LncRNA PVT1 promotes malignant progression by regulating the miR-7-5p/CDKL1 axis in oral squamous cell carcinoma.

Oral squamous cell carcinoma (OSCC), one of the most common types of head and neck squamous cell carcinoma (HNSCC), is characterized by high incidence and mortality. PVT1 is a long non-coding RNA (lncRNA) that plays an oncogenic role in various cancer types. This study aims to reveal the role and underlying molecular mechanism of PVT1 in OSCC progression.

Retroperitoneal leiomyoma located in the broad ligament: A case report.

Background: Retroperitoneal leiomyoma is a rare benign tumor. Retroperitoneal leiomyomas located in the latissimus uterine ligament are even rarer. Retroperitoneal leiomyomas have similar characteristics to uterine leiomyomas in terms of tissue, which results in confusion during diagnosis.

Long non-coding RNA LINC00992 promotes hepatocellular carcinoma cell proliferation, metastasis, and invasiveness by downregulating MicroRNA miR-361-5p expression to increase levels of the transcription factor twist1.

Hepatocellular carcinoma (HCC) is one of the most common cancers, and has an extremely poor prognosis. Our previous study confirmed that the microRNA miR-361-5p inhibited the proliferation, metastasis, invasiveness, and epithelial-to-mesenchymal transition (EMT) process of HCC by targeting the transcription factor Twist1. Long non-coding RNAs (lncRNAs) are key regulators of processes such as cell differentiation, inflammation, tumor formation, and immune escape.

1,3-Benzodioxole Derivatives Improve the Anti-Tumor Efficiency of Arsenicals.

Arsenicals have been widely used in the treatment of cancers such as leukemia and other tumors. However, their side effects limit their clinical application. Stiripentol, a second-line adjunctive treatment for epilepsy with a good safety profile, inhibits microsomal cytochrome-P450-family enzymes to extend the retention time of co-administration.

Mitochondrial Toxicity of Organic Arsenicals.

Arsenic is either notorious toxicant or miracle cure for acute promyelocytic leukemia and several other diseases. It interacts with mitochondria directly or indirectly, by interacting with mitochondrial enzymes, such as respiratory chain complexes and tricarboxylic acid cycle proteins, or affecting mitochondrial homeostasis via ROS or mitochondrial outer membrane permeabilization. Given the ubiquitous presence of mitochondria and indispensable role in cellular metabolism, arsenical-mitochondrial interactions may manifest clinical importance by revealing mechanism of disease curation, preventing severe side effects, and foreseeing potential health issues.

Upregulation of lncRNA NONRATG019935.2 suppresses the p53-mediated apoptosis of renal tubular epithelial cells in septic acute kidney injury.

Although increasing evidence has confirmed that the apoptosis of renal tubular epithelial cells (RTECs) is a crucial contributor to the onset and development of septic acute kidney injury (AKI), the pathological mechanism by which RTEC apoptosis is upregulated during septic AKI is not entirely clear. In this study, a rat model of septic AKI was induced by a cecal ligation puncture procedure or lipopolysaccharide (LPS) injection. Four differentially expressed long noncoding RNAs (DE-Lncs) in the rat model of septic AKI were determined using RNA-sequencing and verified by qRT-PCR.

[Effect of Bmi-1 Silencing on the Proliferation of K562/ADM Cells in vitro and in vivo].

Objective: To investigate the effect of Bmi-1 gene silencing on the proliferation of K562/ADM cells in vitro and in vivo and to explore its possible molecular mechanism.

Methods: The small interference RNA (siRNA) sequences of Bmi-1 were transfected into K562/ADM cells for decreasing the expression of Bmi-1. The effect of Bmi-1 silencing on the proliferation of K562/ADM cells in vitro and in vivo was detected by using MTT method, cell colony-forming test and tumoriganicity of nude mice; the expression of Bmi-1, PTEN and PAKT proteins was detected by Wertern blot.

Dual Inhibition of Pyruvate Dehydrogenase Complex and Respiratory Chain Complex Induces Apoptosis by a Mitochondria-Targeted Fluorescent Organic Arsenical in vitro and in vivo.

Based on the potential therapeutic value in targeting mitochondria and the fluorophore tracing ability, a fluorescent mitochondria-targeted organic arsenical PDT-PAO-F16 was fabricated, which not only visualized the cellular distribution, but also exerted anti-cancer activity in vitro and in vivo via targeting pyruvate dehydrogenase complex (PDHC) and respiratory chain complexes in mitochondria. In details, PDT-PAO-F16 mainly accumulated into mitochondria within hours and suppressed the activity of PDHC resulting in the inhibition of ATP synthesis and thermogenesis disorder. Moreover, the suppression of respiratory chain complex I and IV accelerated the mitochondrial dysfunction leading to caspase family-dependent apoptosis.

LDHA Suppression Altering Metabolism Inhibits Tumor Progress by an Organic Arsenical.

Based on the potential therapeutic value in targeting metabolism for the treatment of cancer, an organic arsenical PDT-BIPA was fabricated, which exerted selective anti-cancer activity in vitro and in vivo via targeting lactate dehydrogenase A (LDHA) to remodel the metabolic pathway. In details, the precursor PDT-BIPA directly inhibited the function of LDHA and converted the glycolysis to oxidative phosphorylation causing ROS burst and mitochondrial dysfunction. PDT-BIPA also altered several gene expression, such as HIF-1α and C-myc, to support the metabolic remodeling.

