[Retracted] miR­34a is downregulated in human osteosarcoma stem­like cells and promotes invasion, tumorigenic ability and self­renewal capacity.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion assay data shown in Fig. 4B on p. 1635 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes, which had either already been published or were submitted at around the same time. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 15: 1631­1637, 2017; DOI: 10.3892/mmr.2017.6187].

[Retracted] miR­133b induces chemoresistance of osteosarcoma cells to cisplatin treatment by promoting cell death, migration and invasion.

[This retracts the article DOI: 10.3892/ol.2017.7432.].

Intense green light emission in Sr2 ZnGe2 O7 :Mn2+ phosphors by the design of high symmetry melilite structure.

A green phosphor Sr2 ZnGe2 O7 :Mn2+ with a melilite structure was prepared using a high-temperature solid-state reaction. When the 535 nm emission was monitored, the excitation spectrum of the Sr2 ZnGe2 O7 :Mn2+ was found to contain two excitation bands in the ultraviolet (UV) region. When excited by UV light, the sample shows bright green emission at 535 nm, which corresponds to the distinctive transition of Mn2+ (4 T1 →6 A1 ). Moreover, the quantum efficiency of Sr2 ZnGe2 O7 :Mn2+ could reach 67.6%. Finally, a high-performance white-light-emitting diode (WLED) with a low correlated colour temperature of 4632 K and a high colour rendering index (CRI) of 92.3 were packaged by coating commercial blue and red phosphors with an optimized Sr2 ZnGe2 O7 :Mn2+ sample on a 310 nm UV chip. This indicated that Sr2 ZnGe2 O7 :Mn2+ has the potential application as a green component in the WLED lighting field.

The cranial vertebral body suffers a higher risk of adjacent vertebral fracture due to the poor biomechanical environment in patients with percutaneous vertebralplasty.

BACKGROUND CONTEXT: Adjacent vertebral fracture (AVF), a frequent complication of PVP, is influenced by factors such as osteoporosis progression, increased intervertebral cement leakage (ICL), and biomechanical deterioration. Notably, the risk of AVF is notably elevated in the cranial vertebral body compared with the caudal counterpart. Despite this knowledge, the underlying pathological mechanism remains elusive. PURPOSE: This study delves into the role of biomechanical deterioration as a pivotal factor in the heightened risk of AVF in the cranial vertebral body following PVP. By isolating this variable, we aim to unravel its prominence relative to other potential risk factors. STUDY DESIGN: A retrospective study and corresponding numerical mechanical simulations. PATIENT SAMPLE: Clinical data from 101 patients treated by PVP were reviewed in this study. OUTCOME MEASURES: Clinical assessments involved measuring Hounsfield unit (HU) values of adjacent vertebral bodies as a representation of patients' bone mineral density (BMD). Additionally, the rates of ICL were compared among these patients. Numerical simulations were conducted to compute stress values in the cranial and caudal vertebral bodies under various body positions. METHODS: In a retrospective analysis of PVP patients spanning July 2016 to August 2019, we scrutinized the HU values of adjacent vertebral bodies to discern disparities in BMD between cranial and caudal regions. Additionally, we compared ICL rates on both cranial and caudal sides. To augment our investigation, well-validated numerical models simulated the PVP procedure, enabling the computation of maximum stress values in cranial and caudal vertebral bodies across varying body positions. RESULTS: The incidence rate of cranial AVF was significantly higher than the caudal side. No notable distinctions in HU values or ICL rates were observed between the cranial and caudal sides. The incidence of AVF showed no significant elevation in patients with ICL in either region. However, numerical simulations unveiled heightened stress values in the cranial vertebral body. CONCLUSIONS: In patients postPVP, the cranial vertebral body faces a heightened risk of AVF, primarily attributed to biomechanical deterioration rather than lower BMD or an elevated ICL rate.

The Long Noncoding RNA ZEB2-AS1 Contributes to Proliferation and Epithelial-to-Mesenchymal Transition of Osteosarcoma.

Background: Long non-coding RNA Zinc finger E-box binding homeobox 2 (ZEB2) antisense RNA 1 (ZEB2-AS1) has been shown to promote tumor progression. However, the clinical significance and fundamental function role of ZEB2-AS1 in osteosarcoma (OS) has been poorly understood. Methods: The expression of ZEB2-AS1 was determined in tumor tissues and matched normal tissues from 67 OS patients using quantitative reverse transcriptase PCR analysis. Clinical value of ZEB2-AS1 was evaluated by χ2 test and Kaplan-Meier method. Cell proliferation was analyzed using CCK-8 assay, colony formation. Cell apoptosis status was determined by caspase-3 activity assay. Cell migration, invasion and epithelial-mesenchymal transition (EMT) were investigated by scratch wound healing, transwell invasion assays and Western blotting. Results: Clinical association analysis revealed that high ZEB2-AS1 expression correlated with tumor size, distant metastasis and poor prognosis of OS patients. Moreover, ZEB2-AS1 expression was identified as an independent prognostic factor for OS patients. Loss-of-function assays demonstrated that ZEB2-AS1 knockdown suppressed the proliferation and induced apoptosis in OS cells. In addition, ZEB2-AS1 knockdown inhibited cell migration, invasion, EMT of OS cells in vitro. Conclusions: Taken together, our data demonstrate that ZEB2-AS1 serves a putative oncogenic role and associates with unfavorable prognosis in OS.

