MiR-182 affects renal cancer cell proliferation, apoptosis, and invasion by regulating PI3K/AKT/mTOR signaling pathway.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-182 affects renal cancer cell proliferation, apoptosis, and invasion by regulating PI3K/AKT/mTOR signaling pathway, by J.-H. Fu, S. Yang, C.-J. Nan, C.-C. Zhou, D.-Q. Lu, S. Li, H.-Q. Mu, published in Eur Rev Med Pharmacol Sci 2018; 22 (2): 351-357-DOI: 10.26355/eurrev_201801_14179-PMID: 29424922" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/14179.

CD18 inhibits progression of kidney cancer by down-regulating Treg cell levels.

OBJECTIVE: Gene mutation is closely related to the occurrence of tumor. Renal cell carcinoma is a malignant tumor, seriously threatening patients' life quality. Regulatory T cells (Treg) play important roles in the development of several cancers. This study aimed to investigate whether CD18 affects renal carcinoma cell proliferation. MATERIALS AND METHODS: Thirty mice with renal cell carcinoma were constructed using gene-engineering mouse with CD18 deficiency, and another 30 normal C57 mice were used as control. Ki67 and micro-vessel density were detected by using immunohistochemistry (IHC) and immunofluorescence, respectively. The expression of CD3, CD4 and CD8 were detected in blood and spleen by quantitative PCR (q-PCR). Flow cytometry was used to detect the changes of Treg cells. RESULTS: The expression of Ki67 in C57 was significantly higher than that in CD18-/- mice (p<0.05). IHC results showed that CD31 was also significantly downregulated in CD18-/- group compared to control group (p<0.05). It was found that only high expression of CD4 in mesenteric lymph nodes of CD18-/- was considered as non-tumor-bearing. Flow cytometry results showed that Treg cells were significantly decreased in CD18-/- compared to C57 group (p<0.05). CONCLUSIONS: CD18-/- down-regulates Treg cells and inhibits the pathogenesis of renal cell carcinoma.

MiR-182 affects renal cancer cell proliferation, apoptosis, and invasion by regulating PI3K/AKT/mTOR signaling pathway.

OBJECTIVE: PI3K/AKT/mTOR signaling pathway plays a crucial role in tumorigenesis and development. It was shown that mTOR overexpression was associated with the pathogenesis of renal cancer. Down-regulation of MiR-182 was found in renal carcinoma tissue. This study thus aims to investigate the influence of miR-182 in regulating mTOR expression and renal carcinoma cell proliferation, invasion, and apoptosis. PATIENTS AND METHODS: The targeted regulatory relationship between miR-182 and mTOR was tested by dual luciferase assay. Renal carcinoma tissue and benign renal tissue were collected to detect miR-182 and mTOR expressions. MiR-182, mTOR, p-mTOR, and Survivin levels were compared between HK-2 and A498 cells. Renal carcinoma A498 cells were divided into four groups, including miR-NC, anti-miR-182 mimic, si-NC, and si-mTOR groups. Cell apoptosis and proliferation were evaluated by flow cytometry. Cell invasion was determined by transwell assay. RESULTS: Bioinformatics analysis revealed the complementary relationship between miR-182 and the 3'-UTR of mTOR mRNA. The level of miR-182 was significantly reduced, while mTOR expression was upregulated in renal carcinoma tissue compared with that in benign lesion, which was associated with TNM stage. MiR-182 expression was markedly declined, whereas mTOR, p-mTOR, and Survivin levels were apparently upregulated in A498 cells compared with that in HK-2 cells. The treatment of miR-182 mimic or si-mTOR transfection significantly downregulated mTOR, p-mTOR, and Survivin expressions, restrained cell proliferation and invasion, and enhanced cell apoptosis. CONCLUSIONS: The decreasing level of miR-182 plays a role in enhancing mTOR expression and promoting renal carcinoma pathogenesis. Overexpression of miR-182 inhibited mTOR expression and weakened cell proliferation and invasion, which provides leads to the future therapy of renal cancer.

