Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
1.
Pathol Res Pract ; 238: 154115, 2022 Oct.
Article in English | MEDLINE | ID: mdl-36084427

ABSTRACT

Hepatocellular carcinoma (HCC) is one of the most common cancers, and has an extremely poor prognosis. Our previous study confirmed that the microRNA miR-361-5p inhibited the proliferation, metastasis, invasiveness, and epithelial-to-mesenchymal transition (EMT) process of HCC by targeting the transcription factor Twist1. Long non-coding RNAs (lncRNAs) are key regulators of processes such as cell differentiation, inflammation, tumor formation, and immune escape. However, the underlying interactions between the lncRNA LINC00992, miR-361-5p, and Twist1 in HCC progression is still elusive. In the current study, the DIANA-lncBase database was used to identify regulatory genes upstream of miR-361-5p. Reverse transcription-quantitative PCR (RT-qPCR) was used to quantify the expression of the genes encoding LINC00992, miR-361-5p, and Twist1 in HCC cells. The cell counting kit-8 (CCK-8) was used to measure HCC cell proliferation and Transwell was used to measure HCC cell migration and invasion. The dual-luciferase reporter assay and RNA pull-down assay were performed to examine the interaction between LINC00992 and miR-361-5p. Western blotting was used to detect the levels of Twist1 protein. The result confirmed that, among three lncRNAs tested, miR-361-5p was the one most significantly affected by LINC00992. RT-qPCR revealed that LINC00992 was highly expressed in HCC tissues and cells. The follow-up results showed that the expression of LINC00992 and miR-361-5p in HCC tissues were closely correlated with the rate of metastasis or recurrence of the HCC patients. Our result showed that the expression of miR-361-5p was lower in the LINC00992 (+) group than in the LINC00992 (-) group. CCK-8 and Transwell showed that LINC00992 promoted HCC cell proliferation, migration, and invasion, whereas dual-luciferase reporter assay and RNA pull-down assay showed that LINC00992 combined with miR-361-5p to act as a miRNA decoy in HCC. RT-qPCR and Western blotting confirmed that LINC00992 upregulated the expression of the Twist1 gene in HCC cells by downregulating expression of miR-361-5p. CCK-8 and Transwell assays confirmed that LINC00992 promoted the proliferation, metastasis, and invasiveness of HCC cells by downregulating miR-361-5p levels and consequently upregulating Twist1 expression, implying that these three elements may be promising targets for HCC therapy.

2.
Biomed Res Int ; 2020: 8891876, 2020.
Article in English | MEDLINE | ID: mdl-33381597

ABSTRACT

MicroRNA-361-5p (miR-361-5p) is a tumor suppressor miRNA that is dysregulated in several types of human cancer. However, the functional significance of miR-361-5p in hepatocellular carcinoma (HCC) is unclear. This study explored the biological function of miR-361-5p in regulating the progression of HCC and the underlying molecular mechanism. RT-qPCR analysis showed that miR-361-5p was downregulated in HCC tissues and cell lines. Functional analysis revealed that miR-361-5p acted as a tumor suppressor, inhibiting cell proliferation, migration, and invasion in HCC cell lines. Bioinformatics analyses identified Twist1 as a direct target of miR-361-5p, which was validated by dual-luciferase reporter assays, RT-qPCR, and western blotting. Rescue experiments indicated that Twist1 may mediate the tumor-suppressive effect of miR-361-5p in HCC cells, and this was supported by the effect of miR-361-5p on inhibiting the epithelial-mesenchymal transition (EMT) by targeting Twist1. This study is the first to suggest that miR-361-5p inhibits tumorigenesis and EMT in HCC by targeting Twist1. These findings are valuable for the diagnosis and clinical management of HCC.


Subject(s)
Carcinoma, Hepatocellular , Epithelial-Mesenchymal Transition/genetics , Liver Neoplasms , MicroRNAs , Nuclear Proteins , Twist-Related Protein 1 , Carcinogenesis/genetics , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/metabolism , Carcinoma, Hepatocellular/mortality , Carcinoma, Hepatocellular/pathology , Cell Line, Tumor , Humans , Liver/metabolism , Liver/pathology , Liver Neoplasms/genetics , Liver Neoplasms/metabolism , Liver Neoplasms/mortality , Liver Neoplasms/pathology , MicroRNAs/genetics , MicroRNAs/metabolism , Nuclear Proteins/genetics , Nuclear Proteins/metabolism , Twist-Related Protein 1/genetics , Twist-Related Protein 1/metabolism
3.
Asian Pac J Cancer Prev ; 16(2): 823-9, 2015.
Article in English | MEDLINE | ID: mdl-25684532