Incomplete insertion of pedicle screws triggers a higher biomechanical risk of screw loosening: mechanical tests and corresponding numerical simulations.

Screw loosening is a widely reported issue after spinal screw fixation and triggers several complications. Biomechanical deterioration initially causes screw loosening. Studies have shown that incomplete insertion of pedicle screws increases the risk of screw breakage by deteriorating the local mechanical environment. However, whether this change has a biomechanical effect on the risk of screw loosening has not been determined. This study conducted comprehensive biomechanical research using polyurethane foam mechanical tests and corresponding numerical simulations to verify this topic. Pedicle screw-fixed polyurethane foam models with screws with four different insertion depths were constructed, and the screw anchoring ability of different models was verified by toggle tests with alternating and constant loads. Moreover, the stress distribution of screw and bone-screw interfaces in different models was computed in corresponding numerical mechanical models. Mechanical tests presented better screw anchoring ability with deeper screw insertion, but parameters presented no significant difference between groups with complete thread insertion. Correspondingly, higher stress values can be recorded in the model without complete thread insertion; the difference in stress values between models with complete thread insertion was relatively slight. Therefore, incomplete thread insertion triggers local stress concentration and the corresponding risk of screw loosening; completely inserting threads could effectively alleviate local stress concentration and result in the prevention of screw loosening.

Enhancing Water-Splitting Efficiency Using a Zn/Sn-Doped PN Photoelectrode of Pseudocubic α-Fe2O3 Nanoparticles.

α-Phase hematite photoelectrodes can split water. This material is nontoxic, inexpensive, and chemically stable; its low energy gap of 2.3 eV absorbs light with wavelengths lower than 550 nm, accounting for approximately 30% of solar energy. Previously, we reported polyhedral pseudocubic α-Fe2O3 nanocrystals using a facile hydrothermal route to increase spatial charge separation, enhancing the photocurrent of photocatalytic activity in the water-splitting process. Here, we propose a p-n junction structure in the photoanode of pseudocubic α-Fe2O3 to improve short carrier diffusion length, which limits its photocatalytic efficiency. We dope Zn on top of an Fe2O3 photoanode to form a layer of p-type semiconductor material; Sn is doped from the FTO substrate to form a layer of n-type semiconductor material. The p-n junction, n-type Fe2O3:Sn and p-type Fe2O3:Zn, increase light absorption and charge separation caused by the internal electric field in the p-n junction.

miR-133b induces chemoresistance of osteosarcoma cells to cisplatin treatment by promoting cell death, migration and invasion.

As an important chemotherapeutic agent for the treatment of osteosarcoma, the effectiveness of cisplatin is considered to be due to its unique properties, which allow it to penetrate the cell membrane and form various DNA-platinum adducts, resulting in genetic alterations or DNA damage. However, chemoresistance to cisplatin remains a major challenge for its use and chemotherapeutic effects. In the present study, an isogenic model of a cisplatin resistant osteosarcoma cell line, MG63-DDP, was generated from the original MG63 cell line. The expression level of microRNA (miR)-133b in the MG63-DDP cisplatin-resistant osteosarcoma cell line was analyzed by reverse transcription-quantitative polymerase chain reaction (PCR). Cisplatin-DNA adduct formation, cell death (carboxyfluorescein succinimidyl ester/propidium iodide staining) and clonogenic survival assays (crystal violet staining) were performed, comparing various cell types. The effect of miR-133b on migration (scratch wound assay) and invasion (Transwell assay) was also evaluated. Characterization studies have previously revealed an increased level of miR-133b in MG63-DDP cells compared with normal MG63 cells. Upregulation of miR-133b was associated with the accumulation of cisplatin-DNA adducts and an increase in cisplatin-induced cell death. Furthermore, increased miR-133b expression levels enhanced the migration and invasion of MG63 cells under cisplatin stress. Concordantly, in MG63-DDP cells the neutralization of miR-133b demonstrated opposite effects, as compared with the upregulation of miR-133b. To the best of our knowledge, the present study demonstrated for the first time that cisplatin-resistant MG63 cells exhibit an increased level of miR-133b expression. The endogenous expression level of miR-133b is sufficient for inducing cisplatin resistance, which suggests that miR-133b may be a biomarker for cisplatin resistance in osteosarcoma.

