LncRNA BX357664 inhibits the proliferation and invasion of non-small cell lung cancer cells.

The article "LncRNA BX357664 inhibits the proliferation and invasion of non-small cell lung cancer cells, by J. Yang, Y.-M. Du, B. Li, published in Eur Rev Med Pharmacol Sci 2019; 23 (2): 660-669-DOI: 10.26355/eurrev_201901_16880-PMID: 30720174" has been withdrawn from the authors due to data miscalculation, p-value (Distance metastasis in Table I) should be 0.161, not 0.034. So the low level of BX357664 was not correlated with distant metastasis of NSCLC. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/16880.

Complete genomic sequence of tea-oil camellia deltapartitivirus 1, a novel virus from Camellia oleifera.

Three viral contig sequences, which represented complete genome of a novel virus with three dsRNAs of 1,712 nucleotides (nt) (dsRNA1), 1,504 nt (dsRNA2) and 1,353 nt (dsRNA3), were found in tea-oil camellia plants by high-throughput sequencing analysis. The three dsRNAs were re-sequenced by RT-PCR cloning. The largest dsRNA, dsRNA1, had a single open reading frame (ORF) that encoded a putative 52.7-kDa protein of a putative viral RNA-dependent RNA polymerase (RdRp). DsRNA2 and dsRNA3 were predicted to encode putative capsid proteins (CPs) of 40.47 kDa and 40.59 kDa, respectively. The virus, which is provisionally named "tea-oil camellia deltapartitivirus 1",  shared amino acid sequence itentities of 36.09-69.18% with members of the genus Deltapartitivirus on RdRp. Phylogenetic analysis based on RdRp also placed the new virus and other deltapartitiviruses together in a group, suggesting that this virus should be considered a new member of the genus Deltapartitivirus.

Effect of bradykinin on rats with thromboangiitis obliterans through PI3K/Akt signaling pathway.

OBJECTIVE: To explore the effect of bradykinin on rats with thromboangiitis obliterans (TAO) through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathway. MATERIALS AND METHODS: The female Wistar rats were injected with lauric acid via the femoral artery to establish the TAO model, and they were randomly divided into control group (healthy rats), model group (TAO rats) and bradykinin group (TAO rats injected with bradykinin B2 receptor-specific inhibitor). The control was set in each group before the operation. The level of serum bradykinin in each group was detected via enzyme-linked immunosorbent assay (ELISA), and the reactive oxygen species (ROS) level, Caspase-3 activity and PI3K/Akt protein concentration in vascular tissues were measured via ELISA, Western blotting, ROS assay, and Caspase-3 activity assay, respectively. Moreover, the specific therapeutic mechanism of bradykinin was analyzed. RESULTS: In control group, the intima of the lower extremity venous tissues was smooth, the extima had no evident changes, and there was no inflammatory cell invasion around the arteries and veins. In model group, there was massive inflammatory cell invasion into the lower extremity venous tissues. In bradykinin group, fibrosis and atrophy occurred in venous tissues, the extima was thickened without fibrosis, and there was phagocytosis of neutrophils and mononuclear macrophages around the arteries and veins, as well as massive inflammatory infiltration. The PI3K/Akt protein concentration in lower extremity venous tissues was the highest in control group and the lowest in bradykinin group, and there were statistically significant differences (p<0.01). At 24 h after administration of doxorubicin (DOX), the level of ROS in lower extremity venous tissues was higher in bradykinin group than that in model group (p<0.05), and it was also higher in model group than that in control group (p<0.05). Besides, the activity of Caspase-3 in lower extremity venous tissues was significantly increased in bradykinin group compared with that in model group and control group, while it was slightly higher in model group than that in control group (p<0.05). CONCLUSIONS: The low expression of bradykinin can promote TAO in rats by the mechanism that it inhibits the PI3K/Akt signaling pathway to raise the oxidative stress level, thereby aggravating TAO.

MiR-637 inhibits proliferation and invasion of hepatoma cells by targeted degradation of AKT1.

