ENST00000534735 inhibits proliferation and migration, promotes apoptosis and pyroptosis of endometrial cancer via OSBPL3 through APMK/SIRT1/NF-κB pathway.

Background: The complete understanding of the biological roles of long non-coding RNAs (lncRNAs) in cancer remains elusive. The findings of this study indicate that the newly discovered lncRNA ENST00000534735 exhibited a decreased expression in both endometrial cancer (EC) tissues and cell lines. Methods: The expression of ENST00000534735 in EC tissues was detected using RNA-sequencing analysis. The effects of ENST00000534735 on cell proliferation, migration, apoptosis, and pyroptosis were determined via in vitro and in vivo experiments. The proteins that interact with ENST00000534735 were confirmed by RNA pull-down assay. Furthermore, an investigation was conducted on the impact of ENST00000534735 on the in vivo growth of EC through a tumorigenicity assay in nude mice. Results: We found that ENST00000534735 was significantly down-regulated in EC tissues compared to their adjacent non-cancerous tissues. The ectopic expression of ENST00000534735 drastically inhibited lung cancer cell proliferation and migration ability and facilitated apoptosis and pyroptosis. Knockdown of ENST00000534735 increased OSBPL3 expression, and the tumor-suppressing effects of ENST00000534735 overexpression were reversed by upregulation of OSBPL3 via the APMK/SIRT1/NF-κB pathway. The in vivo tumorigenic assays conducted on nude mice revealed that the excessive expression of ENST00000534735 impeded the growth of EC. Conclusions: All results elucidated the role and molecular mechanism of ENST00000534735 in the malignant development of EC. ENST00000534735, a new antioncogene in EC, may serve as a survival biomarker or therapeutic target for EC.

LncRNA TCF7 contributes to high glucose-induced damage in human podocytes by up-regulating SEMA3A via sponging miR-16-5p.

AIMS/INTRODUCTION: Long non-coding RNAs (lncRNAs) exert essential functions in the pathogenesis of diabetic nephropathy (DN). LncRNA T-cell factor 7 (TCF7) and semaphorin-3A (SEMA3A) have been found to be involved in the progression of diabetic nephropathy. However, whether the effect of TCF7 on the pathogenesis of diabetic nephropathy is mediated by SEMA3A remains unclear. MATERIALS AND METHODS: TCF7, miR-16-5p, and SEMA3A were quantified by a qRT-PCR or immunoblotting method. A CCK-8 assay gauged the cell viability. Measurement of cell apoptosis was done using flow cytometry. RNA immunoprecipitation (RIP), dual-luciferase reporter, and RNA pull-down assays were utilized to assay the targeted interactions among the variables. RESULTS: The TCF7 and SEMA3A levels were elevated in serum from patients with diabetic nephropathy. TCF7 silencing or SEMA3A depletion ameliorated high glucose (HG)-induced podocyte injury. Moreover, TCF7 silencing protected against HG-induced podocyte injury by down-regulating SEMA3A. TCF7 targeted miR-16-5p, and miR-16-5p targeted SEMA3A. Furthermore, TCF7 affected the expression of SEMA3A by competing specifically for shared miR-16-5p. CONCLUSIONS: These findings suggested that TCF7 silencing attenuated high glucose-induced podocyte damage partially through the miR-16-5p/SEMA3A regulation cascade.

General 5-Halomethyl Isoxazoline Synthesis Enabled by Copper-Catalyzed Oxyhalogenation of Alkenes.

A general and efficient oxyhalogenation of unsaturated ketoximes has been achieved through copper catalysis with diethyl bromomalonate, N-chlorosuccinimide, and N-iodosuccinimide, yielding 5-chloromethyl, 5-bromomethyl, and 5-iodomethyl isoxazolines in good to excellent yields.

The successful treatment of flat warts with auricular acupuncture.

BACKGROUND: Flat warts are a common presenting complaint in adolescents and adults and may be a cosmetic problem as well. Patients suffering from flat warts are often unsatisfied with conventional medical care because of adverse effects such as intolerable pain, hyperpigmentation, hypopigmentation, or occasionally allergic contact dermatitis. To offset the possibilities of hyperpigmentation, hypopigmentation, and scar formation, the method of auricular acupuncture was used. METHODS: Single-blind method adopted, 60 subjects with flat warts were all outpatients and randomly allocated to a treatment group or a control group, with 30 patients in each group. Thirty subjects in the treatment group were treated with weekly auricular acupuncture for 10 weeks while the other subjects in the control group were treated with 0.1% of tretinoin ointment topically for 10 weeks. RESULTS: Sixteen subjects in the treatment group (53.33%) recovered fully from flat warts without recurrence during the ensuing six months' follow-up after 10 weeks' surgery compared with only one subject in the control group (3.33%). The therapeutic effect of the treatment group was statistically better than that of the control group by Mann-Whitney U-test with SPSS software (P < 0.01). During the treatment period and the ensuing six months' follow-up, no adverse effects were observed by the investigators or reported by patients. CONCLUSIONS: Our findings suggest that auricular acupuncture may be a viable alternative for the treatment of flat warts. Larger randomized studies are needed to fully evaluate auricular acupuncture against more conventional treatments, and these are planned.