Medical Genetics Branch, National Human Genome Research Institute, 10 Center Dr, Bethesda, MD 20892, USA.
J Natl Cancer Inst. 2010 Jun 16;102(12):866-80. doi: 10.1093/jnci/djq153. Epub 2010 May 18.
BACKGROUND Secretory GTPases like Rab27B control vesicle exocytosis and deliver critical proinvasive growth regulators into the tumor microenvironment. The expression and role of Rab27B in breast cancer were unknown. METHODS Expression of green fluorescent protein (GFP) fused with wild-type Rab3D, Rab27A, or Rab27B, or Rab27B point mutants defective in GTP/GDP binding or geranylgeranylation, or transient silencing RNA to the same proteins was used to study Rab27B in estrogen receptor (ER)-positive human breast cancer cell lines (MCF-7, T47D, and ZR75.1). Cell cycle progression was evaluated by flow cytometry, western blotting, and measurement of cell proliferation rates, and invasion was assessed using Matrigel and native type I collagen substrates. Orthotopic tumor growth, local invasion, and metastasis were analyzed in mouse xenograft models. Mass spectrometry identified proinvasive growth regulators that were secreted in the presence of Rab27B. Rab27B protein levels were evaluated by immunohistochemistry in 59 clinical breast cancer specimens, and Rab3D, Rab27A, and Rab27B mRNA levels were analyzed by quantitative real-time polymerase chain reaction in 20 specimens. Statistical tests were two-sided. RESULTS Increased expression of Rab27B promoted G(1) to S phase cell cycle transition, proliferation and invasiveness of cells in culture, and invasive tumor growth and hemorrhagic ascites production in a xenograft mouse model (n = 10; at 10 weeks, survival of MCF-7 GFP- vs GFP-Rab27B-injected mice was 100% vs 62.5%, hazard ratio = 0.26, 95% confidence interval = 0.08 to 0.88, P = .03). Mass spectrometric analysis of purified Rab27B-secretory vesicles identified heat-shock protein 90alpha as key proinvasive growth regulator. Heat-shock protein 90alpha secretion was Rab27B-dependent and was required for matrix metalloproteinase-2 activation. All Rab27B-mediated functional responses were GTP- and geranylgeranyl-dependent. Presence of endogenous Rab27B mRNA and protein, but not of Rab3D or Rab27A mRNA, was associated with lymph node metastasis (P < .001) and differentiation grade (P = .001) in ER-positive human breast tumors. CONCLUSIONS Rab27B regulates invasive growth and metastasis in ER-positive breast cancer cell lines, and increased expression is associated with poor prognosis in humans.
分泌型 GTP 酶(如 Rab27B)控制囊泡的胞吐作用,并将关键的促侵袭生长调节剂递送到肿瘤微环境中。Rab27B 在乳腺癌中的表达和作用尚不清楚。
使用表达绿色荧光蛋白(GFP)融合野生型 Rab3D、Rab27A 或 Rab27B、或 Rab27B 点突变体(在 GTP/GDP 结合或 geranylgeranylation 中缺陷)、或针对相同蛋白的瞬时沉默 RNA 的 MCF-7、T47D 和 ZR75.1 等雌激素受体(ER)阳性人乳腺癌细胞系,研究 Rab27B。通过流式细胞术、Western blot 和细胞增殖率测量评估细胞周期进程,通过 Matrigel 和天然 I 型胶原底物评估侵袭。在小鼠异种移植模型中分析原位肿瘤生长、局部侵袭和转移。质谱鉴定了存在 Rab27B 时分泌的促侵袭生长调节剂。在 59 例临床乳腺癌标本中通过免疫组织化学评估 Rab27B 蛋白水平,在 20 例标本中通过实时定量聚合酶链反应分析 Rab3D、Rab27A 和 Rab27B mRNA 水平。统计检验为双侧。
Rab27B 表达增加促进细胞周期从 G1 期向 S 期过渡、培养细胞的增殖和侵袭性以及异种移植小鼠模型中的侵袭性肿瘤生长和出血性腹水产生(n = 10;在 10 周时,GFP-Rab27B 注射 MCF-7 GFP-的小鼠的存活率为 100%对 62.5%,风险比 = 0.26,95%置信区间 = 0.08 至 0.88,P =.03)。纯化的 Rab27B 分泌小泡的质谱分析鉴定了热休克蛋白 90alpha 为关键的促侵袭生长调节剂。热休克蛋白 90alpha 的分泌依赖于 Rab27B,并且需要基质金属蛋白酶-2 的激活。所有 Rab27B 介导的功能反应都依赖于 GTP 和 geranylgeranyl。在 ER 阳性人乳腺癌中,存在内源性 Rab27B mRNA 和蛋白,但不存在 Rab3D 或 Rab27A mRNA,与淋巴结转移(P <.001)和分化程度(P =.001)相关。
Rab27B 调节 ER 阳性乳腺癌细胞系的侵袭性生长和转移,表达增加与人类预后不良相关。