细胞中表达降低并可能通过调控β-catenin表达参与紫杉醇耐药过程且与其发生、发展及侵袭有关，是涉及到乳腺癌发展的一种新的分子，可为临床诊断、治疗乳腺癌提供新的理论依据。

Role of long non-coding RNA LINC00173 in paclitaxel-resistant breast cancer cells

ObjectiveTo investigate the effects of long non-coding RNA LINC00173 on the proliferation, invasion and migration of paclitaxel-resistant breast cancer cells, and its possible mechanism of action.MethodsThe expression levels of LINC00173 in breast cancer cell lines(MCF-7, MDA-MB-231 and SKBR-3) and normal breast cancer epithelial cell lines(MCF-10A) were detected using qRT-PCR.The LINC00173 overexpression vector and interference fragment were constructed, and transfected into breast cancer cell lines, respectively.The qRT-PCR was used to detect the expression level of transfected LINC00173.The proliferation ability of breast cancer cells was detected using CCK8 assay.The transwell invasion and scratch assay were used to detect the invasion and migration of cells.The expression levels of CyclinD1, β-catenin and P-gp proteins were detected using Western blotting.ResultsCompared with MCF-10A cells, the expression level of LINC00173 in breast cancer cell line was low.After MCF-7 cells transfected with interference fragments and MCF-7/PR resistant cell lines transfected with overexpression vector of si-LINC00173, the expression level of si-LINC00173 decreased compared with the negative control group(si-NC).Compared with the LV-NC group, the overexpression of LV-LINC00173 increased, and the difference of which was statistically significant(P < 0.01).After interfering the expression of LINC00173, the proliferation and migration of MCF-7 cells enhanced(P < 0.01).After overexpression of LINC00173, the proliferation, invasion and migration of MCF-7/PR cells decreased(P < 0.01).After the interfering with LINC00173, the expression levels of CyclinD1, β-catenin and P-gp in MCF-7 cells significantly increased(P < 0.01).After the overexpression of LINC00173, the expression levels of CyclinD1, β-catenin and P-gp in MCF-7/PR decreased significantly(P < 0.01).ConclusionsThe decreasing expression level of LINC00173 in breast cancer cells may participate in the process of paclitaxel-resistance by regulating β-catenin expression and its occurrence, development and invasion.LINC00173 is a new molecule involved in the development of breast cancer, and which can provide a new theoretical basis for clinical diagnosis and treatment of breast cancer.