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p75NTR promotes survival of breast cancer resistant cells by regulating Bcl-2/Bax and MAPK pathway

机译:p75NTR通过调节Bcl-2 / Bax和MAPK途径促进乳腺癌耐药细胞的存活

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摘要

In breast cancer, the neurotrophin receptor p75NTR is a critical factor that promotes resistance to the drug, however, its mechanism of action remains unclear. In our study, the 10 cases of positive expressions of p75NTR were detected in 86 cases of breast cancer tissues, accounting for 11.6% of cases detected. The immunohistochemistry detection of p75NTR was in the cytoplasm and cell membrane. The expression of p75NTR was significantly associated with histological grade (P<0.01), however, not with the menopause, tumor size and lymph node metastasis. Western blot result showed that p75NTR protein was induced by overexpression in the multidrug-resistant breast cancer cell lines. After transfection of pcDNA3.1-p75NTR, MDA-MB-231/ADR-p75NTR cell cycle was arrested in G0/G1 phase. However, the number of cells in G0/G1 phase increased and decreased in S phase cells (P<0.05). Additionally, apoptosis rate decreased (P<0.05). The p75NTR overexpression increased the expression of MDR related protein and activated MAPK signaling pathway.
机译:在乳腺癌中,神经营养蛋白受体p75NTR是提高对该药耐药性的关键因素,但是其作用机理仍不清楚。在我们的研究中,在86例乳腺癌组织中检测到10例p75NTR阳性表达,占所检测病例的11.6%。 p75NTR的免疫组织化学检测在细胞质和细胞膜中。 p75NTR的表达与组织学分级显着相关(P <0.01),而与更年期,肿瘤大小和淋巴结转移无关。 Western印迹结果表明,p75NTR蛋白是由多药耐药乳腺癌细胞株中的过表达诱导的。转染pcDNA3.1-p75NTR后,MDA-MB-231 / ADR-p75NTR细胞周期被阻滞在G0 / G1期。然而,S期细胞中G0 / G1期的细胞数量增加和减少(P <0.05)。另外,凋亡率降低(P <0.05)。 p75NTR的过表达增加了MDR相关蛋白的表达并激活了MAPK信号通路。

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