Novel insights into the roles of migrasome in cancer.

Cell migration, a hallmark of cancer malignancy, plays a critical role in cancers. Improperly initiated or misdirected cell migration can lead to invasive metastatic cancer. Migrasomes are newly discovered vesicular cellular organelles produced by migrating cells and depending on cell migration.

The Impact of miR-122 on Cancer.

MiRNAs are confirmed to be a kind of short and eminently conserved noncoding RNAs, which regulate gene expression at the post-transcriptional level via binding to the 3'- untranslated region (3'-UTR) of targeting multiple target messenger RNAs. Recently, growing evidence stresses the point that they play a crucial role in a variety of pathological processes, including human cancers. Dysregulated miRNAs act as oncogenes or tumor suppressor genes in many cancer types.

Emerging roles of noncoding RNAs in human cancers.

Studies have found that RNA encoding proteins only account for a small part of the total number, most RNA is non-coding RNA, and non-coding RNA may affect the occurrence and development of human cancers by affecting gene expression, therefore play an important role in human pathology. At present, ncRNAs studied include miRNA, circRNA, lncRNA, piRNA, and snoRNA, etc. After decades of research, the basic role of these ncRNAs in many cancers has been clear.

Effect of the Application of Exosome on Gastric Cancer.

Gastric cancer is one of the most common and highest mortality rate cancers in the world. Exosomes are vesicles secreted by cells carrying different types of molecules, such as protein and RNA. Numerous studies have confirmed that exosomes are involved in various stages of the occurrence and development of gastric cancer and play an important role.

Microrna-96 In Human Cancers.

MicroRNAs (miRNAs) are small non-coding RNAs 19-25 nucleotides in size involved in gene regulation and diverse processes in tumor cells. Abnormal expression of miRNAs is closely related to carcinogenesis. MiR-96 is a salient cancer-related miRNA in a variety of tumors.

The Role of NcRNAs to Regulate Immune Checkpoints in Cancer.

At present, the incidence of cancer is becoming more and more common, but its treatment has always been a problem. Although a small number of cancers can be treated, the recurrence rates are generally high and cannot be completely cured. At present, conventional cancer therapies mainly include chemotherapy and radiotherapy, which are the first-line therapies for most cancer patients, but there are palliatives.

Tumor-derived or non-tumor-derived exosomal noncodingRNAs and signaling pathways in tumor microenvironment.

The tumor microenvironment (TME) involved in multiple pathological processes of tumors is highly complex. Exosomes, as organelles, can be produced by some cells in the TME and have been verified as a special carriers and a key factor for communication between tumor and TME-associated cells. Noncoding RNAs (ncRNAs) involved in tumorigenesis and development have been demonstrated to be released into the TME by exosomes.

Surface plasmon resonance biosensor for the determination of 3-methyl-quinoxaline-2-carboxylic acid, the marker residue of olaquindox, in swine tissues.

To monitor the illegal use of olaquindox in animals, a monoclonal antibody-based surface plasmon resonance (SPR) biosensor method has been developed to detect 3-methyl-quinoxaline-2-carboxylic acid, the marker residues of olaquindox, in swine tissues. The limit of detection was 1.4 µg kg in swine muscle and 2.

Effect of Intranasal Instillation of Lipopolysaccharide on Lung Development and Its Related Mechanism in Newborn Mice.

Premature infants are prone to repeated lung infections after birth, which can disrupt the development of lung structure and function. However, the effects of postnatal pulmonary inflammation on lung development in newborn mice have not been reported and may play an important role in the development of bronchopulmonary dysplasia (BPD). This study aimed to establish a BPD model of postnatal pulmonary inflammation in premature infants and to explore its role and possible mechanisms in the pathogenesis of BPD.

Transforming Growth Factor-β-Neutralizing Antibodies Improve Alveolarization in the Oxygen-Exposed Newborn Mouse Lung.

