[Retracted] Anticancer activity of taraxerol acetate in human glioblastoma cells and a mouse xenograft model via induction of autophagy and apoptotic cell death, cell cycle arrest and inhibition of cell migration.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (Figs. 3, 4, 7 and 10) contained apparent anomalies, including repeated patternings of data within the same figure panels. Furthermore, Fig. 3 contained data that bore striking similarities to data published in Fig. 6 in another paper published in Molecular Medicine Reports, which has now been retracted [Zhu Y­Y, Huang H­Y and Wu Y­L: Anticancer and apoptotic activities of oleanolic acid are mediated through cell cycle arrest and disruption of mitochondrial membrane potential in HepG2 human hepatocellular carcinoma cells. Mol Med Rep 12: 5012­5018, 2015]. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Molecular Medicine Reports 13: 4541­4548, 2016; DOI: 10.3892/mmr.2016.5105].

Anticancer activity of taraxerol acetate in human glioblastoma cells and a mouse xenograft model via induction of autophagy and apoptotic cell death, cell cycle arrest and inhibition of cell migration.

The aim of the present study was to investigate the in vitro and in vivo anticancer and apoptotic effects of taraxerol acetate in U87 human glioblastoma cells. The effects on cell cycle phase distribution, cell cycle-associated proteins, autophagy, DNA fragmentation and cell migration were assessed. Cell viability was determined using the MTT assay, and phase contrast and fluorescence microscopy was utilized to determine the viability and apoptotic morphological features of the U87 cells. Flow cytometry using propidium iodide and Annexin V-fluorescein isothiocyanate demonstrated the effect of taraxerol acetate on the cell cycle phase distribution and apoptosis induction. Western blot analysis was performed to investigate the effect of the taraxerol acetate on cell cycle­associated proteins and autophagy­linked LC3B­II proteins. The results demonstrated that taraxerol acetate induced dose­ and time­dependent cytotoxic effects in the U87 cells. Apoptotic induction following taraxerol acetate treatment was observed and the percentage of apoptotic cells increased from 7.3% in the control cells, to 16.1, 44.1 and 76.7% in the 10, 50 and 150 µM taraxerol acetate­treated cells, respectively. Furthermore, taraxerol acetate treatment led to sub­G1 cell cycle arrest with a corresponding decrease in the number of S­phase cells. DNA fragments were observed as a result of the gel electrophoresis experiment following taraxerol acetate treatment. To investigate the inhibitory effects of taraxerol acetate on the migration of U87 cell, a wound healing assay was conducted. The number of cells that migrated to the scratched area decreased significantly following treatment with taraxerol acetate. In addition, taraxerol acetate inhibited tumor growth in a mouse xenograft model. Administration of 0.25 and 0.75 µg/g taraxerol acetate reduced the tumor weight from 1.2 g in the phosphate­buffered saline (PBS)­treated group (control) to 0.81 and 0.42 g, respectively. Similarly, 0.25 and 0.75 µg/g taraxerol acetate injection reduced the tumor volume from 1.3 cm3 in the PBS-treated group (control) to 0.67 and 0.25 cm3, respectively.

The Clinical Characteristics and Treatment of Cerebral Microarteriovenous Malformation Presenting with Intracerebral Hemorrhage: A Series of 13 Cases.

OBJECT: The aim of this report was to explore the clinical presentation, radiological features, treatment methods, and outcome of micro-AVMs presenting with intracerebral hemorrhage. METHODS: The clinical data, radiological features, treatment, and follow-up results for a consecutive series of 13 cases with micro-AVMs were retrospectively analyzed. RESULTS: All 13 patients presented with intracerebral hemorrhage. Ten cases were confirmed by enhanced thin layer CT scanning and CTA, and the other 3 cases were confirmed by DSA. Treatment consisted of surgical removal in 10 cases, endovascular embolization in 1, and radiosurgery in 2. The modified GOS score was achieved in the third month after discharge: 10 cases were rated with 5 points (good recovery), 1 case was rated with 4 points (mild disability), and 2 cases were rated with 3 points (severe disability). During follow-up, No case of rebleeding was reported. CONCLUSIONS: Intracerebral hemorrhage is the main clinical manifestation of micro-AVMs. It is beneficial to find a tiny nidus of dense vessels located on hematoma wall on enhanced thin layer CT scanning for a clear diagnosis and to detect any abnormal feeding artery or venous drainage for an indirect diagnostic evidence. Resection is the main method of treatment for micro-AVMs.

miR-630 targets LMO3 to regulate cell growth and metastasis in lung cancer.

MicroRNAs (miRNAs) are a class of small non-coding RNAs that play key roles in cancer development and progression. Therefore, the discovery of miRNAs may provide a new and powerful tool for understanding the mechanism of carcinogenesis. In the present study, we aimed to investigate the functional significance of miR-630 and to identify its possible target genes in human non-small cell lung cancer (NSCLC). Our results showed that miR-630 was significantly down-regulated in NSCLC tissues and cell lines. The enforced expression of miR-630 was able to inhibit cell proliferation, migration, and invasion of NSCLC cells. Moreover, our results further revealed that LMO3, a nuclear LIM-only proteins, was identified as a target of miR-630. Restoration of LMO3 remarkably reversed the tumor-suppressive effects of miR-630 on cell proliferation, migration, and invasion in NSCLC cells. Therefore, we demonstrated that miR-630 suppressed the proliferation, migration, and invasion of NSCLC cells by down-regulating LMO3 expression, suggesting miR-630 as a potential therapeutic target for the treatment of human NSCLC in the future.