Soluble interleukin-1 receptor, a potential negative regulator of orange-spotted grouper Epinephelus coioides interleukin-1 system.

In this study, the cDNA sequence encoding interleukin-1 (Il-1) receptor-like protein of orange-spotted grouper Epinephelus coioides was obtained. The newly identified sequence was named soluble type I Il-1 receptor (sIl-1rI) owing to its structural composition, which had two Ig-like domains, lack of transmembrane region and the Toll/interleukin-1 receptor (TIR) domain, similar to the brown rat Rattus norvegicus soluble Il-1rI. In addition, sequence comparison and phylogenetic analysis indicated that E. coioides sequence had a closer relationship with Il-1rI than Il-1rII. Real-time PCR revealed that sil-1rI mRNA expression presented a process of decrease, restoration and increase in Cryptocaryon irritans-infected E. coioides. The negative correlation between Il-1ß and sil-1rI mRNA in C. irritans-infected head-kidney implied the potential negative regulatory role of sil-1rI in E. coioides Il-1 system. The leucocytes incubated with lipopolysaccharide or polyriboinosinic polyribocytidylic acid exhibited different expression profiles of sil-1rI. Recombinant Il-1ß (rIl-1ß) protein was capable of inducing sil-1rI mRNA under the concentration of 100 ng ml(-1) , suggesting that high dosage or excess Il-1ß would stimulate the expression of sil-1rI to maintain the homoeostasis of E. coioides Il-1 system. For the first time, the role of teleost Il-1rI in parasite infection has been identified, and soluble Il-1r was found in fish.

Identification and expression analysis of major histocompatibility complex IIB gene in orange-spotted grouper Epinephelus coioides.

In this study, complementary DNA (cDNA) and DNA sequences of major histocompatibility complex (MHC) class IIB genes (mhcIIB) were cloned from orange-spotted grouper Epinephelus coioides. The gene structure of E. coioides mhcIIB consists of five exons and four introns, and its deduced amino acid sequence length is 249 amino acids, including a signal peptide, a peptide-binding region, an IGC1 domain, a transmembrane region and a cytoplasmic tail. A phylogenetic study showed that E. coioides mhcIIB shared 32.0-79.1% identity with those of other teleosts and mammals. Real-time reverse transcriptase (RT)-PCR was performed to detect the class IIB gene expression in eight different tissues. To characterize the relationship between E. coioides mhcIIB gene and pathogens, in vivo and in vitro studies were performed. Challenge of Cryptocaryon irritans revealed that class IIB genes were down-regulated after 24 and 48 h of challenge, and their expression was later restored at 72 h. Stimulation of isolated E. coioides leukocytes with lipopolysaccharide (LPS) and polyinosinic:polycytidylic acid (PolyI:C) significantly increased peripheral blood and spleen mhcIIB expression, while head kidney mhcIIB expression remained constant.

50-Hz magnetic field induces EGF-receptor clustering and activates RAS.

PURPOSE: In a previous study, we found that exposure to a 50 Hz magnetic field (MF) could activate stress-activated protein kinase (SAPK) and P38 mitogen-activated protein (MAP) kinase (P38 MAPK) in Chinese hamster lung (CHL) fibroblast cells, and simultaneous exposure to a 'noise' MF of the same intensity inhibited these effects. In order to explore the possible target sites and upstream signal transduction molecules of SAPK and P38 MAPK, and further validate the interference effects of 'noise' MF on 50 Hz MF, the effects of MF exposure on clustering of epidermal growth factor (EGF) receptors and Ras protein activation were investigated. MATERIALS AND METHODS: CHL cells were exposed to a 50 Hz sinusoidal MF at 0.4 mT for different durations, and clustering of EGF receptors on cellular membrane and Ras protein activation were analyzed using immunofluorescence confocal microscopy and co-precipitation technology. EGF treatment served as the positive control. RESULTS: The results showed that, compared with sham-exposed cells, exposure to a 50 Hz MF at 0.4 mT for 5 min slightly induced EGF receptor clustering, whereas exposure for 15 min enhanced receptor clustering significantly. Corresponding to receptor clustering, Ras protein was also activated after exposure to the 50 Hz MF. Exposure to a 'noise' MF (with frequency ranges from 30 - 90 Hz) at the same intensity and durations, did not significantly affect EGF receptor clustering and Ras protein. However, by superimposing the 'noise' MF, receptor clustering and Ras activation induced by 50 Hz MF were inhibited. CONCLUSION: The results suggested that membrane receptors could be one of the most important targets where extremely low frequency (ELF) MF interacts with cells, and Ras may participate in the signal transduction process of 50 Hz MF. Furthermore, a 'noise' MF could inhibit these effects caused by ELF-MF.

