Translationally controlled tumor protein: the mediator promoting cancer invasion and migration and its potential clinical prospects

Translationally controlled tumor protein (TCTP) is a highly conserved multifunctional protein localized in the cytoplasm and nucleus of eukaryotic cells. It is secreted through exosomes and its degradation is associated with the ubiquitin-proteasome system (UPS), heat shock protein 27 (Hsp27), and chaperone-mediated autophagy (CMA). Its structure contains three α‍-helices and eleven β‍-strands, and features a helical hairpin as its hallmark. TCTP shows a remarkable similarity to the methionine-R-sulfoxide reductase B (MsrB) and mammalian suppressor of Sec4 (Mss4/Dss4) protein families, which exerts guanine nucleotide exchange factor (GEF) activity on small guanosine triphosphatase (GTPase) proteins, suggesting that some functions of TCTP may at least depend on its GEF action. Indeed, TCTP exerts GEF activity on Ras homolog enriched in brain (Rheb) to boost the growth and proliferation of Drosophila cells. TCTP also enhances the expression of cell division control protein 42 homolog (Cdc42) to promote cancer cell invasion and migration. Moreover, TCTP regulates cytoskeleton organization by interacting with actin microfilament (MF) and microtubule (MT) proteins and inducing the epithelial-mesenchymal transition (EMT) process. In essence, TCTP promotes cancer cell movement. It is usually highly expressed in cancerous tissues and thus reduces patient survival; meanwhile, drugs can target TCTP to reduce this effect. In this review, we summarize the mechanisms of TCTP in promoting cancer invasion and migration, and describe the current inhibitory strategy to target TCTP in cancerous diseases.     

Serum levels of bone alkaline phosphatase in breast and prostate cancers with bone metastasis

BALP activity in the sera of metastatic patients of breast and prostate malignancy has increased significantly. Our studies with patients in India conform the earlier reports that BALP may have a useful complementary role in the early diagnosis of bone metastases.     

乳腺癌细胞粘附分子CD_(15)的表达及其与预后因素的关系

应用免疫组化SP法对94例乳腺癌、41例乳腺良性病变和10例正常乳腺组织进行了细胞粘附分子CD_(15)检测。结果发现,CD_(15)。在乳腺癌和乳腺良性病变的阳性率分别为79.8％和58.3％,两者有显著差异性(P<0 01),10例正常乳腺组织仅4例呈CD_(15)弱阳性反应。CD_(15)表达与患者年龄和肿瘤大小无显著关系。CD_(15)表达阳性率在浸润性导管癌中显著高于单纯癌(P<0.05),组织学Ⅱ～Ⅲ级显著高于Ⅰ级者(P<0.05),临床Ⅲ一Ⅳ期显著高于Ⅰ期和Ⅱ期者(P<0.05),淋巴结转移阳性组显著高于阴性组(P<0.01)。在一组原发部位和淋巴结转移性乳腺癌配对标本中,CD_(15)表达无明显差异性。CD_(15)阳性的乳腺癌Cath-D和c-erbB-2的表达阳性率均显著高于CD_(15)阴性者(P<0.001)。结果提示,CD_(15)的表达与乳腺癌的发生发展、浸润转移及预后有密切关系。     

中药对乳腺癌内分泌治疗的减毒作用研究

中药治疗乳腺癌有着广泛的临床适应证,尤其在内分泌治疗毒副反应研究方面有着显著的优势。对提高患者生存率,降低复发转移率,改善患者的生活质量具有极其重要的临床意义和广泛的应用前景。     

E-cadherin在涎腺粘液表皮样癌的表达及其与浸润转移的关系

目的:细胞粘附功能下降是恶性肿瘤发展的关键因素,为探讨E-cadherin在涎腺粘液表皮样癌发病机制中的作用,我们研究了E-cadherin在涎腺粘液表皮样癌的表达情况,并分析其与临床病理特征的关系。方法:采用免疫组织化学S-P法对46例涎腺粘液表皮样癌进行E-cadherin的检测。结果:E-cadherin在涎腺粘液表皮样癌中的表达强弱与癌组织的分化程度及淋巴结转移有关(P<0.05),而与患者的性别、年龄无关(P>0.05)。结论:E-cadherin表达与涎腺粘液表皮样癌的浸润转移有关,可作为一种新的肿瘤标志物,其表达对判断预后有一定的价值。     

基质金属蛋白酶-2在乳腺癌中的表达及与侵袭、转移的关系

[目的]探讨乳腺癌细胞基质金属蛋白酶-2的表达及其与侵袭、转移的关系.[方法]免疫组织化学方法检测60例乳腺癌患者癌组织中MMP-2表达.[结果]MMP-2的表达在乳腺癌细胞明显高于正常乳腺细胞(P<0.01);淋巴结转移组明显高于非淋巴结转移组(P<0.01);在中、低分化组明显高于高分化组(P.<0.01).但与组织学类型无关(P<0.05).[结果]乳腺癌的MMP-2的表达与其侵袭、转移可能相关.     