Abnormal alveolar formation and excessive disordered elastin accumulation are key pathological features in bronchopulmonary dysplasia. Transforming growth factor (TGF)-β is an important regulator of the extracellular matrix in the developing lung. To determine if increased TGF-β would injure alveolar development by activating TGF-β signaling and by influencing the expression of elastogenesis-related protein, we performed intraperitoneal injection of newborn mice with the TGF-β-neutralizing antibody 1D11 and observed whether 1D11 had a protective role in the oxygen (O)-exposed newborn mouse lung.

Quinocetone induces mitochondrial apoptosis in HepG2 cells through ROS-dependent promotion of VDAC1 oligomerization and suppression of Wnt1/β-catenin signaling pathway.

Quinocetone (QCT) has been used as an animal feed additive in China since 2003. However, investigations indicate that QCT has potential toxicity due to the fact that it shows cytotoxicity, genotoxicity, hepatotoxicity, nephrotoxicity and immunotoxicity in vitro and animal models. Although QCT-induced mitochondrial apoptosis has been established, the molecular mechanism remains unclear.

AKT/TSC2/p70S6K signaling pathway is involved in quinocetone-induced death-promoting autophagy in HepG2 cells.

Quinocetone (QCT, 3-methyl-2-quinoxalin benzenevinylketo-1, 4-dioxide) is widely used as a veterinary drug and animal feed additive in China. Although it promotes growth and improves feed efficiency, QCT's in vitro and in vivo toxicities remain uncertain. This study was conducted to explore the mechanism of QCT-induced autophagy in HepG2 cells.

Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells and both processes are regulated by ROS-dependent pathway.

Thapsigargin (TG), is widely used to induce endoplasmic reticular stress. Treated with TG for a long time, cells suffer the unfolded protein response (UPR) to elude apoptosis, but may activate autophagy. However, the switch between autophagy and apoptosis is unclear.

P21(Waf1/Cip1) plays a critical role in furazolidone-induced apoptosis in HepG2 cells through influencing the caspase-3 activation and ROS generation.

Furazolidone (FZD), a synthetic nitrofuran with a broad spectrum of antimicrobial activities, has been shown to exhibit marked genotoxity and cytotoxicity in vitro, but the proper mechanism was unclear. P21(Waf1/Cip1) (p21), a cyclin-dependent kinase, is critically involved in cell cycle arrest and apoptosis in response to DNA injury. This study was aimed to explore the role of p21 in FZD-induced apoptosis in HepG2 cells and uncover its possible mechanism.

ML-7 amplifies the quinocetone-induced cell death through akt and MAPK-mediated apoptosis on HepG2 cell line.

The study aims at evaluating the combination of the quinocetone and the ML-7 in preclinical hepatocellular carcinoma models. To this end, the effect of quinocetone and ML-7 on apoptosis induction and signaling pathways was analyzed on HepG2 cell lines. Here, we report that ML-7, in a nontoxic concentration, sensitized the HepG2 cells to quinocetone-induced cytotoxicity.

Furazolidone induces apoptosis through activating reactive oxygen species-dependent mitochondrial signaling pathway and suppressing PI3K/Akt signaling pathway in HepG2 cells.

Furazolidone (FZD), a synthetic nitrofuran with a broad spectrum of antimicrobial activities, has been shown to be genotoxic and potentially carcinogenic in several types of cells. However, the proper molecular mechanisms of FZD toxicity remain unclear. This study was aimed to explore the effect of FZD on apoptosis in HepG2 cells and uncover signaling pathway underlying the cytotoxicity of FZD.

Lycopene attenuates colistin-induced nephrotoxicity in mice via activation of the Nrf2/HO-1 pathway.

Nephrotoxicity is the major dose-limiting factor for the clinical use of colistin against multidrug-resistant (MDR) Gram-negative bacteria. This study aimed to investigate the protective effect of lycopene on colistin-induced nephrotoxicity in a mouse model. Fifty mice were randomly divided into 5 groups: the control group (saline solution), the lycopene group (20 mg/kg of body weight/day administered orally), the colistin group (15 mg/kg/day administered intravenously), the colistin (15 mg/kg/day) plus lycopene (5 mg/kg/day) group, and the colistin (15 mg/kg/day) plus lycopene (20 mg/kg/day) group; all mice were treated for 7 days.