ABSTRACT

The aim of the present study was to investigate the expression of the transcription factor Ki-67, ER, PR, Her2/neu, p21, EGFR, and TOP II-α in the tumor tissue of patients with invasive ductal carcinoma(IDC); in addition, we examined correlations between these markers. Two hundred and sixteen IDC patients, who were not previously been treated with chemo- or radiotherapy, were included in the study. All tumors were grade I-III. Expression of molecular markers was determined by immunohistochemical analysis on paraffin-embedded tissue sections. Follow-up data were collected for 3 months to 10 years and analyzed for tumor recurrence, survival time, and prognostic risk factors. We determined Ki-67 expression correlates with the expression of ER, PR, HER-2, EGFR, and TOP-α, as well as lymph node involvement, high tumor grade, lymphovascular invasion, high tumor stage, and high TNM stage in IDC. Positive Ki-67 expression was a risk factor for rapid tumor recurrence and may help tumor progression, leading to poor prognosis in IDC. Ki-67 was directly correlated with EGFR, TOP II-α, lymph node involvement, high tumor grade, lymphovascular invasion, high tumor stage, and high TNM stage in the hormone receptor subtypes of breast cancer. In triple negative breast cancer, Ki-67 correlated with TOP II-α. Expression of Ki-67 correlated with that of ER, PR, HER-2, EGFR, TOP II-α, and p21. In addition, the biomarker Ki-67 has a role as a prognostic factor and indicates a poor prognosis in IDC.


Subject(s)
Antigens, Neoplasm/metabolism , Breast Neoplasms/pathology , Carcinoma, Ductal, Breast/pathology , Cyclin-Dependent Kinase Inhibitor p21/metabolism , DNA Topoisomerases, Type II/metabolism , DNA-Binding Proteins/metabolism , Ki-67 Antigen/metabolism , Neoplasm Recurrence, Local/pathology , Receptor, ErbB-2/metabolism , Receptors, Estrogen/metabolism , Receptors, Progesterone/metabolism , Adult , Aged , Biomarkers, Tumor/metabolism , Breast Neoplasms/metabolism , Breast Neoplasms/mortality , Carcinoma, Ductal, Breast/metabolism , Carcinoma, Ductal, Breast/mortality , Female , Follow-Up Studies , Humans , Lymphatic Metastasis , Middle Aged , Neoplasm Grading , Neoplasm Invasiveness , Neoplasm Recurrence, Local/metabolism , Neoplasm Recurrence, Local/mortality , Neoplasm Staging , Prognosis , Survival Rate , Young Adult
4.
PLoS One ; 9(5): e96080, 2014.
Article in English | MEDLINE | ID: mdl-24867183

ABSTRACT

BACKGROUND AND AIMS: An immune imbalance in the cytokine profile exerts a profound influence on the progression of hepatitis B virus (HBV) infections and hepatocellular carcinoma (HCC). The present study evaluated the immune status of T helper (Th) 17 and Th1 cells in patients with HBV-related and non-HBV-related HCC. METHODS: We randomly enrolled 150 patients with HCC. Blood samples and tissue samples were obtained. The distributions and phenotypic features of Th17 and Th1 cells were determined by flow cytometry and/or immunohistochemistry. RESULTS: Compared to corresponding non-tumor regions, the levels of Th17 and Th1 cells were significantly increased in tumors of patients with HCC (P<0.001). The intratumoral densities of IL-17-producing cells and IFN-γ-producing cells were associated with overall survival (OS, P = 0.001) and disease-free survival (DFS, P = 0.001) of patients with HCC. The ratio of Th17 to Th1 in HBV-related HCC was higher than in non-HBV-related HCC. A multivariate Cox analysis revealed that the Th17 to Th1 ratio was an independent prognostic factor for OS (HR = 2.651, P = 0.007) and DFS (HR = 2.456, P = 0.002). CONCLUSIONS: HBV infections can lead to an imbalance in immune status in patients with HCC. An elevated Th17 to Th1 ratio may promote tumor progression. The Th17 to Th1 ratio could serve as a potential prognostic marker for scoring the severity of HCC.


Subject(s)
Carcinoma, Hepatocellular/immunology , Hepatitis B/immunology , Interleukin-17/immunology , Liver Neoplasms/immunology , T-Lymphocytes, Helper-Inducer/immunology , Th1 Cells/immunology , Th17 Cells/immunology , Carcinoma, Hepatocellular/mortality , Carcinoma, Hepatocellular/virology , Case-Control Studies , Cytokines/metabolism , Disease Progression , Flow Cytometry , Follow-Up Studies , Hepatitis B/mortality , Hepatitis B/virology , Hepatitis B virus/isolation & purification , Humans , Immunoenzyme Techniques , Interleukin-17/metabolism , Liver Neoplasms/mortality , Liver Neoplasms/virology , Prognosis , Survival Rate , T-Lymphocytes, Regulatory/immunology
SELECTION OF CITATIONS
SEARCH DETAIL
...