Millimeter wave exposure reverses TPA suppression of gap junction intercellular communication in HaCaT human keratinocytes.

The effect of 30.16 GHz millimeter wave (MMW) exposure at 1.0 and 3.5 mW/cm2 on gap junction intercellular communication (GJIC) was studied in cultured HaCaT keratinocytes, using the fluorescence recovery after photobleaching (FRAP) technique and laser confocal scanning microscopy to follow the intracellular movement of 5,6-carboxyfluorescein diacetate dye. While MMW exposure alone for 1 h at either 1.0 or 3.5 mW/cm2 did not affect GJIC, MMW exposure in combination with 5 ng/ml TPA treatment reversed TPA induced suppression of GJIC. Exposure at 1.0 mW/cm2 resulted in a partial reversal, and exposure at 3.5 mW/cm2 resulted in essentially full reversal of the TPA suppression.

ELF magnetic fields induce internalization of gap junction protein connexin 43 in Chinese hamster lung cells.

We have previously demonstrated that exposure of Chinese hamster lung (CHL) cells to 50 Hz magnetic fields (MFs) and/or 12-O-tetradecanoylphorbol-3-acetate (TPA)-inhibited gap junctional intercellular communication (GJIC). To explore and compare the mechanisms of GJIC inhibition induced by extremely low frequency (ELF) MF and TPA, the number and localization of connexin 43 (C x 43) were studied. The localization of C x 43 was determined with indirect immunofluorescence histochemical analysis and detected by confocal microscopy after exposing CHL cells to 50 Hz sinusoidal magnetic field at 0.8 mT for 24 h without or with TPA (5 ng/ml) for the last 1 h. The C x 43 levels in nuclei and in cytoplasm were examined by Western blotting analysis. The results showed that the cells exposed to MF and/or TPA displayed individual plaques at regions of intercellular contact, which were fewer than the normal cells in number, while the number of C x 43 in cytoplasm increased and congregated near the nuclei. Western blot analysis further demonstrated the quantity of changes in location of Cx43. These results suggest that reduction of C x 43 at regions of intercellular contact may be one of the mechanisms of GJIC inhibition induced by ELF MF.

[Effects of electromagnetic field emitted by electric blankets on brain catecholamine in fetal mice].

A study of effects of electromagnetic field emitted by electric blankets on brain catecholamine (CA) content in fetal mice under development was carried out, to determine which component of the electromagnetic field, electric field or magnetic field or both, causes the effects, and to improve the design of the electric blankets. Forty-eight NIH pregnant mice were divided into three groups exposed to electric field, magnetic field and electromagnetic field, respectively for five hours daily during mice's whole gestational periods, and one control group. Twelve infant mice in each group were decapitated at the seventh day after delivery, and sagittal sections of the middle part of their brain were prepared for quantitative histofluorescence analysis of CA with a microspectrophotometer. Results showed brain CA content in all the exposed groups was lower than that in controls, with F values of 18.5 and 37.6 in hypothalamus and hippocampus, respectively. Both electric and magnetic fields could decrease brain CA content in mice, but electric fields had greater effects. It suggested the focus in production of electric blankets should be put on reducing electric field, as well as reducing magnetic field by cloth wiring design. Electric field lowered to less than 100 V/m for the electric blankets with such design from 1 kV/m, and magnetic field to less than 0.08 microT from 1 microT.