[Corrigendum] The effect of NFATc1 on vascular generation and the possible underlying mechanism in epithelial ovarian carcinoma.

Subsequently to the publication of the above article [and an already published Corrigendum that has indicated a corrected version of Fig. 6 (DOI: 10.3892/ijo.2020.5131; published online on October 12, 2020)], the authors have realized that some incorrect data were also included in Fig. 3 in their paper; essentially, Fig. 3A, which was intending to show the siRNA knockdown data for NFATc1 expression in xenograft tumor tissue via immunohistochemical staining, was inadvertently derived from the same data as that shown for Fig. 4F. The corrected version of Fig. 3, featuring the correct data for Fig. 3A, is shown below. The authors confirm that this error did not significantly influence either the results or the conclusions in their paper. The authors are grateful to the Editor of International Journal of Oncology for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 48: 1457­1466, 2016; DOI: 10.3892/ijo.2016.3355].

Holomorphology and neotype designation of Microperla retroloba (Wu, 1937).

Microperla retroloba (Wu, 1937) is a poorly described species from Gansu Province of China and the types of which were apparently lost. Herein, a neotype of M. retroloba is designated based on new material from Ningxia Hui Autonomous Region adjacent to Gansu Province. Male, female, larva and egg morphology of M. retroloba are described, illustrated and compared with all congeners.

[Corrigendum] The effect of NFATc1 on vascular generation and the possible underlying mechanism in epithelial ovarian carcinoma.

Following the publication of the above article, the authors have realized that some incorrect data were included in Fig. 6 in their paper; essentially, the CXCR2 protein bands that were included in the figure were irrelevant, and data for interleukin­8 (IL­8) should have been selected and included in the figure instead. The corrected version of Fig. 6 is shown opposite, now featuring the IL­8 data. The authors confirm that these errors did not significantly influence either the results or the conclusions in their paper. The authors are grateful to the Editor of International Journal of Oncology for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 48: 1457­1466, 2016; DOI: 10.3892/ijo.2016.3355].

Association between Visceral Fat and Bone Mineral Density in Both Male and Female Patients with Adult Growth Hormone Deficiency.

AIM: Adult growth hormone deficiency (AGHD) is associated with an increased risk of fractures. The interactions between various body composition and bone are known to be complex in nature. However, very few studies have examined this crosstalk in AGHD. In this study, we sought to investigate the relationship between various parameters of body composition and bone mineral density (BMD) as well as determine the role of visceral fat in determining the bone mass in patients with AGHD. METHODS: We conducted a cross-sectional study on 57 patients with AGHD. Anthropometry, biochemistry, and analysis of body composition and BMD were performed according to standard protocols. Male and female patients were classified into those with osteoporosis and those without osteoporosis (normal subjects and patients with osteopenia). Further, we analyzed the correlation between the BMD and measurements obtained for various body composition parameters in male and female AGHD patients. RESULTS: Our findings indicated that among female AGHD patients, those with osteoporosis had a significantly higher levels of fat mass (FM) and visceral adipose tissue mass (VATM) (both, P < 0.05) than those without osteoporosis. Further, Pearson correlation analysis showed that the values of age, body mass index (BMI), FM, and VATM correlated negatively with BMD in women with AGHD (all P < 0.05); however, this association was not noted in men. After adjusting for the other covariates, VATM was found to be independently correlated with the BMD in female patients with AGHD. CONCLUSIONS: A close correlation was noted between VATM and BMD in female patients with AGHD.

Effect of PPARγ agonist (rosiglitazone) on the secretion of Th2 cytokine in asthma mice.

OBJECTIVE: To explore the effect of PPARγ agonist (rosiglitazone) on the secretion of Th2 cytokines and the proportion of immune cell subsets in asthma mice. METHODS: Ovalbumin (OVA)-sensitized mice were used to build asthma models. Those mice were divided into the normal control group, model group and rosiglitazone group. Differences of the changes in lung histopathology of mice in the three groups were observed through hematoxylin and eosin (HE) strain, and the numbers of the total cells, eosinophils and neutrophils in BALF of mice in the three groups were compared. ELISA and real-time PCR were employed to detect the protein levels of interleukin (IL)-5, IL-13, IL-4 and IL-10 and mRNA level, respectively. Flow cytometry number was implied to analyze the proportion of immune cell subsets in peripheral blood of mice. RESULTS: Compared with the mice in the control group, and mice of the model group, the infiltration of inflammatory cells in BALF increased, bronchial smooth muscle became thickened, a large amount of collagen deposited, the secretion of Th2 cytokine increased significantly, the ratio of regulatory T cells (Treg) decreased, the ratio of T17 cells rose distinctly; while in mice of the rosiglitazone group, the changes of their lung histopathology were improved obviously, the number of infiltration of inflammatory cells declined, the thickened smooth muscle relieved, the deposition of collagen decreased, the secretion of Th2 cytokine was inhibited, the ratio of Treg went up, and the increased of the ratio of T17 cells was inhibited but still not return to normal level. CONCLUSIONS: Rosiglitazone can regulate the proportion of Treg and Th17 cells and inhibit the secretion of Th2 cytokines, which inhibit the airway inflammatory response for asthma mice effectively.

