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The article titled "[Retracted] Upregulation of CENPF is linked to aggressive features of osteosarcoma" was published in Oncology Letters in 2021. However, it has since been retracted by the editor due to concerns raised by a reader. The reader pointed out that certain data and images in the article were similar to those published by different authors at different research institutes. The authors were asked for an explanation but did not respond. The editor apologizes for any inconvenience caused. [Extracted from the article]

The present study assessed the effects of the tankyrase (TNKS) small molecule inhibitor XAV939 on the proliferation and migration of lung adenocarcinoma A549 cells and the possible underlying mechanism. To do this, the association between TNKS and the WNT/β‑catenin signaling pathway in lung acinar adenocarcinoma was investigated. Immunohistochemistry was performed, which demonstrated that TNKS, β‑catenin and Myc proto‑oncogene protein (c‑Myc) proteins are positively expressed in lung adenocarcinoma tissue; this expression was significantly higher than that in normal adjacent non‑carcinoma tissues. A549 cell proliferation was inhibited in all XAV939‑intervention groups examined. In the wound‑healing assay, cells treated with different concentrations of XAV939 exhibited a significantly increased scratch width compared with the control group. Reverse transcription‑semi‑quantitative polymerase chain reaction analysis revealed that β‑catenin mRNA expression was significantly decreased in A549 cells in response to different XAV939 concentrations compared with the control group. Immunofluorescence revealed that β‑catenin protein, initially localized in the nucleus/cytoplasm, gradually translocated to the cytoplasm/membrane, an effect that was associated with increased drug concentration. TNKS, β‑catenin and c‑Myc protein expression in A549 cells treated with XAV939 was reduced compared with that in untreated cells. Therefore, abnormally high TNKS expression may promote the occurrence of lung cancer. The TNKS inhibitor XAV939 inhibited lung adenocarcinoma A549 cell proliferation and migration in vitro. The underlying mechanism by which XAV939 exerted its inhibitory effects may be associated with attenuation of the WNT signaling pathway. [ABSTRACT FROM AUTHOR]

Hypoxic microenvironments and angiogenesis have been a focus of tumor research in previous years. The aim of the the present study was to create a hypoxic model and observe the effect of hypoxia on the expression of hypoxia inducible factor-1α (HIF-1α), insulin-like growth factor I (IGF-1) and vascular endothelial growth factor expression. The hypoxia model was generated using cobalt chloride (CoCl2) and an MTT assay was used to observe the influence of hypoxia on HepG2 cells. Reverse transcription-polymerase chain reaction, western blotting, ELISA and confocal immunofluorescence microscopy were used to detect the expression of HIF-1α, IGF-1 and VEGF in HepG2 cells, in which hypoxia was induced by various concentrations of CoCl2 and for various incubation times. The cell viability worsened with increasing concentrations of CoCl2. The expression of HIF-1α and IGF-1R was observed in hypoxic HepG2 cells, with the exception of HIF-1α mRNA. The expression of IGF-1R and VEGF mRNA and protein was correlated with the concentration of CoCl2 and the time that hypoxia was induced for. The expression of HIF-1α mRNA and protein was positively correlated with the expression of the VEGF mRNA and protein in a dose- and time-dependent manner under hypoxic conditions. Using immunofluorescence, it was observed that IGF-1R and HIF-1α were secreted from the hypoxic HepG2 cells. It was concluded that hypoxia induces the accumulation of IGF-1R and HIF-1α mRNA and protein, which regulates the expression of VEGF mRNA and protein in hypoxic HepG2 cells. [ABSTRACT FROM AUTHOR]

Centromere protein F (CENPF) plays a key role in the regulation of the cell cycle. The present study revealed that CENPF was overexpressed in a variety of tumors and associated with the poor prognosis of osteosarcoma. The mRNA expression levels of CENPF were analyzed using the Gene Expression Profiling Interactive Analysis database and the protein levels of CENPF were detected in the specimens from patients with osteosarcoma using immunohistochemistry. Cell proliferation, cell cycle and flow cytometry assays were performed after the transfection of control or CENPF plasmids into osteosarcoma cells. A xenografts assay was used to determine the effects of CENPF on tumor growth in vivo. The results showed that CENPF was upregulated in osteosarcoma tissues and associated with high-grade tumor stage (P=0.023) and intraglandular dissemination (P=0.046). The transfection-induced depletion of CENPF in human osteosarcoma MG-63 and U-2 OS cell lines inhibited cell proliferation, stimulated apoptosis and induced cell cycle arrest. Induced CENPF depletion in MG-63 cells inhibited tumor growth of osteosarcoma cells in mice. These findings suggested that elevated CENPF levels contributed to increased cell proliferation by mediating apoptosis and cell cycle in osteosarcoma. Therefore, CENPF might be a potential biomarker for poor prognosis of osteosarcoma. [ABSTRACT FROM AUTHOR]

