粘附分子CD44v6在宫颈癌组织中的表达及意义

目的:了解粘附分子CD44v6在宫颈癌组织中的表达及其意义。方法:采用免疫组织化学法(SP法)检测CD44v6在69例宫颈癌组织及20例正常宫颈组织中的表达。结果:正常宫颈组织中的CD44v6呈阴性表达。69例宫颈癌组织中CD44v6的阳性表达率为68.1％(47/69)。CD44v6的阳性表达在不同的病灶大小、临床分期、细胞分化程度及有无淋巴结转移的宫颈癌组织中差异有统计学意义(P<0.05～0.01);在不同的病理类型及年龄的患者中差异无统计学意义(P>0.05)。结论;CD44V6可能在宫颈癌的生长、浸润及转移过程中起重要作用,可望作为反映宫颈癌恶性潜能的新指标。     

Effect of Oversulfation on the Composition,Structure, and In Vitro Anti-Lung Cancer Activity of Fucoidans Extracted from Sargassum aquifolium

Intensive efforts have been undertaken in the fields of prevention, diagnosis, and therapy of lung cancer. Fucoidans exhibit a wide range of biological activities, which are dependent on the degree of sulfation, sulfation pattern, glycosidic branches, and molecular weight of fucoidan. The determination of oversulfation of fucoidan and its effect on anti-lung cancer activity and related signaling cascades is challenging. In this investigation, we used a previously developed fucoidan (SCA), which served as a native fucoidan, to generate two oversulfated fucoidan derivatives (SCA-S1 and SCA-S2). SCA, SCA-S1, and SCA-S2 showed differences in compositions and had the characteristic structural features of fucoidan by Fourier transform infrared (FTIR) and nuclear magnetic resonance (NMR) analyses. The anticancer properties of SCA, SCA-S1, and SCA-S2 against human lung carcinoma A-549 cells were analyzed in terms of cytotoxicity, cell cycle, Bcl-2 expression, mitochondrial membrane potential (MMP), expression of caspase-3, cytochrome c release, Annexin V/propidium iodide (PI) staining, DNA fragmentation, and the underlying signaling cascades. Our findings indicate that the oversulfation of fucoidan promotes apoptosis of lung cancer cells and the mechanism may involve the Akt/mTOR/S6 pathway. Further in vivo research is needed to establish the precise mechanism whereby oversulfated fucoidan mitigates the progression of lung cancer.     

信号通路在肝癌发生过程中的作用及靶向治疗策略

肝癌是一种多病因参与、多阶段病变的复杂疾病。研究表明,参与调节机体重要生理过程的一些信号通路异常与癌变密切相关。该文综述了在肝癌发生过程中一些信号通路的异常现象,总结并分析了以信号通路为靶点的临床药物研究策略及未来发展方向。对这些信号通路作用机制进行深入细致了解将有助于寻找更为合适而有效的治疗靶点。     

Squamous cell carcinoma in a digit of the hind limb with systemic metastasis in a 17-year-old female koala

We encountered a case of cutaneous squamous cell carcinoma (SCC) in a 17-year-old female koala at a zoo. A fragile, papillary, elevated mass was found on the third digit of the right hind limb. SCC was identified histopathologically: squamous cell-like polygonal tumor cells showed a nest-like growth pattern with epidermal down growth, central keratinization and necrotic foci, and invaded dermal connective tissues. Metastatic lesions were observed in various organs, including the lung and axillary lymph node: in the lung, multiple metastatic foci similar to the primary lesion, and in the axillary lymph node, individual polygonal tumor cells infiltrated the sinusoids. Immunohistochemistry revealed that the tumor cells were positive for proliferating cell nuclear antigen, which exhibited 32–33% of labeling indices in the tumor cells. To our knowledge, this is the first report of a case of SCC in a digit of a koala.     

洛伐他汀影响人高转移卵巢癌细胞系HO-8910PM转移相关能力的研究

目的研究洛伐他汀对人高转移卵巢癌细胞系HO-8910PM转移相关能力的影响。方法分别运用MTT法、Transwell小室法、细胞粘附人工重组基底膜实验检测洛伐他汀对HO-8910PM细胞的细胞毒作用,对细胞的侵袭能力和趋化运动及对细胞粘附能力的影响。结果洛伐他汀作用HO-8910PM细胞6h后能抑制其体外侵袭、趋化运动和粘附能力,其中8μmol/L抑制率分别为(79.18±0.21)%、(59.40±0.80)%和(14.08±1.28)%。结论洛伐他汀能有效地抑制人高转移卵巢癌细胞系HO-8910PM的侵袭、趋化运动和粘附能力,是潜在的抗肿瘤转移药物。     