The urinary levels of CTX-II, C2C, PYD, and Helix-II increased among adults with KBD: a cross-sectional study.

Background: Kashin-Beck disease (KBD) is an endemic osteoarthropathy, and its pathogenesis is still not entirely clear. Pathologically, many KBD changes are similar to those of osteoarthritis (OA). Therefore, this study aimed to identify changes in the levels of potential urinary biomarkers for OA, including C-telopeptide of type II collagen (uCTX-II), type II collagen cleavage neoepitope (uC2C), pyridinoline (uPYD), and uHelix-II, among adults with KBD.

[Bmi-1-siRNA Regulates the Proliferation of K562 Leukemia Cells in vitro and in vivo by PTEN/pAKT Pathway].

Objective: To investigate the effect of Bmi-1 gene silence on the proliferation ability of K562 cells in vitro and in vivo, and to explore the relation of molecular mechanism between proliferation ability of K562 cells in vitro and in vivo with PTEN/pAKT signaling pathway.

Methods: The Bmi-1 small interference RNA (siRNA) sequences were transfected into K562 cells for decreasing Bmi-1 expression. The effect of Bmi-1 siRNA on the proliferation of K562 cells in vitro and in vivo was detected by MTT method and colony-forming test, the effect of Bmi-1 siRNA on the tumorogenicity of K562 cells was observed by subcutaneous inoculation of K562 cells, LY294002 and Bpv treated K562 cells in nude mice, the expression of Bmi-1, PTEN and pAKT proteins were detected by Western blot.

A mitochondria-targeted organic arsenical accelerates mitochondrial metabolic disorder and function injury.

Considering the vital role of mitochondria in the anti-cancer mechanism of organic arsenical, the mitochondria-targeted precursor PDT-PAO-TPP was designed and synthesized. PDT-PAO-TPP, as a delocalization lipophilic cation (DLCs) which mainly accumulated in mitochondria, contributed to improve anti-cancer efficacy and selectivity towards NB4 cells. In detail, PDT-PAO-TPP inhibited the activity of PDHC resulting in the suppression of ATP synthesis and thermogenesis disorder.

Oxidative stress-mediated intrinsic apoptosis in human promyelocytic leukemia HL-60 cells induced by organic arsenicals.

Arsenic trioxide has shown the excellent therapeutic efficiency for acute promyelocytic leukemia. Nowadays, more and more research focuses on the design of the arsenic drugs, especially organic arsenicals, and on the mechanism of the inducing cell death. Here we have synthesized some organic arsenicals with Schiff base structure, which showed a better antitumor activity for three different kinds of cancer cell lines, namely HL-60, SGC 7901 and MCF-7.

Degradation of the Separase-cleaved Rec8, a Meiotic Cohesin Subunit, by the N-end Rule Pathway.

The Ate1 arginyltransferase (R-transferase) is a component of the N-end rule pathway, which recognizes proteins containing N-terminal degradation signals called N-degrons, polyubiquitylates these proteins, and thereby causes their degradation by the proteasome. Ate1 arginylates N-terminal Asp, Glu, or (oxidized) Cys. The resulting N-terminal Arg is recognized by ubiquitin ligases of the N-end rule pathway.

[Microcystin safety study during Cyanobacteria removal by pressure enhanced coagulation process].

Pressure enhanced coagulation and sedimentation technique is an effective way for blue algae treatment. It is not clear whether Cyanobacteria balloon rupture will cause Cyanobacteria cells rupture, resulting in high intracellular concentrations of microcystin LR leak into the water, affecting drinking water safety. Therefore, in this study experimental comparative study of pressure and pre-oxidation of water containing Cyanobacteria was carried out to examine the microcystin LR concentration changes and Cyanobacteria removal efficiency.

[Variation of water DOC during the process of pre-pressure and coagulation sedimentation treatment].

The aim of the study was to explore whether the pre-pressure and coagulation sedimentation process would result in algal cell disruption, leading to increased dissolved organic carbon (DOC) in water, based on which, the pressure application mode would be optimized and safe and efficient pre-pressure algae removal process would be obtained. The changes in DOC during the process of pre-pressure and preoxidation treatment, the distribution of molecular weight in water as well as the removal efficiency of algae, turbidity and DOC after coagulation and sedimentation were investigated. The results showed that the DOC in water did not increase but decreased, and the molecular weight decreased after treated with 0.

[Isolation, identification and oxidizing characterization of an iron-sulfur oxidizing bacterium LY01 from acid mine drainage].

An acidophilic iron-sulfur oxidizing bacterium LY01 was isolated from acid mine drainage of coal in Guizhou Province, China. Strain LY01 was identified as Acidithiobacillusferrooxidans by morphological and physiological characteristics, and phylogenetic analysis of its 16S rRNA gene sequence. Strain LY01 was able to grow using ferrous ion (Fe2+), elemental sulfur (S0) and pyrite as sole energy source, respectively, but significant differences in oxidation efficiency and bacterial growth were observed when different energy source was used.