乳腺癌组织中c-erbB-2、p53和nm23蛋白表达及相互关系和意义

目的　探讨c erbB 2、p53和nm2 3蛋白在乳腺癌组织中的表达与乳腺癌临床病理参数、雌激素受体 (ER)、孕激素受体 (PR)的关系。方法　应用免疫组化ABC法对 5 5例乳腺癌组织中的c erbB 2、p53和nm2 3蛋白表达进行检测。结果　 5 5例乳腺癌中c erbB 2、p53及nm2 3的阳性率分别为 49 1 % (2 7/5 5 )、47 3 % (2 6 /5 5 )和 49 1 % (2 7/5 5 ) ,c erbB 2和p53蛋白在乳腺癌中的阳性率与肿瘤病理分级及淋巴结转移有显著意义 (P <0 0 5 ) ,与雌孕激素受体状况呈负相关 (P <0 0 1 )。nm2 3蛋白在乳腺癌中的阳性率与肿瘤病理分级、淋巴结转移有密切的关系 (p <0 0 5 ) ,与雌孕激素受体状呈正相关 (p <0 0 1 )。 70 9% (3 9/5 5 )肿瘤有上述蛋白的异常表达 ,其中 49 1 % (2 7/5 5 )的肿瘤同时有多个蛋白异常表达。结论　肿瘤的多因素分析比单因素分析更有价值 ,癌基因c erbB 2、nm2 3和抑癌基因p53蛋白的表达异常及协同作用在乳腺癌的发生发展中起重要使用     

Knockdown of OLA1, a regulator of oxidative stress response, inhibits motility and invasion of breast cancer cells

To explore the role of a novel Obg-like ATPase 1 (OLA1) in cancer metastasis, small interference RNA (siRNA) was used to knockdown the protein, and the cells were subjected to in vitro cell migration and invasion assays. Knockdown of OLA1 significantly inhibited cell migration and invasion in breast cancer cell line MDA-MB-231. The knockdown caused no changes in cell growth but affected ROS production. In wound-healing assays, decreased ROS in OLA1-knockdown cells were in situ asso-ciated with the cells' decreased motile morphology. Further, treatment of N-acetylcysteine, a general ROS scavenger, blunted the motility and invasiveness of MDA-MB-231 cells, similar to the effect of OLA1-knockdown. These results suggest that knock-down of OLA1 inhibits breast cancer cell migration and invasion through a mechanism that involves the modulation of intracel-lular ROS levels.     

Vascular architecture:is it a helpful histopathological biomarker for hepatocellular carcinoma?

Hepatocellular carcinoma(HCC) remains one of the major public health problems throughout the world.Although originally associated with tumorigenic processes,liver angiogenesis has also been observed in the context of different liver in-flammatory,fibrotic,and ischemic conditions.Here we investigate the fractal dimension as a quantitator of non-Euclidean two-dimensional vascular geometry in a series of paired specimens of primary HCC and surrounding non-tumoral tissue,and discuss why this parameter might provide additional information regarding cancer behavior.The application of fractal geometry to the measurement of liver vascularity and the availability of a computer-aided quantitative method can eliminate errors in visual interpretation,and make it possible to obtain closer-to-reality numerals that are compulsory for any measurement process.     

基于WoS和CSCD的肿瘤类高被引文章分析

[目的]对WoS和CSCD数据库中1000篇肿瘤类高被引文献的特点进行分析,以期为杂志组稿约稿提供依据。[方法]分别检索2005-2014年间WoS和CSCD数据库中年被引频次前50的肿瘤类文献,分析其第一作者、总被引频次、发表后1~5年内被引频次、文章类型、作者单位、基金情况、学科分布、研究内容和研究方向等,并对其进行统计分析。[结果]WoS数据库中高被引文献的被引频次远高于CSCD数据库[(29218.5±16693.9)次vs. (552.3±308.7)次]。高被引文献中,论著类文章占比重较高(72.8%),且在文章发表后5年内,年被引频次波动不大。流行病学研究、大型临床多中心试验研究、指南类文章以及知名专家述评是被引用的热点文章。[结论]国内外文献学术质量仍存在较大差距。杂志组稿应从流行病类文章、知名专家述评以及多中心临床试验入手,以提高整体被引频次以及学术质量。