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Background Cervical cancer seriously threatens both the health and life of women. We aimed to investigate whether RNA interference of long non-coding RNA (lncRNA) DCST1-AS1 could promote miR-874-3p expression to affect the proliferation, migration and invasion of cervical cancer cells. Methods DCST1-AS1 expression levels in cervical cancer cells and transfection effects were detected by quantitative reverse transcriptase-polymerase chain reaction analysis. Proliferation, invasion and migration of cells were separately shown by cell-counting kit-8, wound healing and transwell assays, and relative protein expression was determined by western blot analysis. Dual-luciferase reporter and RNA immunoprecipitation assays verified the interaction of DCST1-AS1 and miR-874-3p. Results DCST1-AS1 expression was increased in cervical cancer tissues and cells. The DCST1-AS1 expression in Hela and SiHa cells was the highest, and so the cells were selected for the next experiment. Inhibition of DCST1-AS1 suppressed the proliferation, invasion and migration of cervical cancer cells and decreased the expression of KI67, proliferating cell nuclear antigen, matrix metalloproteinase (MMP)-2 and MMP-9. miR-874-3p expression was increased when cells were transfected with miR-874-3p mimic or shRNA-DCST1-AS1-1, and DCST1-AS1 expression was down-regulated when cells were transfected with miR-874-3p mimic. DCST1-AS1 can directly target miR-874-3p. Furthermore, inhibition of miR-874-3p could effectively alleviate the effect of inhibition of DCST1-AS1 with respect to the proliferation, invasion and migration of cervical cancer cells. Conclusions Inhibition of DCST1-AS1 suppressed the proliferation, migration and invasion of cervical cancer cells by increasing miR-874-3p expression, which could be alleviated by the inhibition of miR-874-3p.

Molecular imaging has received increased attention worldwide, including in China, because it offers noninvasive characterization of widely diverse clinically significant pathologies. To achieve these goals, nanomedicine has evolved into a broad interdisciplinary field with flexible designs to accommodate and concentrate imaging and therapeutic payloads into pathological cells through selective binding to disease specific cell membrane biomarkers. This concept of personalized medicine reflects the vision of "magic bullets" proposed by German biochemist Paul Ehrlich over 100 years ago. As happening worldwide, Chinese scientists are contributing to this tsunami of science and technologies through impactful national programs and international research collaborations. This review provides a comprehensive update of Chinese innovations to address intractable unmet medical need in China and worldwide in the optical sciences. This article is categorized under: Diagnostic Tools > in vivo Nanodiagnostics and Imaging.

The nickel-catalyzed intermolecular cycloadditions of benzocyclobutenones with 1,3-dienes developed by Martin and co-workers are featured with the exclusive proximal C-C bond cleavage and a high chemoselectivity of the [4+4] over the [4+2] cycloaddition. In this report, the detailed reaction mechanism and the origins of the selectivities were investigated by means of density functional theory calculations. The results show that the reaction is initiated by a C-C oxidative addition of the benzocyclobutenone to form the five-membered nickelacycles. A subsequent exo 1,4-insertion/C-C reductive elimination and an endo 1,4-insertion/C-C reductive elimination lead to the [4+4] and [4+2] cycloaddition products, respectively. The 1,4-insertion of the 1,3-diene into the Ni-C bond was calculated to be the rate- and selectivity-determining step of the reaction. The calculations reproduced quite well the experimentally observed exclusive proximal C-C bond cleavage and the high chemoselectivity of the [4+4] over the [4+2] cycloaddition. In particular, it was found that the steric repulsion between the phosphine ligand and the α-substituent of the benzocyclobutenone has a dramatic impact on the 1,4-insertion, which enables the experimentally observed selectivities.

The novel HLA-C*08:125 allele differs from the closest allele C*08:02:01:01 in exon 3.

In this report, the mechanism of the rhodium-catalyzed intermolecular cycloaddition of vinylaziridines with alkynes is investigated by means of density functional theory calculations. The calculations show that the reaction is initiated by a C−N oxidative addition to form the Rh–allyl complex, from which the migratory insertion of the alkyne into the Rh−N bond was found to take place in a 1,2-fashion. The subsequent competing direct C−C reductive elimination and alkenyl isomerization/ C−C reductive elimination led to the [3+2] and [5+2] cycloadditions, respectively. The experimentally observed ligand-controlled selectivity is reproduced quite well by the calculations. Importantly, it turns out that the steric repulsion between the ligand and the alkenyl moiety has a profound impact on the direct C−C reductive elimination and the alkenyl isomerization, which enables the selectivity switch between the [3+2] and [5+2] cycloaddition upon change of ligand.

Mammalian cortical expansion is tightly controlled by fine-tuning of proliferation and differentiation of neural progenitors in a region-specific manner. How extrinsic cues interface with cell-intrinsic programs to balance proliferative versus neurogenic decisions remains an unsolved question. We examined the function of Semaphorin receptors Plexin-B1 and -B2 in corticogenesis by generating double mutants, whereby Plexin-B2 was conditionally ablated in the developing brain in a Plexin-B1 null mutant background. Absence of both Plexin-Bs resulted in cortical thinning, particularly in the caudomedial cortex. Plexin-B1/B2 double, but not single, mutants exhibited a reduced neural progenitor pool, attributable to decreased proliferation and an altered division mode favoring cell cycle exit. This resulted in deficient production of neurons throughout the neurogenic period, proportionally affecting all cortical laminae. Consistent with the in vivo data, cultured neural progenitors lacking both Plexin-B1 and -B2 displayed decreased proliferative capacity and increased spontaneous differentiation. Our study therefore defines a novel function of Plexin-B1 and -B2 in transmitting extrinsic signals to maintain proliferative and undifferentiated states of neural progenitors. As single mutants displayed no apparent cortical defects, we conclude that Plexin-B1 and -B2 play redundant or compensatory roles during forebrain development to ensure proper neuronal production and neocortical expansion. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 76: 882-899, 2016.

Double minute chromosomes (DMs) are extrachromosomal cytogenetic structures found in tumour cells. As hallmarks of gene amplification, DMs often carry oncogenes and drug-resistance genes and play important roles in malignant tumour progression and drug resistance. The mitogen-activated protein kinase (MAPK) signalling pathway is frequently dysregulated in human malignant tumours, which induces genomic instability, but it remains unclear whether a close relationship exists between MAPK signalling and DMs. In the present study, we focused on three major components of MAPK signalling, ERK1/2, JNK1/2/3 and p38, to investigate the relationship between MAPK and DM production in tumour cells. We found that the constitutive phosphorylation of ERK1/2, but not JNK1/2/3 and p38, was closely associated with DMs in tumour cells. Inhibition of ERK1/2 activation in DM-containing and ERK1/2 constitutively phosphorylated tumour cells was able to markedly decrease the number of DMs, as well as the degree of amplification and expression of DM-carried genes. The mechanism was found to be an increasing tendency of DM DNA to break, become enveloped into micronuclei (MNs) and excluded from the tumour cells during the S/G2 phases of the cell cycle, events that accompanied the reversion of malignant behaviour. Our study reveals a linkage between ERK1/2 activation and DM stability in tumour cells.