CMTM5与表皮生长因子受体在前列腺癌中的表达及意义

目的：通过检测CMTM5（CKLF-like MARVEL transmembrane domain containing 5）及表皮生长因子受体（epidermal growth factor receptor，EGFR）在前列腺癌中的表达，分析其在前列腺癌发生及发展中可能存在的联系。方法：免疫组织化学检测前列腺癌和良性前列腺增生（benigh prostatic hyperlasia，BPH）组织中CMTM5的表达，分析其与前列腺癌临床病理学特征的关系；免疫组织化学检测EGFR在前列腺癌组织中的表达，并分析其与CMTM5在前列腺癌中表达水平的关系；Western blot检测CMTM5和EGFR在BPH组织及各前列腺癌细胞系的表达。结果：免疫组织化学结果显示，CMTM5在75%（27/36）BPH和35.9%（23/64）前列腺癌组织中高表达，差异有统计学意义（P=0.000 2）。CMTM5的表达水平与年龄、临床分期、有无转移之间无明显关系（P>0.05）， 在中高度分化（Gleason评分≤7）的肿瘤组织中，CMTM5的表达水平高于低度分化（Gleason评分≥8）的肿瘤组织，差异有统计学意义（P=0.003）。EGFR在57.8%的前列腺癌组织中高表达（37/64），其与CMTM5表达水平的差异有统计学意义（P=0.021）。23例前列腺癌组织CMTM5低表达且EGFR高表达，占35.9%。Western bolt结果显示CMTM5在BPH组织中表达，但在各前列腺癌细胞系中均表达缺失，而EGFR在BPH组织中的表达低于各前列腺癌细胞系，特别是激素非依赖性细胞系PC3和DU145。结论：CMTM5的表达缺失与EGFR的过表达可能同时参与了前列腺癌的发生与发展。

Expression and significance of CMTM5 and epidermal growth factor receptor in prostate cancer

Objective：To investigate the expression patterns of CKLF-like MARVEL transmembrane domain containing 5 (CMTM5), a novel tumor suppressor, and epidermal growth factor receptor (EGFR) in prostate cancer (PCa) tissues and cells and to analyze the relationship between CMTM5 and EGFR in PCa. Methods: The expression patterns of CMTM5 and EGFR in PCa tissues and cells were detected by immunohistochemistry and Western blot, respectively. Results: CMTM5 was highly expressed in 75% (27/36) of benigh prostatic hyperplasia(BPH) tissues but 35.9% (23/64) of PCa tissues (P<0.001). There was a significant difference of CMTM5 expression between the two groups of PCa tissues with different Gleason scores (P=0.003), though its expression was not related to the age, clinical stage, and metastatic situation (P>0.05). EGFR was highly expressed in 57.8% (37/64) of PCa tissues, it had statistical significance between EGFR and CMTM5 expressions in PCa tissues. Furthermore, 23 cases (35.9%) had low CMTM5 expression and high EGFR expression. Western blot showed that CMTM5 was undetectable in PCa cells, in which the EGFR expression was upregulated. Conclusion: The loss of CMTM5 may participate in the progression of PCa resulting from deregulated EGFR.