[Inhibition of 1,25-(OH)2D3 on passively sensitized human airway smooth muscle cells].

OBJECTIVE: To investigate the effects of 1,25-(OH)(2)D(3) on the proliferation of passively sensitized human airway smooth muscle cells (HASMCs) and their expressions of MMP-9 and a disintegrin and metalloprotease 33(ADAM33). METHODS: HASMCs were passively sensitized with 10% serum from asthmatic patients. MTT colorimetry assay was used to examine the effect of 1,25-(OH)(2)D(3) on cell proliferation at different concentrations (10(-10) mol/L, 10(-9) mol/L, 10(-8) mol/L, 10(-7) mol/L).By this way, its optimal inhibitory concentration was determined. And then the effects of 1,25-(OH)(2)D(3) at the optimal concentration on cell proliferation was examined by the same MTT assay and cell cycle analysis by flow cytometry. The expressions of MMP-9 and ADAM33 in HASMCs were studied by real-time quantitative RT-PCR and Western blotting analysis. RESULTS: (1) Inhibition of cell proliferation by 1,25-(OH)(2)D(3) was barely detectable at 10(-10) mol/L. But with the increasing concentration ranging from 10(-9) mol/L to 10(-7) mol/L, 1,25-(OH)(2)D(3) markedly inhibited the cell proliferation concentration-dependently and reached the maximum effect at the concentration of 10(-7) mol/L. Accordingly, 10(-7) mol/L was chosen as the optimal concentration of 1,25-(OH)(2)D(3) for the following study. (2) At the concentration of 10(-7) mol/L, 1,25-(OH)(2)D(3) inhibited the cell proliferation of passively sensitized HASMCs in a time-dependent manner and hampered the G(1)/S transition. (3) 1,25-(OH)(2)D(3) pretreatment attenuated the MMP-9 and ADAM33 protein levels in passively sensitized HASMCs by (63.4 ± 3.6)% and (50.9 ± 2.9)%, respectively (P < 0.01). (4) 1,25-(OH)(2)D(3) significantly inhibited the MMP-9 and ADAM33 mRNA levels in passively sensitized HASMCs by (52.2 ± 2.5)% and (67.8 ± 3.2)%, respectively (P < 0.01). CONCLUSION: 1,25-(OH)(2)D(3) has a direct inhibitory effect on passively sensitized HASMCs in vitro, including the inhibition of cell proliferation and the expressions of MMP-9 and ADAM33, which maybe associated with the beneficial role of 1,25-(OH)(2)D(3) in the prevention and therapy of asthmatic airway remodeling.

[Effect of huangqi and dangshen extraction on angiogenesis in Matrigel implant of mice].

AIM: To study the inhibitory effect of huangqi and dangshen extraction (SQ) on angiogenesis induced by b-FGF. METHODS: Matrigel implant assay was used. Matrigel(500 microL) containing b-FGF and heparin was injected subcutaneously into the abdomens of mice and harvested 5 d later. The amount of hemoglobin and micro-vascular area present in the implant were measured and compared. The mice were given different dosage of SQ (experimental group) or the same volume of glucose (vehicle group) once a day by intraperitoneal injection. Inhibitory experiment started 3 d before Matrigel implant and continued until the end of study. RESULTS: SQ in lower dosage (< or = 50% V/V) increased hemoglobin content and micro-vascular area in Matrigel implant while SQ in higher dosage (> or = 60%, V/V) reduced hemoglobin content and micro-vascular area in Matrigel implant. The effect of enhance ment and inhibition was in a limited concentration-effect manner. CONCLUSION: SQ in different dosage has different effects on angiogenesis. We should use different dosage in different purpose.

[Inhibitory effect of huangqi and dangshen extraction with pacilitaxel on metastasis and angiogenesis on mouse Lewis lung carcinoma model].

AIM: To study enhance effect of huangqi and dangshen extraction (Shenqi) on pacilitaxel inhibitory metastasis and angiogenesis on mouse Lewis lung carcinoma model. METHODS: Lewis lung carcinoma cells were inoculated into right hind footpad of C57BL/6 mice. Six hour after tumor inoculated, the mice were randomly divided into 3 groups.Shenqi (paclitaxel plus Shenqi) or paclitaxel was intraperitoneally injected in two group since the second day of the establishment of animal model. The third group simply administered with normal saline was set as placebo-control. Tumor volume, quantitation of microvessel density (MVD) in inoculated tumor, the number of metastasis in the lungs and survival analysis were compared in 3 groups. RESULTS: Paclitaxel plus Shenqi can effectively reduced MVD in inoculated tumor and the number of lung metastasis as compared with other two group (P<0.05). The survival time of Shenqi group was also significantly longer (P<0.05). Tumor volume was no statistical difference in three group (P>0.05). CONCLUSION: Shenqi can amplify the paclitaxel effect of anti-angiogenesis and anti-metastasis, enhances the survival time of mice bearing LLC, might has possible therapeutic applications in the treatment of lung cancer.