Dual-modality imaging probes synergistically combine magnetic resonance (MR) and fluorescence into a single nanocomposite. This promising technique affords a new level of flexibility for molecular imaging uses in biomedical research. In this study, we report a new strategy for the synthesis of a novel attapulgite nanorod-based atta@FeO@[Ru(bpy)(fmp)]Cl nanocomposite (atta@FeO@Ru NC). Our synthesized NC has both photoluminescent and magnetic properties, bright fluorescence, as well as significant magnetic resonance. Transmission electron microscopy, energy dispersive spectroscopy, fluorescence spectrometry, and magnetization measurements were all used to validate its properties. In vitro studies showed that our functionalized NC had high cellular biocompatibility and was successfully used to label living cells through endocytosis of cells. Moreover, a CCK8 assay showed that even high concentrations of the atta@FeO@Ru NC had low toxicity. Finally, the intravenous administration of the atta@FeO@Ru NC to a rabbit model of hepatic carcinoma resulted in a marked and negatively enhanced T-weighted MRI in both normal liver and tumor, which can further enhance the visibility of the liver cancer tissue and normal liver tissue. Collectively, these results suggest that the atta@FeO@Ru NC can be used for tumor discovery and diagnosis.

Long non-coding RNA musculin antisense RNA 1 (lncRNA MSC-AS1) has been recognized as an oncogene in pancreatic cancer, hepatocellular carcinoma, nasopharyngeal carcinoma, and renal cell carcinoma. However, the functional significance of MSC-AS1 and its underlying mechanism in gastric cancer (GC) progression remain unclear. In this study, we demonstrated that the expression of MSC-AS1 in GC tissues was significantly higher than that in non-tumor tissues. Moreover, the elevated level of MSC-AS1 was detected in GC cells (MKN-45, AGS, SGC-7901, and MGC-803) compared to normal GES-1 gastric mucosal cells. The cancer genome atlas (TCGA) data further indicated that the high level of MSC-AS1 was closely correlated with advanced tumor stage and poor prognosis of GC. Next, we revealed that MSC-AS1 knockdown inhibited the proliferation, glucose consumption, lactate production, and pyruvate production of MGC-803 cells. Conversely, MSC-AS1 overexpression enhanced the proliferation and glycolysis of AGC cells. Mechanistically, modulating MSC-AS1 level affected the expression of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), but did not impact the levels of hexokinase 2 (HK2) and pyruvate kinase M2 (PKM2) in GC cells. Based on this, we reversed the MSC-AS1 knockdown-induced the inhibition of cell proliferation and glycolysis by restoring PFKFB3 expression in MGC-803 cells. In conclusion, MSC-AS1 facilitated the proliferation and glycolysis of GC cells by maintaining PFKFB3 expression.

Abstract. The reaction of divalent transition metal salts and (E)-N'-(1-(pyridin-2-yl)ethylidene)nicotinohydrazide (penh) led to the formation of [Mn(penh) 2 ] (complex 1), [Co(penh) 2 ] (complex 2), [Cu(penh) 2 ] (complex 3) and [Cd (penh) 2 ] (complex 4) complexes. The four complexes were characterized using elemental analyses, infrared spectra and single-crystal X-ray diffraction analyses. Subsequently, the complexes were used for in vitro cell level experiments to determine potential antitumor effects. The results demonstrated that the complexes exhibited a similar structure; however, they were crystallized with distinct space groups. In comparison with the uncomplexed penh ligand, all four complexes were able to markedly decrease the proliferation rate of various types of tumor cell, including the human lung cancer cell line A549, human gastric cancer cell line BGC823 and human esophageal cancer cell line Eca109, in a concentration-dependent manner. Furthermore, the complexes promoted tumor cell apoptosis, as demonstrated in the apoptosis assay, and this was confirmed using electrophoresis. IntroductionHydrazide-hydrazone derivatives are an important class of biologically active molecules, which have attracted the attention of medicinal chemists due to their wide-ranging pharmacological properties and their potential application as antitumor, antineoplastic, antiviral and anti-inflammatory agents (1-6).In particular, aroylhydrazone complexes of transition metals are known to provide useful models for the elucidation of the underlying molecular mechanism of enzyme inhibition by hydrazine derivatives (7) and for their potential pharmacological application (8,9). Hydrazone derivatives of isoniazid and other hydrazides have been reported to exhibit marked antimicrobial activity (10-14). Furthermore, a number of substituted hydrazone derivatives have been synthesized and evaluated for their antitumor activity, with certain promising results having been reported (15-17).The aim of the present study was to develop potent anticancer agents. (E)-N'-(1-(pyridin-2-yl)ethylidene) nicotinohydrazide (penh), and [Mn(penh) 2 ] (complex 1), [Co (penh) 2 ] (complex 2), [Cu(penh) 2 ] (complex 3) and [Cd(penh) 2 ] (complex 4) metal complexes were synthesized, and their cytotoxicity against human lung cancer (A549), human gastric cancer (BGC823) and human esophageal cancer (Eca109) cell lines was investigated. Materials and methodsMaterials. All starting materials were obtained commercially and used as received. The A549 human lung cancer, BGC823 human gastric cancer and Eca109 human esophageal cancer cell lines were obtained from the Cell Culture Center of the Basic Institute of Medical Sciences (Peking Union Medical College, Beijing, China). Cell culture reagents were purchased from Gibco (Thermo Fisher Scientific, Inc., Waltham, MA, USA). An Annexin V/propidium iodide (PI) double staining kit was purchased from BD Biosciences (Franklin Lakes, NJ, USA). MTT and dimethyl sulfoxide (DMSO) were purchased from Sigma-Aldrich (Merc...