Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1.

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, "Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1, by Z.-B. Zhong, Y.-J. Wu, J.-N. Luo, X.-N. Hu, Z.-N. Yuan, G. Li, Y.-W. Wang, G.-D. Yao, X.-F. Ge, published in Eur Rev Med Pharmacol Sci 2019; 23(24): 10867-10873-DOI: 10.26355/eurrev_201912_19790-PMID: 31858555" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19790.

Knockdown of long noncoding RNA DLX6-AS1 inhibits migration and invasion of thyroid cancer cells by upregulating UPF1.

OBJECTIVE: Recently, long non- coding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in the development of thyroid cancer (TC), and to explore the underlying mechanism. PATIENTS AND METHODS: DLX6-AS1 expression in both TC cells and tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, transwell assay and wound healing assay were conducted. QRT-PCR and Western blot assay were used to explore the underlying mechanism. Furthermore, the function of DLX6-AS1 was identified in vivo. RESULTS: DLX6-AS1 expression level in TC tissues was significantly higher than that of the corresponding normal tissues. Moreover, TC cell migration and invasion were markedly inhibited after DLX6-AS1 was knocked down in vitro. The mRNA and protein expressions of UPF1 were both remarkably up-regulated after knockdown of DLX6-AS1. Meanwhile, the expression level of UPF1 was negatively correlated with the expression of DLX6-AS1 in TC tissues. Furthermore, knockdown of DLX6-AS1 significantly inhibited tumor metastasis in vivo. CONCLUSIONS: Knockdown of DLX6-AS1 could inhibit TC cell migration and invasion via upregulating UPF1, which might be a potential therapeutic target in TC.

SOX2 gene expression and its role in triple negative breast cancer tissues.

The aim of this work was to study the expression of SOX2 gene in triple negative breast cancer and its role. One hundred and twenty specimens of paraffin-embedded triple negative breast cancer (TNBC) tissues were collected from Harbin Medical University Cancer Hospital, Heilongjiang, China between January 2014 and March 2018. The expression of SOX2 was detected using immunohistochemistry, and the relationship between the expression of SOX2 and clinical features was analyzed. Breast cancer cell lines (normal group, SOX2 interference group, SOX2 overexpression group) were cultured in vitro to detect the proliferation and cloning ability of the cell lines. The expression of SOX2 was related to lymph node metastasis and stage of breast cancer (P less than 0.05), but was not related to age, menopause or tumor size (P > 0.05); the expression of SOX2 in the overexpression group was significantly greater than that in the normal group after 72 hours, and no significant difference between the overexpression group and the interference group was observed. The number of clone cells with a diameter of 0.5 mm in the interference group was lower compared to the normal group, and that of the overexpression group was higher, but not significant. SOX2 is associated with the high invasiveness of breast cancer and can be used as a therapeutic target to inhibit the metastasis of cancer cells. SOX2 can promote the proliferation of breast cancer cells and affect the size of clone cells in its involvement in clone.

High expression of KIF14 is associated with poor prognosis in patients with epithelial ovarian cancer.

OBJECTIVE: Kinesin family member 14 (KIF14) is a mitotic kinesin and plays an important role in tumor progression. KIF14 overexpression has been observed in multiple cancers and has been correlated with a poor prognosis. However, its protein expression and prognostic significance in epithelial ovarian cancer (EOC) remain unclear. In this research, we aimed to explore the relationship of KIF14 expression with clinicopathological parameters and prognosis in EOC. MATERIALS AND METHODS: In this study, we measured KIF14 expression in 170 EOC carcinoma tissue samples with immunohistochemistry and correlated these data with clinicopathological characteristics. RESULTS: The expression of KIF14 in EOC tissues was significantly higher than that in normal tissues. Furthermore, KIF14 expression was significantly associated with metastasis (p = 0.047), histological type (p = 0.001), Ki67 expression (p = 0.004) and residual tumor (p = 0.038). Also, Kaplan-Meir survival curves showed that a high level of KIF14 expression was a predictor for worse PFS (p = 0.013) and OS (p = 0.009) in patients with EOC. CONCLUSIONS: KIF14 expression may be associated with poor prognosis, suggesting that it has potential value as an effective prognostic predictor in EOC patients.

Effect of recombinant human endostatin on the expression of c-Myc and bFGF in mouse gastric cancer cells.