Honokiol suppresses proliferation and induces apoptosis via regulation of the miR­21/PTEN/PI3K/AKT signaling pathway in human osteosarcoma cells.

Honokiol (HNK) is a small biphenolic compound, which exerts antineoplastic effects in various types of cancer. However, the mechanism underlying the antitumor effects of HNK in osteosarcoma (OS) cells is not yet fully understood. Emerging evidence has indicated that microRNAs (miRNAs/miRs) serve key roles in numerous pathological processes, including cancer. It has previously been reported that Chinese medicinal herbs harbor anticancer properties via modulating miRNA expression. Therefore, the present study aimed to determine whether HNK could suppress OS cell growth by regulating miRNA expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometric analysis were used to evaluate the cell proliferation and apoptosis in human OS cells after treatment with HNK, respectively. The results demonstrated that HNK inhibits proliferation and induces apoptosis of human OS cells in a dose­dependent manner. Furthermore, HNK­induced apoptosis was characterized by upregulation of proapoptotic proteins, including cleaved­caspase­3, cleaved­poly (ADP­ribose) polymerase and B­cell lymphoma 2 (Bcl­2)­associated X protein, and downregulation of the anti­apoptotic protein Bcl­2. Reverse transcription­quantitative polymerase chain reaction (RT­qPCR) verified that HNK was able to induce aberrant expression of miRNAs in human OS cells, and miR­21 was one of the miRNAs that was most significantly downregulated. To further investigate miR­21 function, the present study validated that HNK reduces miR­21 levels in a dose­dependent manner. In addition, restoration of miR­21 expression abrogated the suppressive effects of HNK on OS cells. Luciferase assay and western blot analysis identified that miR­21 inhibits the expression of phosphatase and tensin homolog (PTEN) by directly targeting its 3'-UTR. Notably, HNK was able to suppress the phosphoinositide 3­kinase (PI3K)/protein kinase B (AKT) signaling pathway; however, it was reactivated by miR­21 overexpression. Taken together, these data indicated that HNK may inhibit proliferation and induce apoptosis of human OS cells by modulating the miR­21/PTEN/PI3K/AKT signaling pathway. Therefore, miR­21 may be considered a potential therapeutic target for the treatment of osteosarcoma with HNK.

miR-34a is downregulated in human osteosarcoma stem-like cells and promotes invasion, tumorigenic ability and self-renewal capacity.

MicroRNA-34 (miR-34), in particular miR-34a, has a negative regulatory effect on osteosarcoma cell proliferation, migration and invasion. Notably, it is also a post­transcriptional regulatory factor of (sex determining region Y)­box 2 (Sox-2), which is required for osteosarcoma cell self­renewal and tumorigenesis. As a direct regulator of Sox­2, miR­34a has been hypothesized to be greatly associated with the regulation of malignancies in osteosarcoma. To investigate the role of miR-34a in the malignancies of osteosarcoma, reverse transcription­quantitative polymerase chain reaction was performed to detect the expression level of miR­34a in osteospheres. The results revealed that the miR­34a, b and c were suppressed in osteosarcoma stem­like cells (OSCs) and osteospheres. The introduction of miR­34a mimics and short hairpin (sh)RNA targeting Sox­2 mRNA (shSox­2) in human OSCs markedly reduced their transformation properties in vitro and their capacity to form tumors in soft agar. Furthermore, the epigenetic expression of miR­34a and shSox­2 inhibited the expression of the stem cell marker, stem cell antigen­1 and led to the failure of osteosphere formation, respectively. The data of the present study indicated that the inhibitory role of miR­34a on tumor growth and metastasis of osteosarcoma may function by reducing the maintenance of osteosphere self­renewal capacity, elimination of tumorigenic ability and invasion of osteosarcoma in vitro. These findings may provide the basis for a novel therapeutic target of osteosarcomas based on inducing the expression of miR-34a.

Resveratrol inhibits canonical Wnt signaling in human MG-63 osteosarcoma cells.

In the last 30 years, the 5-year-survival rate of patients with osteosarcoma has not improved as a result of the low prevalence and large tumor heterogeneity. Therefore, the development of novel drugs for the treatment of osteosarcoma is urgently required. The present study aimed to identify potential novel drugs for the treatment of osteosarcoma, thus used ß­catenin as a target and performed high content screening. In a total of 14 botanical extracts assessed, resveratrol markedly downregulated the expression of ß­catenin and significantly inhibited MG­63 cell proliferation. CCK­8 assay was used to confirm the anti­osteosarcoma effect of resveratrol and flow cytometry and western blotting were performed to analyze the underlying mechanisms of the proapoptotic effects of resveratrol. ß­catenin is a vital member of the canonical Wnt signaling pathway and, therefore, the target genes of this pathway were further analyzed. The results of this analysis demonstrated that resveratrol suppressed the MG­63 cells by inhibiting the canonical Wnt signaling pathway.