OBJECTIVE: This study aimed at investigating whether miR-637 could promote proliferation of hepatocarcinoma cells by targeted regulation of AKT1 expression, leading to enhanced cell invasion and thus participating in the progression of liver cancer. PATIENTS AND METHODS: The miR-637 and AKT1 expressions in cancer tissues and adjacent tissues of liver cancer patients were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The effects of miR-637 on cell proliferation and cell invasion were examined by cell counting kit-8 (CCK-8) and cell invasion assays. Dual-luciferase reporter gene assay was performed to evaluate the regulating relationship between miR-637 and AKT1. Also, the expression of AKT1 after overexpression or knockdown of miR-637 was analyzed by Western blot to evaluate whether miR-637 could affect proliferative and invasive ability of hepatoma cells by inhibiting the expression of AKT1. RESULTS: The qRT-PCR results revealed that miR-637 expression in cancer tissues of liver cancer patients was markedly lower than that in corresponding adjacent tissues, which was consistent with its low expression in HCC cell lines. However, AKT1 expression in cancer tissues was markedly higher than that in corresponding adjacent tissues. Overexpression of miR-637 in hepatoma cells inhibited cell proliferation and attenuated cell invasion, while inhibition of miR-637 showed the opposite effect. Results of dual-luciferase reporting assay and Western blot demonstrated that miR-637 can selectively degrade AKT1 and that overexpression of AKT1 in HCC cells can partially reverse the effect of miR-637 on cell proliferation and invasion. CONCLUSIONS: MiR-637 can promote the proliferation of hepatoma cells and enhance invasive cell ability, the mechanism of which may be related to the targeted regulation of AKT1 expression.

LncRNA BX357664 inhibits the proliferation and invasion of non-small cell lung cancer cells.

OBJECTIVE: To explore the level of long non-coding RNA (lncRNA) BX357664 in non-small cell lung cancer (NSCLC) and its role in the development of NSCLC. Meanwhile, the potential regulatory mechanism of BX357664 was also what we were interested in. PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to examine the level of BX357664 in 82 pairs of cancer tissues and adjacent normal tissues collected from patients with NSCLC, and the relationship between BX357664 level and pathological parameters or prognosis of NSCLC patients was analyzed. Further verification by RT-qPCR was to examine BX357664 expression in NSCLC cell lines, and BX357664 overexpression model was constructed using lentivirus in NSCLC cell lines including SPCA1 and H1299. In addition, cell counting kit-8 (CCK-8), cell clone formation assay, and transwell assay were performed to analyze the influence of BX357664 on the biological function of NSCLC cells. Western Blot was conducted to explore its underlying mechanisms. RESULTS: RT-qPCR results indicated that BX357664 in NSCLC was remarkably lower than that in normal tissues. Compared with patients with highly-expressed BX357664, patients with lowly-expressed had worse tumor stage, higher incidence of lymph node metastasis or distant metastasis and lower overall survival rate. In addition, compared with NC group, the proliferation, invasion and migration ability of cells in BX357664 overexpression group was attenuated significantly, and the key proteins in TGF-ß1/Smad pathway including transforming growth factor-ß1 (TGF-ß1), p-Smad2, p-Smad3, N-cad, Vimentin and MMP-9 were also remarkably reduced. CONCLUSIONS: BX357664 level was significantly reduced in tumor tissues of NSCLC patients, resulting in advanced tumor staging, lymph node metastasis, distant metastasis, and poor prognosis. Additionally, BX357664 may inhibit the proliferation as well as invasion and migration of NSCLC cells by regulating TGF-ß1/Smad pathway.

Transmembrane 7 superfamily member 4 regulates cell cycle progression in breast cancer cells.

OBJECTIVE: TM7SF4 (transmembrane 7 superfamily member 4) gene encodes a seven-pass transmembrane protein that is primarily expressed in dendritic cells called as dendritic cell-specific expressed seven transmembrane protein (DC-STAMP). This protein regulates immunological functions, osteoclastogenesis and myeloid differentiation. Although the roles of TM7SF4 have been currently studied on Paget's disease of bone and papillary thyroid cancers, it is unclear whether TM7SF4 plays a role in breast cancer. In current study, we investigated the expression of TM7SF4 in human breast cancer cell lines. MATERIALS AND METHODS: In this study, five breast cancer lines were cultured. Small hairpin RNA against TM7SF4 using a lentiviral vector was generated and transfected into MCF-7 breast cancer cells. Effects of down-regulating TM7SF4 in transfected cells were examined by Western blot, RT-PCR, apoptotic rate, colony formation, and cell cycle analyses. RESULTS: The results demonstrated that down-regulation of TM7SF4 led to a decrease in colony formation in MCF-7 cells compared to the control group. This is likely due to a decrease in proliferation and cell cycle and an increase in apoptosis. CONCLUSIONS: To our knowledge, our data demonstrate for the first time that TM7SF4 plays an essential role in regulating cell cycle progression in breast cancer.