肝癌细胞系中Runx3基因表达及启动子区异常甲基化分析

目的：通过检测6种肝癌细胞中Runx3基因异常甲基化状态及表达情况,探讨药物5-aza-2＇-deoxycytidine（decitabine）激活Runx3基因重新表达的能力及对肝癌细胞生长的影响。方法：采用DNA甲基化特异性PCR（MSP）技术分别对6种肝细胞癌细胞系Runx3基因启动子区域甲基化状态进行检测,同时采用逆转录一聚合酶链反应（RT—PCR）检测5种肝癌细胞中Runx3的表达情况及药物5-aza-2＇-deoxycytidine处理其中3种肝癌细胞前后Runx3表达变化。结果：6种肝癌细胞系中,有3种细胞Runx3基因启动子区域存在甲基化异常,药物5-aza-2＇-deoxycytidine处理3种肝癌细胞后,Runx3基因明显表达或表达活性增强。结论：启动子区异常甲基化是导致Runx3基因失活的主要原因之一,与肝细胞癌发生早期密切相关,可作为肝细胞癌早期诊断的分子标记物及分子治疗的靶点。     

茶叶提取物对抗肺癌细胞(A549)体外试验研究

观察表没食子儿茶素没食子酸酯(EGCG)、茶黄素-3、3'-双没食子酸酯(TFDG)、茶黄素(TF)、茶黄素复合物(TFs)、葡萄籽提取物(GrapeSeedExtract,GSE)、松树皮提取物(PineBarkExtract,PBE)、咖啡因(Caf)、槲寄生(VCE)和茶氨酸(The)的体外抗癌活性,通过人肺癌细胞(A549)进行体外试验,结果表明除咖啡因、槲寄生、茶氨酸的作用较小以外其他几种均有很强的促进人肺癌细胞(A549)凋亡的作用,并且EGCG的作用最强,顺序为EGCG、TFs>GSE>PBE、TFDG>TF。用作图法求得EGCG、GSE、PBE、TFDG和TF的IC50值分别为1.01μM、21.91μM、31.01μM、32.87μM和279.67μM。     

Mortalin expression in cervical squamous-cell carcinoma and its effect on tumor metastasis

AIM: To investigate the significance of mortalin expression in clinical pathology of cervical squamous-cell carcinoma. METHODS: Immunofluorescence staining was used to detect the location of mortalin in human cervical squamous-cell carcinoma SiHa cells. The protein expression of mortalin was detected in 59 cases of normal cervical epithelial tissues and 93 cases of cervical squamous-cell carcinoma tissues by immunohistochemical staining, and its correlation with clinicopathological features of cervical squamous-cell carcinoma was also analyzed. MTT assay was used to evaluate the optimal concentration and dosing time of mortalin inhibitor MKT-077. After the protein expression of mortalin in SiHa cells was inhibited, wound-healing and migration assays were performed. The protein expression of epithelial-mesenchymal transition (EMT)-related molecules was determined by Western blot. RESULTS: Immunofluorescence staining showed that mortalin was located in the cytoplasm of SiHa cells. The positive rate and strongly positive rate of mortalin in the cervical squamous-cell carcinoma patients were 88.7% (55/62) and 61.3% (38/62), respectively, and they were significantly higher than those in normal cervical epithelial tissues (23.7% and 5.1%, P < 0.01). Additionally, mortalin expression was statistically correlated with the histological grade, clinical stage and lymph node metastasis. After inhibiting the expression of mortalin in the SiHa cells by MKT-077, the results of wound-healing and migration assays showed that the migration ability of SiHa cells was down-regulated. The protein expression of E-cadherin was up-regulated, and vimentin and Snail were significantly down-regulated. CONCLUSION: Mortalin over-expression is an effective biomarker for prediction of malignant potential and poor prognosis of cervical squamous-cell carcinoma.     

IL-17 promotes viability and migration ability of endometrial carcinoma cells by inhibiting miR-195-5p expression

AIM:To investigate the potential mechanism of interleukin-17 (IL-17) promoting the viability, migration and invasion of human endometrial carcinoma cells. METHODS:The expression of IL-17 and microRNA-195-5p (miR-195-5p) in the human endometrial carcinoma and benign uterine lesion samples were detected by RT-qPCR. The expression of miR-195-5p in human endometrial carcinoma HEC-1-B cells after treatment with IL-17 at different concentrations for 48 h was detected by RT-qPCR. The viability, migration and invasion of HEC-1-B cells after treatment with IL-17 at 100 μg/L or transfection of miR-195-5p mimics were detected by MTT assay and Transwell assays. The viability, migration and invasion of HEC-1-B cells after over-expression of miR-195-5p combined with 100 μg/L IL-17 intervention were also observed. RESULTS:The expression of IL-17 was increased while the expression of miR-195-5p was decreased in the human endometrial carcinoma samples (P<0.05). The expression of miR-195-5p in the HEC-1-B cells after treatment with IL-17 at 10,100 and 300 μg/L for 48 h was significantly decreased (P<0.05). The results of MTT assay and Transwell experiments indicated that IL-17 at 100 μg/L enhanced the viability, migration and invasion of HEC-1-B cells, while over-expression of miR-195-5p resulted in the opposite effect. CONCLUSION:Over-expression of miR-195-5p inhibits the enhancing effects of IL-17 on the viability, invasion and migration of HEC-1-B cells.