Renal cell carcinoma (RCC) is one of the most common urinary tumors. Previous studies have demonstrated that microRNA (miR)‑181a‑5p has an important role in numerous types of cancer. However, the function of miR‑181a‑5p in RCC remains unknown. In the present study, the expression levels of miR‑181a‑5p in RCC tissues and cell lines were investigated using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis. The results of the RT‑qPCR analyses suggested that the expression of miR‑181a‑5p was upregulated in RCC tissues and cells lines compared with adjacent normal renal tissues and normal renal cell lines. Furthermore, the effect of miR‑181a‑5p on cell proliferation, migration, invasion and apoptosis was investigated in the present study. Overexpression of miR‑181a‑5p was revealed to suppress the apoptosis of 786‑O and ACHN cells, in addition to enhancing the proliferation, migration and invasion abilities of 786‑O and ACHN cells in vitro, thus suggesting that miR‑181a‑5p may function as an oncogene in RCC. However, further studies are required to investigate the underlying mechanism of miR‑181a‑5p and its potential role as a biomarker for early detection and prognosis, in addition to as a therapeutic target in RCC.
Although miR-29c has been shown to be expressed less in various kinds of solid cancers, its expression pattern and tumor-suppressive effects in gliomas remain largely unknown. In this study, we detected miR-29c in 10 nontumoral brain tissues and 60 gliomas of various grades and found that its labeling indexes were significantly lower in gliomas (53.7% for the nontumoral brain tissues, and 18.9, 5.5, and 1.8% for the WHO grade I–II, grade III, and grade IV glioma groups, respectively). We then overexpressed miR-29c in the SNB19 glioblastoma cell line and found that it markedly downregulated the expression level of CDK6, and accordingly increased the percentage of the tumor cells in the G1 phase from 44.5 to 69.1% and decreased the colony formation efficiency from 81.1 to 51.5%. miR-29c overexpression also increased the percentage of apoptotic cells from 27.2 to 54.8%, and led to a more than 50% decrease in the migratory and invasive abilities of the tumor cells. Our study shows that miR-29c can effectively block the proliferation of glioblastoma cells by inducing G1 arrest, promote their apoptosis, and inhibit their migration and invasion. At least some of its tumor-suppressive effects are mediated by specifically downregulating the expression of CDK6. Therefore, miR-29c can be used as a tumor suppressor in the gene therapy of malignant gliomas.
Renal cell carcinoma (RCC) is the third most common urological malignancy in the USA and represents 2‑3% of all adult malignancies. Furthermore, the incidence of RCC has been progressively increasing over recent years. Although the morbidity of treatment has decreased with the use of multidisciplinary synthetic therapy, the prognosis of terminal cancer remains poor, with a 5‑year survival rate of 5‑10%. MicroRNAs (miRs) have been correlated with the regulation of 30‑60% of the protein-coding genes and act as oncogenes or anti‑oncogenes in RCC. Considering this research, miRNAs are likely to be the biomarkers for tumor diagnosis, prognosis and the targets for RCC management. In the present study, 42 formalin‑fixed paraffin‑embedded RCC samples were used. The expression of miR‑572 and the role of miR‑572 in RCC cell proliferation, migration and apoptosis was determined by performing reverse transcription‑quantitative polymerase chain reaction analysis, wound scratch assays, cell proliferation assays, Transwell assays and flow cytometry assays, respectively. Further experiments were conducted to clarify the correlation between miR‑572 expression and clinicopathological variables or overall survival. Furthermore, the expression levels of miR‑572 were evaluated for the prognosis value of patients with RCC. Upregulation of miR‑572 was observed in RCC tissues and RCC cell lines. miR‑572 promoted 786‑O and ACHN cell proliferation and mobility and inhibited early apoptosis. In Cox proportional hazard regression analyses, results of the univariate and multivariate analysis indicated that the patients with low miR‑572 expression had a significantly longer overall survival compared with the patients with high miR‑572 expression (univariate analysis, P=0.037; multivariate analysis, P=0.034). Results of the Kaplan‑Meier survival curves revealed that the patients with downregulated miR‑572 have a significantly longer overall survival compared with the patients with highly expressed miR‑572 (P=0.019). To conclude, the results of the present study suggest that tumor oncogene miR‑572 is a potential biomarker for the diagnosis, treatment and prognosis for RCC.