At present, the regulatory mechanisms of various microRNAs (miRNAs/miRs) have been elucidated in human cancers including osteosarcoma (OS). This study mainly focused on the role of miR-615 in OS, which has not yet been reported. Ninety-two OS tissues and normal samples were used in this study. Human osteoblast hFOB1.19 cells and OS cell line HOS were utilized to detect the expression of miR-615. The expression of miR-615 and gene expression were assessed by RT-qPCR and western blot analysis. Transwell, MTT and luciferase reporter assays were used to investigate the regulatory mechanism of miR-615 in OS. The results revealed that miR-615 expression was reduced in OS tissues and cells, and was associated with poor clinical outcomes and prognosis in OS patients. In addition, overexpression of miR-615 restrained cell viability and metastasis in OS. Furthermore, hexokinase 2 (HK2) was confirmed as a direct target of miR-615. Upregulation of HK2 was detected in OS tissues. The upregulation of HK2 weakened the tumor-suppressive effect of miR-615 in OS. Moreover, miR-615 blocked epithelial-mesenchymal transition (EMT) and inactivated the PI3K/AKT pathway in OS. To conclude, miR-615 acts as a tumor suppressor in OS, thus miR-615 can be used as a target for OS treatment. [ABSTRACT FROM AUTHOR]

Although several computational tools using next-generation sequencing (NGS) data have been proposed to detect microsatellite instability (MSI) status, they still have limitations and need improvement. We developed a NovoPM-MSI method to detect MSI status based on NGS data. This method evaluated target mononucleotide microsatellite loci that were sequenced during targeted gene enrichment analysis and reported sample instability score as the fraction of unstable loci within the target set after assessing locus instability by comparing length distribution in paired tumor-normal samples. We validated this method against the conventional MSI-PCR method in 113 paired colorectal cancer (CRC) specimens and compared the performance of NovoPM-MSI to that of mSINGS and MANTIS in accuracy and runtime efficiency. By using the MSI status from MSI-PCR as the gold standard, the three computational methods showed the same sensitivity of 88.9% but different specificities (NovoPM-MSI 97.1%, MANTIS 86.5% and mSINGS 99.0%). Only NovoPM-MSI could greatly improve both the sensitivity and specificity by setting an ambiguous interval. MANTIS had the shortest average runtime (16.3 sec), followed by NovoPM-MSI (18.3 sec) and mSINGS (109.0 sec). In short, the NovoPM-MSI method provides a fast and reliable MSI detection method with accuracy comparable to MSI-PCR in paired CRC samples. [ABSTRACT FROM AUTHOR]

Micheliolide (MCL), a sesquiterpene lactone isolated from Michelia compressa and Michelia champaca, has been used previously to inhibit the NF-κB signaling pathway. MCL has exerted various therapeutic effects in numerous types of disease, such as inflammatory and cancer. However, to the best of our knowledge, its underlying anticancer mechanism remains to be understood. The present study aimed to investigate the effects of MCL on human glioma U251MG cells and to determine the potential anticancer mechanism of action of MCL. From Cell Counting Kit-8, colony formation assay, apoptosis assay and Confocal immunofluorescence imaging analysis, the results revealed that MCL significantly inhibited cell viability in vitro and induced cell apoptosis via activation of the cytochrome c/caspase-dependent apoptotic pathway. In addition, MCL also suppressed cell invasion and metastasis via the wound healing and Transwell invasion assays. Furthermore, western blot and reverse transcription PCR analyses demonstrated that MCL significantly downregulated cyclooxygenase-2 (COX-2) expression levels, which may have partially occurred through the inactivation of the NF-κB signaling pathway. In conclusion, the results of the present study indicated that MCL may inhibit glioma carcinoma growth by downregulating the NF-κB/COX-2 signaling pathway, which suggested that MCL may be a novel and alternative antitumor agent for the treatment of human glioma carcinoma. [ABSTRACT FROM AUTHOR]