Potential Therapeutic Effects of Policosanol from Insect Wax on Caenorhabditis elegans Models of Parkinson's Disease.

Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide. The standard treatments for PD focus on symptom relief rather than attempting to address the underlying degenerative processes completely. This study aimed to evaluate the potential therapeutic effects of policosanol derived from insect wax (PIW) by investigating improvements in disease symptoms represented in Caenorhabditis elegans models of PD. For our assessments, we used the following three models: NL5901, which is a transgenic model for α-synuclein aggregation; wild-type N2 induced with 6-hydroxydopamine (6-OHDA); and 6-OHDA-induced BZ555 as a model for loss of dopaminergic neurons (DNs). Specifically, we examined the effects of PIW treatment on α-synuclein aggregation, the loss of DNs, lipid abundance, and the lifespan of treated organisms. Further, we examined treatment-related changes in the levels of reactive oxygen species (ROS), malondialdehyde (MDA), adenosine triphosphate (ATP), glutathione S-transferase (GST), and superoxide dismutase (SOD), as well as the mRNA production profiles of relevant genes. A 10 µg/mL dose of PIW reduced the aggregation of α-synuclein in NL5901 and suppressed the loss of DNs in 6-OHDA-induced BZ555. Overall, PIW treatment decreased ROS and MDA levels, restored lipid abundance, and prolonged the lifespans of worms in all the three models, which may be associated with changes in the expression profiles of genes related to cell survival and oxidative stress response pathways. Our findings show that PIW alleviated the symptoms of PD in these models, possibly by regulating the stress responses initiated by injuries such as α-synuclein aggregation or 6-OHDA treatment.

Long Noncoding RNA CASC2 Facilitated Wound Healing through miRNA-155/HIF-1α in Diabetic Foot Ulcers.

Diabetic foot ulcers (DFU) are among the serious complications which are closely linked to diabetes mellitus. However, there is still a lack of accurate and effective standard prevention and treatment programs for DFU. In this manuscript, we have investigated the function of lncRNA cancer susceptibility candidate 2 (CASC2)/miR-155/hypoxia-inducible factor 1-alpha (HIF-1α) in the wound healing of DFU. We have analyzed lncRNA CASC2`s expression in the marginal tissues of ulcers in patients and mice with DFU. Additionally, the interaction relationship and mechanism between lncRNA CASC2, miR-155, and HIF-1α were determined, which proved the effects of lncRNA CASC2/miR-155/HIF-1α on fibroblasts apoptosis, proliferation, and migration. According to our study, the lncRNA CASC2's expression was low in the tissues of ulcers of DFU mice and patients. lncRNA CASC2's overexpression promoted fibroblasts migration, proliferation, and inhibited apoptosis and was beneficial for the healing of wounds, preferably in the DFU mice. In addition, lncRNA CASC2 directly targets miR-155 and HIF-1α functions as miR-155's target gene. Overexpression of miR-155 abrogated the function of lncRNA CASC2. Similarly, HIF-1α's inhibition has reversed the effect of miR-155 downregulation on fibroblasts. In general, overexpression of lncRNA CASC2 facilitated wound healing through miR-155/HIF-1α in DFU.

[Corrigendum] FNDC3B promotes epithelial­mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment.

After the publication of the article, and also the publication of a Corrigendum (see doi: 10.3892/or.2020.7744), there are further errors in the published paper that the authors wish to correct in a subsequent corrigendum. In the printed version of Fig. 5, the "NC" images were mistakenly presented in the data panels showing the results of the TCA8113 and TSCCA invasion assay experiments. Furthermore, in Fig. 4A and 6A, the ß­actin control bands were erroneously selected for these figures. The corrected versions of Figs. 4, 5 and 6 are shown opposite and on the next page, incorporating the correct data for Figs. 4A, 5 and 6A. These further corrections do not affect the results and conclusions of this work. The authors all agree to this Corrigendum, and are grateful to the Editor of Oncology Reports for allowing them to have the opportunity to correct these additional errors. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused. [the original article was published in Oncology Reports 39: 1853­1859, 2018; DOI: 10.3892/or.2018.6231].

[Corrigendum] FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment.

During the preparation of the above article, the authors inadvertently selected an incorrect pair of data panels for Fig. 5B. Essentially, in the published version of Fig. 5B, the images were presented incorrectly for the NC migration and KD#3 migration and invasion data panels associated with the TSCCA cell Transwell assay experiments. Furthermore, in Fig. 7A, the GAPDH control bands were erroneously selected for the figure. Figs. 5 and 7 as they should have appeared in the Journal are shown opposite, incorporating the correct data for Figs. 5B and 7A. These errors did not affect either the results or the conclusions of this work. The authors all agree to this Corrigendum, and thank the Editor of Oncology Reports for allowing them to have the opportunity to present their corrected data. Furthermore, the authors apologize to the readership for any inconvenience these errors may have caused. [the original article was published in Oncology Reports 39: 1853­1859, 2018; DOI: 10.3892/or.2018.6231].

Identification of prognostic biomarkers in colorectal cancer using a long non-coding RNA-mediated competitive endogenous RNA network.

Colorectal cancer (CRC) is a highly malignant gastrointestinal tumor accompanied by poor prognosis. Long non-coding RNA (lncRNA) plays an important role in the progression and physiology of tumors as it competes with endogenous RNAs, including miRNA and mRNA. In the present study, a multi-step computational method was used to build a CRC-related functional lncRNA-mediated competitive endogenous RNA (ceRNA) network (LMCN). lncRNAs with more degrees and betweenness centrality (BC) were screened out as hub lncRNAs. Then functional enrichment analyses of lncRNAs were carried out from the Gene Ontology (GO) and Reactome pathway databases based on the 'guilt by association' principle. As a result, lncRNAs in the LMCN displayed specific topological characteristics in accordance with the regulatory correlation of coding mRNAs in CRC pathology. HCP5, EPB41L4A-AS1, SNHG12, and LINC00649 were screened out as hub lncRNAs which were more significantly related to the development and prognosis of CRC. The hub lncRNAs in CRC were obviously involved in functions of cell cycle arrest, vacuolar transport, histone modification, and in pathways of GPCR, signaling by Rho GTPases, axon guidance pathways, meaning that they might be potential biomarkers for diagnosis, evaluation and gene-targeted therapy of CRC. Thus, the LMCN construction method could accelerate lncRNA discovery and therapeutic development in CRC.

FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment.

The primary reasons for the treatment failure of patients with oral tongue squamous cell carcinoma (OTSCC) are metastasis and tumor recurrence. Identifying the exact mechanisms underlying metastasis is a key point in improving patient prognosis. It has been reported that a hypoxic microenvironment plays an important role during the metastasis of malignancies. We found that the expression of fibronectin type III domain containing 3B (FNDC3B) is positively correlated with lymph node metastasis and advanced cTNM stage of OTSCC by IHC assay and correlation analysis. Furthermore, we found that knockdown of FNDC3B could suppress the migratory and invasive abilities of OTSCC cells. In addition, treating OTSCC cells with CoCl2 (a hypoxia mimetic agent) upregulated the mRNA and protein expression of FNDC3B via HIF-1α. Moreover, the resultant increase in FNDC3B expression significantly induced epithelial-mesenchymal transition (EMT) in OTSCC cells. The present study elucidated the important role played by FNDC3B in OTSCC metastasis and indicates FNDC3B as a potential target for the treatment of OTSCC metastasis. However, many questions remain to be explored.