Retraction Notice to: A Novel Mechanism of Doxorubicin Resistance and Tumorigenesis Mediated by MicroRNA-501-5p-Suppressed BLID.

[This retracts the article DOI: 10.1016/j.omtn.

Sea-level rise will reduce net CO uptake in subtropical coastal marshes.

Coastal marshes have a significant capacity to sequester carbon; however, sea-level rise (SLR) is expected to result in prolonged flooding and saltwater intrusion in coastal regions. To explore the effects of SLR projections on net CO uptake in coastal marshes, we conducted a "double-check" investigation, including the eddy covariance (EC) measurements of the CO fluxes in subtropical coastal marshes along inundation and salinity gradients, in combination with a mesocosm experiment for analyzing CO flux components under waterlogging and increased salinity conditions. During the same measurement periods, the net ecosystem CO exchange (NEE based on the EC dataset) in an oligohaline marsh was higher than that in a low-elevation mesohaline marsh, whereas the NEE was lower than that in a high-elevation freshwater marsh.

[Differences and Relationship Between Rhizosphere Characteristics and Methane Emissions of Double-cropping Rice Variety].

Six field varieties of early rice and late rice were selected as test materials for field experiments to explore the difference in CH emissions among different rice varieties, and Static Obscura-Gas Chromatography was used to determine the CH gas. The results demonstrated a significant difference in the CH emissions flux between early and late rice varieties. The average yield of total fertility CH emissions was highest in Xiangzaoxian 24 and lowest in Zhuliangyou 819, with a difference of 34.

A Novel Mechanism of Doxorubicin Resistance and Tumorigenesis Mediated by MicroRNA-501-5p-Suppressed BLID.

Doxorubicin is a widely used anthracycline-based anti-tumor agent for both solid and liquid tumors. Mounting evidence has demonstrated that microRNAs (miRNAs) are involved in chemoresistance and tumorigenesis. However, the roles of microRNA-501-5p (miR-501) in doxorubicin resistance and gastric cancer cell proliferation and invasion are still not fully understood.

In vivo and in vitro effect of hepatocarcinoma lymph node metastasis by upregulation of Annexin A7 and relevant mechanisms.

We unveiled the association of Annexin A7 with vascular endothelial growth factor-C (VEGF-C) and the effect of upregulation of Annexin A7 in Hca-F and Hca-P cells on inhibiting hepatocarcinoma (HCC) lymph node metastasis (LNM) in vitro and in vivo. A total of 200 inbred 615 mice were randomly divided into four equal groups inoculated with Hca-F, Hca-P, FAnxa7-upregulated, and PAnxa7-upregulated cells, respectively. The primary tumor, popliteal, inguinal, and iliac lymph nodes were prepared for immunohistochemical (IHC) staining, real-time quantitative polymerase chain reaction (qRT-PCR) analysis, Western blot, and hematoxylin-eosin (H&E) staining.

[Apoptosis of MDA-MB-231 cells induced by berberine alpha-hydroxy beta-decanoylethyl sulfonate].

To investigate the cell proliferation inhibition and apoptosis induced by berberine a-hydroxy f-decanoylethyl sulfonate (HB) on MDA-MB-231 cells in vitro, and the inhibitory effect of HB on the expression of poly adenosine diphosphate RNA polymerase (PARP), MTT assay was used to detect the viability of MDA-MB-231 cells and cell cycle was examined by flow cytometry. The results showed that HB could significantly inhibit the proliferation of MDA-MB-231 cells, and mildly arrested cell cycle progression at S phase. The IC50S for 24, 48 and 72 h treatment were 4.

Galectin-3 in cancer.

Galectin-3 (Gal-3) plays important roles in cell proliferation, adhesion, differentiation, angiogenesis and apoptosis in normal and pathologic tissues. Accumulated evidences indicate that Gal-3 is closely involved in tumor cell transformation, migration, invasion and metastasis. In this review, the associations of the expression and localization of Gal-3 as well as its potential action mechanism in tumorigenesis in a variety of cancers were summarized and concluded.

Annexin A7 and its binding protein galectin-3 influence mouse hepatocellular carcinoma cell line in vitro.

