N-Myc promotes angiogenesis and therapeutic resistance of prostate cancer by TEM8.

N-Myc promotes angiogenesis and therapeutic resistance of prostate cancer by TEM8.
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DOI:
10.1007/s12032-021-01575-x
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发表时间:
2021-09-14
期刊:
Medical oncology (Northwood, London, England)
影响因子:
--
通讯作者:
Yin Y
Yin Y
中科院分区:
其他
文献类型:
--
作者:
Li M;Fang L;Kwantwi LB;He G;Luo W;Yang L;Huang Y;Yin S;Cai Y;Ma W;Zhan H;Tong Z;Zhang L;Liang C;Yin Y

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虽然早期局限性前列腺癌患者可以存活更长时间,但随着雄激素剥夺疗法(ADT)的使用,耐去势前列腺癌(CRPC)逐渐出现。N-Myc和TEM8在几种癌症类型的进展中起着至关重要的作用。然而,N-Myc和TEM8如何促进前列腺癌进展的潜在机制仍不清楚。本研究采用免疫组织化学方法检测N-Myc和TEM8在良性前列腺增生症(BPH)和前列腺癌(PCa)组织中的表达。LNCaP细胞系在添加10%去炭胎牛血清的RPMI1640培养液中维持。随后,使用R语言软件对结果进行了验证。采用人脐静脉内皮细胞(HUVEC)小管形成实验,观察N-Myc和TEM8过表达对前列腺癌细胞血管生成的影响。免疫组化结果显示N-Myc和TEM8在前列腺癌组织中的表达呈正相关。进一步分析表明,N-Myc和TEM8与前列腺癌患者的临床病理特征和预后不良有关。此外,N-Myc和TEM8的过表达促进了前列腺癌细胞的增殖和血管生成。此外,N-Myc和TEM8的过表达与化疗耐药有关。我们进一步发现,N-Myc通过TEM8促进前列腺癌的血管生成和治疗耐药。因此,在前列腺癌中靶向N-Myc/TEM8通路将是加强前列腺癌患者治疗的一种新的治疗策略。网上版载有补充材料,可在10.1007/s12032-021-01575-x查阅。
Although patients with early localized prostate cancer can survive longer, castration-resistant prostate cancer (CRPC) has gradually emerged with the use of androgen deprivation therapy (ADT). N-Myc and TEM8 play a vital role in the progression of several cancer types. However, the underlying mechanism of how N-Myc and TEM8 promote the progression of prostate cancer remains unclear. In this study, the expression of N-Myc and TEM8 was detected in benign prostatic hyperplasia (BPH) and prostate cancer (PCa) tissues by immunohistochemistry (IHC). LNCaP cell lines were maintained in RPMI 1640 medium supplemented with 10% charcoal-stripped fetal bovine serum. Subsequently, R language software was used to verify our results. Tubule formation assay of human umbilical vein endothelial cell (HUVEC) was conducted to examine the effect of N-Myc and TEM8 overexpression on angiogenesis in prostate cancer cells. IHC results showed a positive correlation between the expression of N-Myc and TEM8 in prostate cancer tissues. Further analysis showed that N-Myc and TEM8 were associated with clinicopathological features and poor prognosis in prostate cancer patients. Moreover, the overexpression of N-Myc and TEM8 promoted proliferation of prostate cancer cells and angiogenesis. Additionally, N-Myc and TEM8 overexpression was associated with therapeutic resistance. We further found that N-Myc promoted angiogenesis and therapeutic resistance in prostate cancer via TEM8. Hence, targeting N-Myc/TEM8 pathway in prostate cancer would be a novel therapeutic strategy to enhance the treatment of prostate cancer patients. The online version contains supplementary material available at 10.1007/s12032-021-01575-x .
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