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Serum mitochondrial tsRNA serves as a novel biomarker for hepatocarcinoma diagnosis

《医学前沿（英文）》 2022年第16卷第2期页码 216-226 doi: 10.1007/s11684-022-0920-7

摘要： Hepatocellular carcinoma (HCC), which makes up the majority of liver cancer, is induced by the infection of hepatitis B/C virus. Biomarkers are needed to facilitate the early detection of HCC, which is often diagnosed too late for effective therapy. The tRNA-derived small RNAs (tsRNAs) play vital roles in tumorigenesis and are stable in circulation. However, the diagnostic values and biological functions of circulating tsRNAs, especially for HCC, are still unknown. In this study, we first utilized RNA sequencing followed by quantitative reverse-transcription PCR to analyze tsRNA signatures in HCC serum. We identified tRF-Gln-TTG-006, which was remarkably upregulated in HCC serum (training cohort: 24 HCC patients vs. 24 healthy controls). In the validation stage, we found that tRF-Gln-TTG-006 signature could distinguish HCC cases from healthy subjects with high sensitivity (80.4%) and specificity (79.4%) even in the early stage (Stage I: sensitivity, 79.0%; specificity, 74.8%; 155 healthy controls vs. 153 HCC patients from two cohorts). Moreover, in vitro studies indicated that circulating tRF-Gln-TTG-006 was released from tumor cells, and its biological function was predicted by bioinformatics assay and validated by colony formation and apoptosis assays. In summary, our study demonstrated that serum tsRNA signature may serve as a novel biomarker of HCC.

关键词： tsRNA biomarker hepatocarcinoma

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Establishment and drug sensitivity evaluation of murine ascites hepatocarcinoma cell line with high lymphatic

Hongying ZHANG, Jianwu TANG, Wenting ZHU, Chunxiu HU, Guowang XU

《医学前沿（英文）》 2009年第3卷第2期页码 119-129 doi: 10.1007/s11684-009-0022-9

摘要： In order to provide a sensitive cell line model for investigating the mechanisms underlying the lymphatic metastasis of tumors and the effect of medicine against cells, a new murine ascites hepatocarcinoma cell line with high lymphatic metastatic potential (Hca-P/L ) was established and the effect of curcumin on biological behavior of Hca-P/L was observed. Murine ascites hepatocarcinoma cell strain with low lymphatic metastatic potential (Hca-P) was subcutaneously inoculated into the medioventral line of a mouse 615 and the first generation of metastatic tumor cells of inguinal lymph node (Hca-P/L ) was obtained. Then, Hca-P/L was screened by the route of mouse foot pad subcutaneously → lymph node → scale-up culture → mouse foot pad subcutaneously for five times consecutively. The sensitivity of two murine ascites hepatocarcinoma cell lines (Hca-P and Hca-P/L ) and two anchorage-dependent human hepatocarcinoma cell lines (SMC7721 and HepG ) to curcumin were studied by use of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay after these cells had been pretreated by curcumin at the concentration of 15-240 μmol/L for 48 h. After pretreatment by curcumin at the maximum non-cytotoxic dose of 15 μmol/L , the effect of curcumin against cell proliferation of Hca-P and Hca-P/L was observed by inverted microscope, cell growth curve and cell population doubling time; the effects of curcumin on cell cycles of Hca-P/L and Hca-P were studied by flow cytometry (FCM). The results showed Hca-P/L spreading to the lymph nodes at multiple sites in mice was screened from Hca-P. The lymph node metastatic rate was 100%. Curcumin had significant growth inhibiting effect on both murine ascites and human hepatocarcinoma cell lines in a dose-dependent manner ( <0. 05). At concentrations of 30-120 μmol/L, curcumin had more inhibition on murine ascites hepatocarcinoma cell lines than on human anchorage-dependent hepatocarcinoma cell lines. At concentrations of 60-240 μmol/L, curcumin had more inhibition on Hca-P/L with (the 50% inhibitory concentration) IC of 51.48 μmol/L than on Hca-P with IC of 90.87 μmol/L. After pretreatment by curcumin at the maximum non-cytotoxic dose of 15 mol/L for 7 days, the proliferations of Hca-P/L and Hca-P were inhibited ( <0.05) in a time-dependent manner ( <0.01) and the population doubling time of Hca-P/L and Hca-P was prolonged ( <0.01), and curcumin had more inhibition on Hca-P/L than on Hca-P ( <0.05). After pretreatment by 15 μmol/L curcumin for 48 h, the morphous of Hca-P/L was influenced more seriously than that of Hca-P and the cell cycle was redistributed with Hca-P/L being blocked in the S phase and Hca-P in the S and G /M phases. Hca-P/L was validated to be more sensitive to curcumin than Hca-P. Hca-P/L is a novel sensitive cell line model for investigating the mechanisms underlying tumor lymphatic metastasis and the effect of the medicine against cells.

关键词： murine ascites hepatocarcinoma cell line metastasis curcumin drug sensitivity

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transporter 2 genes for increased retention of metaiodobenzylguanidine labeled with iodine 131 in malignant hepatocarcinoma

null

《医学前沿（英文）》 2017年第11卷第1期页码 120-128 doi: 10.1007/s11684-017-0501-3

摘要：

Norepinephrine transporter (NET) transfection leads to significant uptake of iodine-131-labeled metaiodobenzylguanidine (¹³¹I-MIBG) in non-neuroendocrine tumors. However, the use of ¹³¹I-MIBG is limited by its short retention time in target cells. To prolong the retention of ¹³¹I-MIBG in target cells, we infected hepatocarcinoma (HepG2) cells with Lentivirus-encoding human NET and vesicular monoamine transporter 2 (VMAT2) genes to obtain NET-expressing, NET-VMAT2-coexpressing, and negative-control cell lines. We evaluated the uptake and efflux of ¹³¹I-MIBG both in vitro and in vivo in mice bearing transfected tumors. NET-expressing and NET-VMAT2-coexpressing cells respectively showed 2.24 and 2.22 times higher ¹³¹I-MIBG uptake than controls. Two hours after removal of ¹³¹I-MIBG-containing medium, 25.4% efflux was observed in NET-VMAT2-coexpressing cells and 38.6% in NET-expressing cells. In vivo experiments were performed in nude mice bearing transfected tumors; results revealed that NET-VMAT2-coexpressing tumors had longer ¹³¹I-MIBG retention time than NET-expressing tumors. Meanwhile, NET-VMAT2-coexpressing and NET-expressing tumors displayed 0.54% and 0.19%, respectively, of the injected dose per gram of tissue 24 h after ¹³¹I-MIBG administration. Cotransfection of HepG2 cells with NET and VMAT2resulted in increased ¹³¹I-MIBG uptake and retention. However, the degree of increase was insufficient to be therapeutically effective in target cells.