The effect of NFATc1 on vascular generation and the possible underlying mechanism in epithelial ovarian carcinoma.

We investigated the effect of nuclear factor of activated T cells c1 (NFATc1) on the growth and vascular generation of human ovarian carcinoma SKOV3 cell-transplanted tumors in nude mice and explored the possible underlying mechanism. NFATc1 siRNA was transfected into the SKOV3 cells, which were then subjected to immunofluorescence tests and real-time reverse transcription polymerase chain reaction (RT-PCR) to determine the transfection-induced inhibition rate. The tumor volumes in the nude mice in all groups were measured to determine the in vivo antitumor effect of NFATc1 siRNA. Immunohistochemical (IHC) methods were employed to detect NFATc1 expression in tumor tissue, combined with cytokeratin (CK) staining to label the epithelial origin of the tumor tissue. CD34 and podoplanin were used as markers for labeling microvessels and microlymphatic vessels, respectively. The densities of microvessels and microlymphatic vessels in each group were calculated and statistically analyzed. RT-PCR and western blotting were performed to detect the protein and mRNA expression levels of NFATc1, the ELR+ CXC chemokine interleukin (IL)-8, fibroblast growth factor-2 (FGF-2), and platelet-derived growth factor BB (PDGF BB) in xenografted tumor tissue in all groups. NFATc1 was highly expressed in tumor tissue in the control groups. The intervention group exhibited a tumor growth inhibition rate of 57.08% and presented a lower tumor weight and volume compared with the two control groups. In the control groups, the microvessel densities were 12.00 ± 1.65 and 11.47 ± 0.32, respectively, and the microlymphatic vessel densities were 10.03 ± 0.96 and 9.95 ± 1.12; these values were significantly higher than in the intervention group. RT-PCR and western blot shows that NFATc1 siRNA could markedly suppress the expression of IL-8, FGF-2 and PDGF BB at the mRNA and the protein level. In conclusion, it was shown that NFATc1 siRNA significantly suppresses the growth and vascular generation of SKOV3 human ovarian carcinoma cell-transplanted tumors subcutaneously xenografted into nude mice. The downregulation of the expression of IL-8, FGF-2 and PDGF BB may be one of the mechanisms underlying the above inhibitory effects.

NFATc1 regulates cell proliferation, migration, and invasion of ovarian cancer SKOV3 cells in vitro and in vivo.

NFATc1 (nuclear factor of activated T­cells c1) is associated with malignancy in several cancer models. However, the expression and function of NFATc1 in ovarian cancer remain elusive. In the present study, we investigated the role of NFATc1 in human epithelial ovarian cancer (EOC) using human ovarian adenocarcinoma SKOV3 cells and patient characteristics. NFATc1 expression was silenced by siRNA in the SKOV3 ovarian cancer cell line and in human ovarian cancer nude mouse xenografts. Real­time PCR, western blotting, immunohistochemical staining, MTT, flow cytometry, transwell, erasion trace and mouse assays were used to detect NFATc1 expression, cell proliferation, apoptosis, cell invasion and migration, tumor growth and angiogenesis. Survival analysis was performed to assess the correlation between NFATc1 expression and survival. NFATc1 was overexpressed in the SKOV3 ovarian cancer cell line and in human serous/mucinous ovarian cancer tissues. The silencing of NFATc1 expression by siRNA reduced cell proliferation and migration and promoted apoptosis in vitro and decreased the ovarian cancer cell tumorigenesis in vivo in nude mice. NFATc1 overexpression in high­grade serous ovarian carcinomas was an independent prognostic factor of poor overall survival and of early relapse (P<0.01) in a univariate analysis. Our present data provide evidence that NFATc1 is overexpressed in human serous/mucinous ovarian cancer and is associated with a poor prognosis. NFATc1 silencing regulates the cell cycle, apoptosis, invasion and migration. NFATc1 thus has the potential to be a therapeutic target and to be used in EOC diagnosis and prognosis.

Anti-inflammatory role of microRNA let-7c in LPS treated alveolar macrophages by targeting STAT3.

OBJECTIVE: To explore the expression of microRNA (miRNA) let-7c and its function in chronic obstructive pulmonary disease (COPD) and alveolar macrophage cells. METHODS: Real time PCR was performed to detect the expression of miRNA let-7c in the lung tissue of COPD patients and COPD model in mice. MiRNA let-7c was overexpressed in alveolar macrophages isolated from mice and its effect was measured by the production of pro-inflammation cytokines and the protein level of signal transducer and activator of transcription 3 (STAT3) as well as phosphorylation level of STAT3 after LPS stimulation. Luciferase assay was used to detect the binding of miRNA let-7c and 3'UTR of STAT3. RESULTS: MiRNA let-7c expression was significantly lower in patients with COPD compared with control group, and the similar result was found in COPD mice and LPS stimulated alveolar macrophages. Overexpression of miRNA let-7c in alveolar macrophages inhibited LPS-induced increasing of tumor necrosis factor alpha, interleukin-6 and interleukin-1ß. Luciferase assay showed STAT3 was a targeting of miRNA let-7c in alveolar macrophages. CONCLUSIONS: MiRNA let-7c low expression in COPD can regulate inflammatory responses by targeting STAT3 in alveolar macrophage, which may provide a new target for COPD treatment strategies.