LINC00662 promotes melanoma progression by competitively binding miR-107 and activating the ß-catenin signaling pathway.

Melanoma is a highly malignant tumor in the body. Long non-coding RNAs (lncRNAs) have been reported to be involved in the development of various tumors. Emerging evidence demonstrates the critical role of lncRNAs in melanoma development. In this study, we aimed to investigate the expression, biological function and regulatory mechanism of LINC00662 in melanomas. First, we found that LINC00662 was up-regulated in melanoma tissues and cell lines. High expression of LINC00662 in melanomas was associated with a poor patient prognosis. Silencing of LINC00662 suppressed the proliferation, migration, and invasion of melanoma cells in vitro and in vivo, while overexpression of LINC00662 promoted melanoma cell proliferation in vitro. Bioinformatics analysis, dual-luciferase assay, and RIP assay confirmed that LINC00662 competitively regulated miR-107. Silencing of LINC00662 upregulated miR-107 expression in a melanoma cell line. Inhibition of miR-107 significantly reversed the inhibitory effect of LINC00662 silencing on cell proliferation and migration. Furthermore, POU3F2 was validated as a downstream target of LINC00662/miR107 and was downregulated when LINC00662 was silenced. Overexpressing POU3F2 attenuated the effect of si-LINC00662 on cellular functions. In addition, the results also showed that the ß-catenin pathway was involved in a si-LINC00662-induced function in melanoma. Overall, our results confirmed that LINC00662 promoted melanoma progression by sponging miR107 and inducing POU3F2, highlighting the mechanism of the LINC00662/miR-107/POU3F2 axis in melanoma cell proliferation and invasion.

Occurrence and treatment of peripheral nerve injuries after cosmetic surgeries.

Although non-invasive and minimally invasive aesthetic procedures increasingly dominate the cosmetic market, traditional plastic surgery remains the most effective improvement method. One of the most common complications in plastic surgery, peripheral nerve injuries, though has a low incidence but intrigued plastic surgeons globally. In this article, a narrative review was conducted using several databases (PubMed, EMBASE, Scopus, and Web of Science) to identify peripheral nerve injuries following cosmetic surgeries such as blepharoplasty, rhinoplasty, rhytidectomy, breast surgeries, and abdominoplasty. Surgery-related nerve injuries were discussed, respectively. Despite the low incidence, cosmetic plastic surgeries can cause iatrogenic peripheral nerve injuries that require special attention. The postoperative algorithm approaches can be effective, but the waiting and treatment processes can be long and painful. Preventive measures are undoubtedly more effective than postoperative remedies. The best means of preventing disease is having a good understanding of anatomy and conducting a careful dissection.

ZNF281 inhibits mitochondrial biogenesis to facilitate metastasis of hepatocellular carcinoma.

Zinc finger protein 281 (ZNF281) has been shown to promote tumor progression. However, the underlying mechanism remains to be further elucidated. In this study, ZNF281 knockdown increased the expression of mitochondrial transcription factor A (TFAM) in hepatocellular carcinoma (HCC) cells, accompanied with increment of mitochondrial content, oxygen consumption rate (OCR) and levels of TCA cycle intermetabolites. Mechanistic investigation revealed that ZNF281 suppressed the transcription of TFAM, nuclear respiratory factor 1 (NRF1) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). Furthermore, ZNF281 interacted with NRF1 and PGC-1α, and was recruited onto the promoter regions of TFAM, TFB1M and TFB2M repressing their expression. Knockdown of TFAM reversed ZNF281 depletion induced up-regulation of mitochondrial biogenesis and function, as well as impaired epithelial mesenchymal transition, invasion and metastasis of HCC cells. Our research uncovered a novel suppressive function of ZNF281 on mitochondrial biogenesis through inhibition of the NRF1/PGC-1α-TFAM axis, which may hold therapeutic potentials for HCC.

Inhibition of Annexin A10 Contributes to ZNF281 Mediated Aggressiveness of Hepatocellular Carcinoma.

