Liao Dai-Xiang, Han Wei-Dong, Zhao Ya-Li, Pu Yong-Dong, Mu Yi-Ming, Luo Cheng-Hua, Li Xiang-Hong
Department of Molecular Biology, Institute of Basic Medicine, PLA General Hospital, Beijing, 100853, P. R. China.
Ai Zheng. 2006 Jul;25(7):866-70.
BACKGROUND & OBJECTIVE: Estrogen directly up-regulates LRP16 gene expression via activating its receptor (ER), and the overexpression of LRP16 promotes the proliferation of human breast cancer cells. This study was to detect the mRNA level of LRP16 gene in breast cancer, and investigate its correlation to the clinicopathologic features.
The mRNA level of LRP16 in carcinoma and matched peritumor tissues from 22 breast cancer patients was detected by Northern blot, and that in the tissues from 30 patients was detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). The expression of Ki-67, ER, and progesterone receptor (PR) in the carcinoma tissues was detected by immunohistochemistry.
According to the results of Northern blot, compared with that in peritumor tissues, LRP16 was overexpressed by 2 folds in 9 (40.9%) out of 22 breast cancer samples. Of the 9 samples with LRP16 overexpression, 7 were ER-positive, and 8 were PR-positive; of the 13 samples without LRP16 overexpression, 6 were ER-positive, and 5 were PR-negative. The positive rates of ER and PR were significantly higher in the samples with LRP16 overexpression than in the samples without LRP16 overexpression (P<0.05). Only 1 of the 9 samples with LRP16 overexpression was negative for both ER and PR, but 7 of the 13 without LRP16 overexpression were negative for both of them. The proportion of the tumors with diameters of 3.0-4.5 cm was significantly higher in the patients with LRP16 overexpression than in those without LRP16 overexpression (8/9 vs. 5/13, P=0.031). Axillary lymph node metastasis was detected in 12 out of 22 patients, including 8 of the 9 patients with LRP16 overexpression and 4 of the 13 without LRP16 overexpression (P=0.011). In addition, LRP16 overexpression was detected in 6 of the 8 patients with Ki-67 overexpression, and 2 of the 14 patients without Ki-67 overexpression (P=0.026). According to the results of RT-PCR, LRP16 was overexpressed in 9 (30%) out of 30 breast cancer samples. All of the 9 samples with LRP16 overexpression were positive for both ER and PR, with Ki-67 overexpression, tumor diameters of more than 3.5 cm and axillary lymph node metastasis. The differences between the patients with or without LRP16 overexpression were significant (P<0.05).
LRP16 overexpression is closely correlated to the positive rates of ER and PR, Ki-67 level, tumor diameter, and axillary lymph node metastasis of breast cancer, and might be involved in the proliferation and metastasis of human breast cancer.
雌激素通过激活其受体（ER）直接上调LRP16基因表达，而LRP16的过表达促进人乳腺癌细胞的增殖。本研究旨在检测乳腺癌中LRP16基因的mRNA水平，并探讨其与临床病理特征的相关性。
采用Northern印迹法检测22例乳腺癌患者癌组织及配对癌旁组织中LRP16的mRNA水平，采用半定量逆转录-聚合酶链反应（RT-PCR）检测30例患者组织中LRP16的mRNA水平。采用免疫组织化学法检测癌组织中Ki-67、ER和孕激素受体（PR）的表达。
根据Northern印迹法结果，与癌旁组织相比，22例乳腺癌样本中有9例（40.9%）LRP16表达上调2倍。在9例LRP16过表达的样本中，7例ER阳性，8例PR阳性；在13例未过表达LRP16的样本中，6例ER阳性，5例PR阴性。LRP16过表达样本中ER和PR的阳性率显著高于未过表达LRP16的样本（P<0.05）。9例LRP16过表达的样本中仅1例ER和PR均为阴性，而13例未过表达LRP16的样本中有7例两者均为阴性。LRP16过表达患者中肿瘤直径为3.0 - 4.5 cm的比例显著高于未过表达LRP16的患者（8/9 vs. 5/13，P = 0.031）。22例患者中有12例检测到腋窝淋巴结转移，其中9例LRP16过表达患者中有8例，13例未过表达LRP16患者中有4例（P = 0.011）。此外，8例Ki-67过表达患者中有6例检测到LRP16过表达，14例未过表达Ki-67的患者中有2例检测到LRP16过表达（P = 0.026）。根据RT-PCR结果，30例乳腺癌样本中有9例（30%）LRP16过表达。9例LRP16过表达的样本ER和PR均为阳性，伴有Ki-67过表达、肿瘤直径大于3.5 cm及腋窝淋巴结转移。LRP16过表达与未过表达患者之间的差异有统计学意义（P<0.05）。
LRP16过表达与乳腺癌的ER和PR阳性率、Ki-67水平、肿瘤直径及腋窝淋巴结转移密切相关，可能参与人乳腺癌的增殖和转移。