Inhibition of autophagy promotes caspase-mediated apoptosis by tunicamycin in HepG2 cells.

Tunicamycin (TM) causes accumulation of unfolded protein in endoplasmic reticulum (ER) lumen and introduces from elsewhere ER stress. This study was to assess the apoptosis and autophagy effect induced by TM on HepG2 cells and the role of autophagy in the system. The viability of HepG2 cells was significantly inhibited by TM in a dose-dependent manner detected by MTT assay.

TNFR1/TNF-α and mitochondria interrelated signaling pathway mediates quinocetone-induced apoptosis in HepG2 cells.

Quinocetone, a new quinoxaline 1, 4-dioxide derivative, has been widely used as an animal feed additive in China. This study was conducted to explore the molecular mechanisms of apoptosis induced by quinocetone in HepG2 cells. MTT assay revealed that the viability of HepG2 cells was significantly inhibited by quinocetone in a dose- and time-dependent manner.

Arsanilic acid causes apoptosis and oxidative stress in rat kidney epithelial cells (NRK-52e cells) by the activation of the caspase-9 and -3 signaling pathway.

Arsenic exists widely in rock, water and air, and arsanilic acid (also known as aminophenyl arsenic acid) is an organoarsenic compound and has been used as feed additives. Organoarsenic compounds in foodstuff cause adverse effects, including acute and chronic toxicity, in animals and humans. However, little is known about the cellular toxicity and mechanisms of organic arsenic on the kidney.

Gossypol acetic acid induces apoptosis in RAW264.7 cells via a caspase-dependent mitochondrial signaling pathway.

To investigate the effects of gossypol acetic acid (GA) on proliferation and apoptosis of the macrophage cell line RAW264.7 and further understand the possible underlying mechanism responsible for GA-induced cell apoptosis, RAW264.7 cells were treated with GA (25~35 μmol/L) for 24 h and the cytotoxicity was determined by MTT assay, while apoptotic cells were identified by TUNEL assay, acridine orange/ethidium bromide staining and flow cytometry.

Enhanced solar cell performance by replacing benzodithiophene with naphthodithiophene in diketopyrrolopyrrole-based copolymers.

Replacing benzodithiophene (BDT) with a naphthodithiophene (NDT) building block, PNDTDPP exhibited enhanced photovoltaic performance with a PCE of 5.37% when compared with BDT-based copolymer PBDDPP, which gave a PCE of 2.91% in conventional device structures.

Cytoprotective effect of trolox against oxidative damage and apoptosis in the NRK-52e cells induced by melamine.

An outbreak of urinary stones associated with consumption of melamine-tainted milk products occurred in 2008 in China, leading to serious illness of many infants and even death. However, the toxicity of melamine in kidney epithelial cells remains unclear. We have explored the effects of melamine and trolox on renal NRK-52e (normal rat kidney 52e) cells.

Zearalenone induces apoptosis and necrosis in porcine granulosa cells via a caspase-3- and caspase-9-dependent mitochondrial signaling pathway.

Zearalenone is a mycotoxin produced mainly by Fusarium. There are numerous incidences of mycotoxicosis in laboratory and domestic animals, especially in pigs. However, little is known about molecular mechanisms of zearalenone toxicity.

DNA damage and decrease of cellular oxidase activity in piglet Sertoli cells exposed to arsanilic acid.

The study was designed to explore the toxic effects of arsanilic acid on piglet Sertoli cells. Sertoli cells were isolated from piglet testes using a two-step enzyme digestion followed by differential plating. Piglet Sertoli cells were cultured and classified into the following five groups: group A, the control without arsanilic acid treatment; group B, cultured with 5 µM arsanilic acid; group C, cultured with 50 µM arsanilic acid; group D, cultured with 0.