Objective: To investigate the involvement and transcriptional targets of zinc finger protein 281 (ZNF281) in the progression of hepatocellular carcinoma (HCC). Methods: The expression of ZNF281 in HCC was detected in tissue microarray and cell lines. The role of ZNF281 in aggressiveness of HCC was examined using wound healing, matrigel transwell, pulmonary metastasis model and assays for expression of EMT markers. RNA-seq was used to find potential target gene of ZNF281. Chromatin immunoprecipitation (ChIP) assay and co-immunoprecipitation (Co-IP) were employed to uncover the mechanism of the transcriptional regulation of ZNF281 on the target gene. Results: ZNF281 was increased in tumor tissues and positively correlated with vascular invasion in HCC. Knockdown of ZNF281 suppressed the migration and invasion with significant alteration of EMT marker expression in HLE and Huh7 HCC cell lines. RNA-seq screening showed that the tumor suppressor gene Annexin A10 (ANXA10) was a most up-regulated gene in response to ZNF281 depletion and responsible for the attenuation of aggressiveness. Mechanistically, ZNF281 interacted with the ANXA10 promoter region harboring ZNF281 recognition sites, and recruited components of nucleosome remodeling and deacetylation (NuRD) complex. By knocking down such components like HDAC1 or MTA1, ANXA10 was released from transcriptional repression by ZNF281/NuRD, and in turn reversed the EMT, invasion and metastasis driven by ZNF281. Conclusion: ZNF281 drives invasion and metastasis of HCC partially through transcriptional repression of tumor suppressor gene ANXA10 by recruiting NuRD complex.

ATF6-Mediated Unfolded Protein Response Facilitates Adeno-associated Virus 2 (AAV2) Transduction by Releasing the Suppression of the AAV Receptor on Endoplasmic Reticulum Stress.

Adeno-associated virus (AAV) is extensively used as a viral vector to deliver therapeutic genes during human gene therapy. A high-affinity cellular receptor (AAVR) for most serotypes was recently identified; however, its biological function as a gene product remains unclear. In this study, we used AAVR knockdown cell models to show that AAVR depletion significantly attenuated cells to activate unfolded protein response (UPR) pathways when exposed to the endoplasmic reticulum (ER) stress inducer, tunicamycin. By analyzing three major UPR pathways, we found that ATF6 signaling was most affected in an AAVR-dependent fashion, distinct from CHOP and XBP1 branches. AAVR capacity in UPR regulation required the full native AAVR protein, and AAV2 capsid binding to the receptor altered ATF6 dynamics. Conversely, the transduction efficiency of AAV2 was associated with changes in ATF6 signaling in host cells following treatment with different small molecules. Thus, AAVR served as an inhibitory molecule to repress UPR responses via a specificity for ATF6 signaling, and the AAV2 infection route involved the release from AAVR-mediated ATF6 repression, thereby facilitating viral intracellular trafficking and transduction. IMPORTANCE The native function of the AAVR as an ER-Golgi localized protein is largely unknown. We showed that AAVR acted as a functional molecule to regulate UPR signaling under induced ER stress. AAVR inhibited the activation of the transcription factor, ATF6, whereas receptor binding to AAV2 released the suppression effects. This finding has expanded our understanding of AAV infection biology in terms of the physiological properties of AAVR in host cells. Importantly, our research provides a possible strategy which may improve the efficiency of AAV-mediated gene delivery during gene therapy.

Giant cell tumor of tendon sheath in the wrist that damaged the extensor indicis proprius tendon: a case report and literature review.

BACKGROUND: Giant cell tumor of the tendon sheath (GCTTS) is a benign soft tissue (synovial membrane) tumor that rarely involves the hands or wrists. And Tendon impairment caused by GCTTS is extremely rare. CASE PRESENTATION: Here, we reported a case of a 60-year-old female with a 10-year history of gradually increasing mass in her left dorsal wrist. The EIP tendon was partially impaired by the mass.The patient was treated with surgical excision of the mass and reconstruction of the EIP tendon. The histopathological examination suggested the presence of GCTTS. After surgery, the patient had adequate functional recovery and no tumor recurrence after 2 years' follow-up. CONCLUSION: GCTTS in hands and wrists rarely damages the tendon. Early diagnosis and proactive interventions may likely contribute to good prognostic outcomes.

Immunotherapy for gastric cancer: dilemmas and prospect.

Gastric cancer remains the second most common cause of cancer-related death worldwide. Because of the poor prognosis of late-stage gastric cancer patients, it is imperative to develop new strategies to improve the survival rate of this disease. Currently, immunotherapy is considered as an innovative approach for cancers such as lung cancer, gastric cancer and breast cancer. In fact, previous works have revealed promising results in this field. With further understanding of immunogenomics of gastric cancer, new immune checkpoint regulators could become more important. In addition, whole-genome sequencing and genome editing provide us with more information on the heterogeneity of gastric cancer, showing helpful tools to identify new predictive biomarkers and to achieve personalized treatment. Further research and better understanding of the functions of immune system will enhance immunotherapy treatment in the future.