Lymph node metastasis is recognized as an important mode of liver cancer metastasis. Our previous study has built two hepatocarcinoma cell lines, Hca-F with high (75%) and Hca-P with low (25%) incidences of lymph node metastasis, and has indicated that annexin A7 is an important factor in the lymphatic metastasis of tumors. There is evidence that galectin-3 is the binding protein of annexin A7 and works in protein complexes.

[Effect of Ech1 overexpression on biological behavior of mouse hepatocarcinoma Hca-P cells in vitro].

Objective: To investigate the effect of enoyl coenzyme A hydratase-1 (Ech1) on the proliferation and invasion ability of mouse hepatocarcinoma Hca-P cells in vitro.

Methods: Recombinant pcDNA3.1(+)-Ech1 gene and pcDNA3.

Annexin A7 gene is an important factor in the lymphatic metastasis of tumors.

In the tumor malignancy progression, lymph node metastasis (LNM) is recognized as an important factor. In this study, RNA interference (RNAi) was employed to down-regulate ANXA7 gene in Hca-F cells, a hepatocarcinoma cell line with high LNM rate. There was no significant effect on cell proliferation ability, but cell division, motility, and invasion abilities were markedly inhibited.

[Down-regulation of Ech1 decreases the adhesion ability of mouse hepatocarcinoma Hca-F cells].

To examine the differential expression pattern of Ech1 protein in mouse Hca-F and Hca-P hepatocarcinoma cell lines with high and low rates of lymphatic metastasis, respectively, and to investigate the relationships between Ech1 expression and adhesion of Hca-F cells. Fluorescence two-dimensional difference in-gel electrophoresis (2D DIGE) and mass spectrometry were used to detect Ech1 expression. Ech1 gene silencing was achieved by stable transfection of Hca-F cells with a plasmid vector harboring short hairpin RNA (shRNA) targeting Ech1, pGPU6/GFP/Neo-shRNA-Ech1.

Chloride intracellular channel 1 is an important factor in the lymphatic metastasis of hepatocarcinoma.

We have previously demonstrated that chloride intracellular channel 1 (CLIC1) is involved in the lymphatic metastasis of tumors. In this study, a self-designed shRNA sequence of mouse CLIC1 gene was synthesized and inserted into a pGPU6/GFP/Neo plasmid, then stably transfected into mouse hepatic carcinoma cell line Hca-F cells to down-regulate the expression of CLIC1 gene. The levels of expression of CLIC1 mRNA and protein were detected by real-time quantitative polymerase chain reaction (qRT-PCR) and western blot (WB) analysis, respectively.

[Expression of enoyl CoA hydratase 1 reduces cell proliferation and migration in mouse hepatocarcinoma cells].

Objective: To study the expression of enoyl CoA hydratase 1 (ECH1) and the effect when down-regulation of ECH1 gene expression in mouse hepatocarcinoma cell.

Methods: Immunofluorescence was used for detecting the expression of ECH1, and stably transfected Hca-F cells with pGPU6/GFP/Neo-shRNA-ECH1 expression plasmids. Cell proliferation was assessed by Cell counting kit-8 (CCK8) assay.

[Localization and expression of CLIC1 in hepatocarcinoma ascites cell lines with high or low potentials of lymphatic spread].

Objective: To study the localization and expression of CLIC1 in mouse hepatocarcinoma ascites cell lines with different metastatic potentials.

Methods: Mouse hepatocarcinoma ascites models (a high potential of lymphatic metastasis cell line-Hca-F, and a low potential of lymphatic metastasis cell line-Hca-P) were investigated using fluorescent two-dimensional difference-gel electrophoresis (2-D DIGE) and mass spectrometry for detecting the localization and expression of CLIC1. Immunofluorescence, immunocytochemistry and Western blot were used to assess CLIC1 protein status in the two cell lines.

Inhibition of JNK1 expression decreases migration and invasion of mouse hepatocellular carcinoma cell line in vitro.

c-Jun N-terminal kinase (JNK) is located in focal adhesion plaque (FAP). JNK is necessary to growth, morphogenesis, and differentiation of cells; especially JNK1 has a close relation with tumors. In this study, we silenced JNK1 by using short hairpin RNA (shRNA) and examined the effect on migration and invasion of mouse hepatocellular carcinoma (HCC) cell line Hca-F in vitro.

