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Downregulation of stathmin 1 in human gallbladder carcinoma inhibits tumor growth in vitro and in vivo.

ABSTRACT: Gallbladder carcinoma (GBC) is a highly lethal malignancy of the gastrointestinal tract. Despite extensive research, the underlying molecular mechanism of GBC remains largely unclear. Stathmin 1 (STMN1) is an important cytosolic protein associated with microtubule stability that was reported to be involved in tumorigenesis. Up to our knowledge, its role in gallbladder carcinoma has not been analyzed. In this study, we found that STMN1 was significantly highly expressed in GBC by immunohistochemistry (IHC). Further research demonstrated that silencing of STMN1 inhibited cell growth in vitro. Moreover, knockdown of STMN1 induced apoptosis and delayed G2/M phase transformation in GBC cells. Our data support a rationale for further studies that the silencing of STMN1 may regulate the activity of p38 MAPK kinase and p53/p21 signal pathway. Besides, xenografted gallbladder carcinoma cells growth were significantly impaired after STMN1 was silenced in vivo. These results suggested that STMN1 played an important role in cell proliferation and migration. This provided a potential clue for investigating the therapeutic target in GBC.

SUBMITTER: Wang J

PROVIDER: S-EPMC4923895 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Downregulation of stathmin 1 in human gallbladder carcinoma inhibits tumor growth in vitro and in vivo.

Wang Jiwen J Yao Yanli Y Ming Yue Y Shen Sheng S Wu Nan N Liu Jiaqi J Liu Han H Suo Tao T Pan Hongtao H Zhang Dexiang D Ding Kan K Liu Houbao H

Scientific reports 20160628

Gallbladder carcinoma (GBC) is a highly lethal malignancy of the gastrointestinal tract. Despite extensive research, the underlying molecular mechanism of GBC remains largely unclear. Stathmin 1 (STMN1) is an important cytosolic protein associated with microtubule stability that was reported to be involved in tumorigenesis. Up to our knowledge, its role in gallbladder carcinoma has not been analyzed. In this study, we found that STMN1 was significantly highly expressed in GBC by immunohistochemi ...[more]

PMID: 27349455

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Project description:Lung cancer is one of the most common malignancies worldwide, but its pathogenesis remains unknown. The current study examined the effects of heterogeneous nuclear ribonucleoprotein K (hnRNP K)-targeted small interfering RNA (siRNA) on the growth and apoptosis of lung cancer cells in vitro. The expression of hnRNP K was studied by the SP method of immunohistochemistry in lung tissue samples of 70 cases of lung cancer. hnRNP K siRNA were transfected into human lung cancer cell line, A549, using Lipofectamine 2000. Cells transfected with siRNAn and untreated served as controls. The inhibitory effect of siRNA on the expression of hnRNP K mRNA and protein was detected by reverse transcription polymerase chain reaction and western blot analysis. The change in cell cycling and cell apoptosis of siRNA-treated cells was detected by flow cytometry. The rates of positive hnRNP K expression in lung tumors of diameters ≤3, 3-5 and ≥5 cm, were 38.5, 95.2 and 91.7%, respectively. A significant difference was identified between lung tumors with diameters of ≤3 and ≥3 cm (P<0.01). The expression of hnRNP K mRNA was significantly inhibited in siRNA-transfected cells compared with that in control cells (P<0.05). Notably, hnRNP K protein decreased in hnRNP K siRNA-transfected cells, but exhibited no effect on the control groups. siRNA targeting human hnRNP K effectively inhibited the growth of lung cancer cell line, A549, and the distribution of the cell cycle. The apoptosis rate was 4.79% and the number of cells increased in the G0/G1 phase from 37.21 to 85.60% and decreased in the S and G2/M phases from 47.71 to 13.50% and 14.00 to 0.32%, respectively, following 24 h of transfection. hnRNP K siRNA promotes A549 apoptosis and the apoptosis rate was 4.79% (P<0.01). Therefore, hnRNP K siRNA may inhibit the proliferation of A549 cells. In addition, hnRNP K promotes the growth of lung cancer cells and, therefore, hnRNP K siRNA may inhibit the growth and increase the apoptosis of lung cancer cells.

Project description:BackgroundThe incidence of cutaneous squamous cell carcinoma (CSCC), a malignant tumor that threatens human life, is increasing every year, and yet its pathogenesis is still unclear. This study found that long noncoding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) was abnormally expressed in CSCC. However, the biochemical mechanisms of lncRNA NEAT1 in carcinogenesis and the development of cancer remain unclear.MethodsFluorescence quantitative polymerase chain reaction (qPCR) was conducted to determine lncRNA NEAT1 expression in CSCC and paracarcinoma tissues and investigate the correlation between NEAT1 levels and patients' clinicopathological features. The invasion, proliferation, and migration of CSCC cells were measured using colony formation, Cell Counting Kit-8, and Transwell assays. Western blot assay was conducted to test whether NEAT1 knockdown affected invasion and migration-related proteins. In addition, a nude mouse subcutaneous tumorigenesis experiment was performed to determine whether the knockdown of NEAT1 affected the proliferation ability of CSCC cells.ResultsChanges in lncRNA NEAT1 expression in CSCC tissues were correlated with the degree of lymph node metastasis and the tumor, regional lymph nodes, and distant metastasis (TNM) grade of patients. The downregulation of NEAT1 lncRNA significantly impeded cell invasion, proliferation, and migration in CSCC. Through lncRNA NEAT1 knockdown, significant reductions in metalloproteinase-2, metalloproteinase-9, N-cadherin, and vimentin expression were observed, and the level of E-cadherin increased. In vivo experiments in nude mice revealed that knockdown of lncRNA NEAT1 greatly inhibited cell proliferation in CSCC.ConclusionsIn CSCC tissues, NEAT1 lncRNA was expressed at high levels and correlated with lymph node metastasis and TNM stage. The knockdown of NEAT1 lncRNA could significantly impede CSCC proliferation, metastasis, and invasion. Additionally, by measuring the expression level of lncRNA NEAT1, we may be able to detect the clinical and pathological characteristics of CSCC.

Dataset Information

Downregulation of stathmin 1 in human gallbladder carcinoma inhibits tumor growth in vitro and in vivo.

Publications

Downregulation of stathmin 1 in human gallbladder carcinoma inhibits tumor growth in vitro and in vivo.

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