Long non-coding RNA NNT-AS1 sponges miR-424/E2F1 to promote the tumorigenesis and cell cycle progression of gastric cancer.

Long non-coding RNAs (lncRNAs) have been illustrated to function as important regulators in carcinogenesis and cancer progression. However, the roles of lncRNA NNT-AS1 in gastric cancer remain unclear. In the present study, we investigate the biological role of NNT-AS1 in gastric cancer tumorigenesis. Results revealed that NNT-AS1 expression level was significantly up-regulated in GC tissue and cell lines compared with adjacent normal tissue and normal cell lines. The ectopic overexpression of NNT-AS1 indicated the poor prognosis of GC patients. In vitro experiments validated that NNT-AS1 knockdown suppressed the proliferation and invasion ability and induced the GC cell cycle progression arrest at G0/G1 phase. In vivo xenograft assay, NNT-AS1 silencing decreased the tumour growth of GC cells. Bioinformatics online program predicted that miR-424 targeted the 3'-UTR of NNT-AS1. Luciferase reporter assay, RNA-immunoprecipitation (RIP) and RNA pull-down assay validated the molecular binding within NNT-AS1 and miR-424, therefore jointly forming the RNA-induced silencing complex (RISC). Moreover, E2F1 was verified to act as the target gene of NNT-AS1/miR-424, indicating the NNT-AS1/miR-424/E2F1 axis. In conclusion, our study indicates that NNT-AS1 sponges miR-424/E2F1 to facilitate GC tumorigenesis and cycle progress, revealing the oncogenic role of NNT-AS1 for GC.

Treatment of Tear Trough Deformity: Fat Repositioning versus Autologous Fat Grafting.

BACKGROUND: Fat-preserving lower blepharoplasty techniques and filling techniques using autologous or non-autologous materials are increasingly used to treat tear trough deformity. However, there has been no definitive comparison of the results of fat repositioning versus autologous fat grafting for this condition. The authors used statistical analysis to compare the results of the two methods. METHODS: From October 2013 to September 2015, a total of 101 patients, aged 20-43 years, underwent fat repositioning or autologous fat grafting in our department. Group 1 (51 patients, 102 eyes) underwent intraorbital fat repositioning with septal reset by transconjunctival lower blepharoplasty. Group 2 (50 patients, 100 eyes) underwent autologous fat grafting by lipoinjection. RESULTS: No significant complications occurred in any patient postoperatively. Four of 102 eyes in Group 1 and seven of 100 eyes in Group 2 had no improvement; the rest had different degrees of improvement. In Grade II and III deformities, fat repositioning resulted in significantly greater improvement of grade compared with autologous fat grafting. The surgical method of Group 1 resulted in better curative effects than that of Group 2. CONCLUSION: In patients with tear trough deformity and without obvious skin or orbicularis oculi muscle laxity, both fat repositioning and autologous fat grafting are acceptable for mild deformity. In patients with higher-grade deformities, fat repositioning produced superior results than autologous fat grafting. LEVEL OF EVIDENCE IV: This journal requires that the authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors http://www.springer.com/00266 .

Presence of aliphatic and polycyclic aromatic hydrocarbons in near-surface sediments of an oil spill area in Bohai Sea.

In order to determine the source of organic matter and the fingerprint of the oil components, 50 samples collected from the near-surface sediments of the oil spill area in Bohai Sea, China, were analyzed for grain size, total organic carbon, aliphatic hydrocarbons (AHs), and polycyclic aromatic hydrocarbons (PAHs). The concentrations of C15-35 n-alkanes and 16 United States Environmental Protection Agency (US EPA) priority pollutant PAHs were found in the ranges of 0.88-3.48µg g(-1) and 9.97-490.13ng/g, respectively. The terrestrial organic matters characterized by C27-C35 n-alkanes and PAHs, resulting from the combustion of higher plants, are dominantly contributed from the transportation of these plants by rivers. Marine organic matters produced from plankton and aquatic plants were represented by C17-C26 n-alkanes in AHs. Crude oil, characterized by C17-C21 n-alkanes, unresolved complex mixture (UCM) with a mean response factor of C19 n-alkanes, low levels of perylene, and a high InP/(InP+BghiP) ratio, seeped into the oceans from deep hydrocarbon reservoirs, as a result of geological faults.