[Effects of silencing chloride intracellular channel 1 gene expression on the proliferation and invasion of mouse hepatocellular carcinoma cell lines].

Objective: To study the effects of silencing CLIC1 gene expression on the proliferation and invasion of Hca-F cells.

Methods: The mouse CLIC1 cDNA sequence was retrieved from NCBI. Three shRNA sequences were designed and cloned into pGPU6/GFP/Neo plasmids.

High expression of osteoglycin decreases gelatinase activity of murine hepatocarcinoma Hca-F cells.

Aim: To investigate the possible correlation between osteoglycin expression and gelatinase activity of mouse hepatocarcinoma Hca-F cells.

Methods: A eukaryotic expression plasmid pIRESpuro3 osteoglycin(+) was constructed and transfected into Hca-F cells to investigate the possible correlation between osteoglycin expression and gelatinase activity of Hca-F cells cultured with extract of lymph node, liver, spleen or in DMEM medium. The activity of gelatinases was examined through zymographic analysis.

[Expression of COX-2 and pregnancy associate plasma protein A in coronary arteries and their relationship with acute coronary syndrome: an autopsy study of 42 cases].

Objective: To study the expression of COX-2 and pregnancy associate plasma protein A (PAPP-A) in coronary arteries and their relationship with acute coronary syndrome.

Methods: Twenty-one autopsy cases with acute coronary syndrome encountered during the period from 2002 to 2007 were enrolled into the study. Another 21 autopsy cases without evidence of acute coronary syndrome were used as the controls.

High-performance liquid chromatography/nano-electrospray ionization tandem mass spectrometry, two-dimensional difference in-gel electrophoresis and gene microarray identification of lymphatic metastasis-associated biomarkers.

The potential biomarkers for the lymphatic metastatic process of mouse hepatocarcinoma were investigated by using two-dimensional difference in-gel electrophoresis (2D DIGE), high-performance liquid chromatography/nano-electrospray ionization tandem mass spectrometry (HPLC/nESI-MS/MS) and GeneChip. 2D DIGE was performed to screen and quantify the differentially expressed proteins between two well-established mouse hepatocarcinoma cell lines, Hca-F with 75% and Hca-P with 25% metastasis rate of lymph node potentials. The protein spots in the gel were visualized by the highly sensitive Deep Purple (GE Healthcare) fluorescent stain.

Identification of differentially expressed genes in mouse hepatocarcinoma ascites cell line with low potential of lymphogenous metastasis.

Aim: To identify genes differentially expressed in mouse hepatocarcinoma ascites cell line with low potential of lymphogenous metastasis.

Methods: A subtracted cDNA library of mouse hepatocarcinoma cell line with low potential of lympho-genous metastasis Hca-P and its synogenetic cell line Hca-F with high metastatic potential was constructed by suppression subtracted hybridization (SSH) method. The screened clones of the subtracted library were sequenced and GenBank homology search was performed.

[Screening for lymphatic metastasis-associated genes in mouse hepatocarcinoma cell lines Hca-F and Hca-P using gene chip].

Background & Objective: Metastasis is a complex process involving multiple genetic changes. The high mortality and poor prognosis caused by metastasis in malignant tumor patients and the uncertain mechanisms are always the prominent problems in the field of oncology. In order to screen for lymphatic metastasis-associated genes, the gene expression profiles of mouse hepatocarcinoma cell lines Hca-F (highly metastatic) and Hca-P (low metastatic) were compared by gene chip.

[Screening of differentially expressed genes in mouse hepatocarcinoma ascites cell line with high potential of lymphatic metastasis].

Objective: To screen genes differentially expressed in mouse hepatocarcinoma ascites cell line with high potential of lymphatic metastasis.

Methods: A subtracted cDNA library of mouse hepatocarcinoma cell line with high potential of lymphatic metastasis Hca-F and its synogenetic cell line Hca-P with low metastatic potential was constructed by suppression subtractive hybridization (SSH) method. The screened clones of the subtracted library were sequenced and GenBank homology search was performed.