The aim of this study was to observe the effects of re-combinant human endostatin on the proliferation and apoptosis of mouse gastric cancer cells, and explore some possible mechanisms of recom-binant human endostatin inhibition of cancer. A murine gastric cancer xenograft model was established. A total of 20 mice were divided into two groups (control and experimental groups). The expression of c-Myc and basic fibroblast growth factor (bFGF) was determined by reverse transcription-polymerase chain reaction, Western blotting, and immu-nohistochemical staining methods. Tumor volume was measured and a growth curve was calculated. The tumor diameter in the experimental group was significantly smaller than that in the control group after treat-ment with endostatin for 21 days. The expression levels of c-Myc and bFGF in the experimental group were significantly lower than those of the control group (P < 0.05). There was a positive correlation between the expression of c-Myc and bFGF in the experimental group. Microvessel density was significantly inhibited in the experimental group (P < 0.05). These results demonstrated that recombinant human endostatin could in-hibit tumor metastasis by inhibition of the expression of c-Myc and bFGF in gastric cancer tissue as well as by inhibition of angiogenesis.

Downregulation of microRNA-383 is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation by targeting IRF1.

Our previous studies have shown that microRNA-383 (miR-383) expression is downregulated in the testes of infertile men with maturation arrest (MA). However, the underlying mechanisms of miR-383 involved in the pathogenesis of MA remain unknown. In this study, we showed that downregulation of miR-383 was associated with hyperactive proliferation of germ cells in patients with mixed patterns of MA. Overexpression of miR-383 in NT2 (testicular embryonal carcinoma) cells resulted in suppression of proliferation, G1-phase arrest and induction of apoptosis, whereas silencing of miR-383 reversed these effects. The effects of miR-383 were mediated through targeting a tumor suppressor, interferon regulatory factor-1 (IRF1), and miR-383 was negatively correlated with IRF1 protein expression in vivo. miR-383 inhibited IRF1 by affecting its mRNA stability, which subsequently reduced the levels of the targets of IRF1, namely cyclin D1, CDK2 and p21. Downregulation of IRF1 or cyclin D1, but not that of CDK2, enhanced miR-383-mediated effects, whereas silencing of p21 partially inhibited the effects of miR-383. Moreover, miR-383 downregulated CDK4 by increasing proteasome-dependent degradation of CDK4, which in turn resulted in an inhibition of phosphorylated retinoblastoma protein (pRb) phosphorylation. These results suggest that miR-383 functions as a negative regulator of proliferation by targeting IRF1, in part, through inactivation of the pRb pathway. Abnormal testicular miR-383 expression may potentiate the connections between male infertility and testicular germ cell tumor.

Effects of 50 Hz magnetic fields on gap junctional intercellular communication.

To explore whether the extremely low frequency (ELF) electromagnetic fields (EMFs) may act as cancer promoters or be synergistic with 12-O-tetradecanoylphorbol-13-acetate (TPA) in cancer promotion, an experiment was conducted on the effects of 50 Hz magnetic fields (MFs) on gap junctional intercellular communication (GJIC) of Chinese hamster lung (CHL) cells. Lucifer dye was loaded into CHL cells by iontophoretic injection, and the number of dye-coupled cells (DCC) 5 min after the injection was adopted as the index of GJIC. The effects of TPA at different concentrations and magnetic fields at different intensities, combined with 5 ng/ml TPA, were studied. The results showed that the suppression of TPA on GJIC was dependent on TPA concentration; the threshold concentration of TPA for CHL cells was between 1 and 5 ng/ml. After exposure to 0.8 mT magnetic field for 24 h, the number of DCC decreased to 6.08 +/- 1.59, whereas the number of DCC in the control group was 9.84 +/- 2.27 (P < .05). When the cells were exposed at 0.2, 0.4, and 0.8 mT for 24 h, combined with 5 ng/ml TPA treatment during the last 1 h, the number of DCC decreased to 5.52 +/- 1.53, 5.00 +/- 1.22, and 4.00 +/- 1.29, respectively, which were significantly lower than the values for the group treated with 5 ng/ml TPA alone (6.38 +/- 1.39). It is suggested that certain intensities of 50 Hz magnetic field might act as cancer promoters, be additive with other promoters in cancer promotion, or both.

[Retinal S-antigen and retinoblastoma--an immunohistochemical study].

A strain of monoclonal antibody, MabAgC6, which defines an epitope in S-antigen, was used to study S-antigen expression in 10 cases of retinoblastoma, where S-antigen immunoactivity was observed in different patterns: the "normal" photoreceptor elements incorporated in 3 cases of growing tumors, 3 of 4 fleurettes and E-W rosettes, and scattered tumor cells in 50% of the cases were stained positive. The results suggest that the expression of S-antigen in retinoblastoma may be used to assess the degree of tumor differentiation, as another of the tumor markers.