// Jing Liu 1, 2, 3, * , Jinling Xu 1, 2, 3, * , Huining Li 1, 2, 3, * , Cuiyun Sun 1, 2, 3 , Lin Yu 4 , Yanyan Li 1, 2, 3 , Cuijuan Shi 1, 2, 3 , Xuexia Zhou 1, 2, 3 , Xiuwu Bian 5 , Yifang Ping 5 , Yanjun Wen 1, 2, 3 , Shujun Zhao 1, 2, 6 , Hui Xu 1, 2, 3 , Linlin Ren 1, 2, 3 , Tongling An 1, 2, 3 , Qian Wang 1, 2, 3 , Shizhu Yu 1, 2, 3 1 Department of Neuropathology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China 2 Tianjin Key Laboratory of Injuries, Variations and Regeneration of the Nervous System, Tianjin 300052, China 3 Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin 300052, China 4 Department of Biochemistry, Basic Medical College of Tianjin Medical University, Tianjin 300070, China 5 Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing 400038, China 6 Laboratory of Hormone and Development, Ministry of Health, Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, China * These authors have contributed equally to this work Correspondence to: Shizhu Yu, e-mail: tjyushizhu@yahoo.com Qian Wang, e-mail: wangqiantni@163.com Keywords: gliomas, miR-146b-5p, TRAF6, proliferation, apoptosis, prognosis Received: May 20, 2015 Accepted: July 24, 2015 Published: August 06, 2015 ABSTRACT Down-regulation of miR-146b-5p contributes to tumorigenesis in several human cancers. However, the relevance of miR-146b-5p to prognosis, proliferation and apoptosis in gliomas remains unknown. In the present study, we demonstrated that miR-146b-5p expression was inversely correlated with grades and Ki-67 index in 147 human glioma specimens, but positively correlated with patients’ survival. Furthermore, two distinct subgroups of patients with grade I-IV gliomas with different prognoses were identified according to miR-146b-5p expression in our specimens. Cox regression showed that miR-146b-5p was an independent predictor for patients’ survival. Overexpression of miR-146b-5p dramatically suppressed glioma cell proliferation and induced apoptosis. Mechanistically, we validated TRAF6 as a direct functional target of miR-146b-5p and found that miR-146b-5p overexpression significantly decreased phosphorylated TAK1 and IκBα, the pivotal downstream effectors of TRAF6. Moreover, TRAF6 expression was positively correlated with glioma grades and Ki-67 index but inversely correlated with miR-146b-5p expression and predicted poor prognosis of glioma patients. In glioblastoma cell lines, silencing of TRAF6 could mimic the anti-tumor effect of miR-146b-5p. Our findings identify miR-146b-5p as a tumor suppressor and novel prognostic biomarker of gliomas, and suggest miR-146b-5p and TRAF6 as potential therapeutic candidates for malignant gliomas.
Butyrophilin 1A1 (BTN1A1) and xanthine oxidoreductase (XOR) are highly expressed in the lactating mammary gland and are secreted into milk associated with the milk fat globule membrane (MFGM). Ablation of the genes encoding either protein causes severe defects in the secretion of milk lipid droplets, suggesting that the two proteins may function in the same pathway. Therefore, we determined whether BTN1A1 and XOR directly interact using protein binding assays, surface plasmon resonance analysis, and gel filtration. Bovine XOR bound with high affinity in a pH- and salt-sensitive manner (KD=101+/-31 nM in 10 mM HEPES, 150 mM NaCl, pH 7.4) to the PRY/SPRY/B30.2 domain in the cytoplasmic region of bovine BTN1A1. Binding was stoichiometric, with one XOR dimer binding to either two BTN1A1 monomers or one dimer. XOR bound to BTN1A1 orthologs from mice, humans, or cows but not to the cytoplasmic domains of the closely related human paralogs, BTN2A1 or BTN3A1, or to the B30.2 domain of human RoRet (TRIM 38), a protein in the TRIM family. Analysis of the protein composition of the MFGM of wild type and BTN1A1 null mice showed that most of the XOR in mice lacking BTN1A1 was released from the MFGM in a soluble form when the milk lipid droplets were disrupted to prepare membrane, compared with wild-type mice, in which most of the XOR remained membrane-bound. Thus BTN1A1 functions in vivo to stabilize the association of XOR with the MFGM by direct interactions through the PRY/SPRY/B30.2 domain. The potential significance of BTN1A1/XOR interactions in the mammary gland and other tissues is discussed.
Following the publication of the above article and a corrigendum (10.3892/etm.2018.6333) that was concerned with changes in the authorship and affiliation details on the paper, an interested reader has drawn to the authors’ attention that, in Fig. 5A on p. 441, the ‘ACHN/cell invasion/miR‑199b‑5p inhibitor’ and ‘ACHN/cell invasion/NCin’ data panels appeared to show an overlapping section of data, such that they were derived from the same original source when they were intended to show the results from differently performed experiments. The authors have re‑examined their data, and realize that the ‘ACHN/cell invasion/NCin’ data panel was inadvertently selected incorrectly. The corrected version of Fig. 5, now containing the correct data for the ‘ACHN/cell invasion/NCin’ experiment, is shown on the next page. Note that the error made during the compilation of this figure did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Experimental and Therapeutic Medicine for offering them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Experimental and Therapeutic Medicine 16: 436‑444, 2018; DOI: 10.3892/etm.2018.6151]
Beneficial effects of green tea (Camellia sinensis, Theaceae) extracts against obesity have been reported; however, the anti-obesity ability of the major components of green tea, polysaccharides, polyphenols and caffeine is not clear. Therefore, experiments with total green tea extracts, polyphenols, polysaccharides, caffeine, and a complex of polysaccharide and polyphenol at a dose of 400 or 800 mg kg⁻¹ were conducted on high-fat diet fed rats for 6 weeks to investigate their anti-obesity effects. The results indicated that polyphenols and polysaccharides were responsible for the suppressive effect of green tea extracts on body weight increase and fat accumulation. Moreover, polyphenols, polysaccharides, or caffeine can improve blood lipid and antioxidant levels, and effectively reduce rat serum leptin levels, inhibit the absorption of fatty acids, and markedly reduce the expression levels of the IL-6 and TNF-α gene. Furthermore, it was shown that polysaccharides and polyphenols were synergistic in reduction of serum leptin levels and in anti-inflammatory activity. These results suggest that the polysaccharide combination with polyphenols might be a potential therapy against obesity.
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