Synergistic neurotoxicity of polystyrene nanoparticles and MEHP in zebrafish (Danio rerio).

The surge in global plastic usage has exacerbated the pollution of nanoplastics and plasticizers in aquatic ecosystems, causing widespread concern about population health issues. We used a zebrafish model to investigate the combined toxicity of polystyrene nanoparticles (PS-NPs) and plasticizer metabolite mono-(2-ethylhexyl) phthalate (MEHP), revealing the synergistic neurotoxic effects and potential mechanisms of compound exposure. Co-exposure amplifies the bioaccumulation of PS-NPs (p < 0.

Neurotoxicity of chronic nano-neodymium oxide exposure in zebrafish: Behavioral and molecular insights.

Rare earth elements (REEs) are crucial in modern technology and essential for the transition to a low-carbon economy. Despite the rising global demand for nano-neodymium oxide (NPs-NdO), a rare earth nanoparticle, comprehensive studies on its neurotoxic effects are limited. This study aims to elucidate the chronic neurotoxic effects of NPs-NdO and explore their molecular mechanisms.

Lanthanum oxide nanoparticles induce AHR-mediated hepatotoxicity in zebrafish via oxidative stress and metabolic dysregulation.

Lanthanum oxide nanoparticles (LaO NPs) are extensively utilized in industrial, medical, and technological fields and are increasingly infiltrating aquatic ecosystems; however, their ecotoxicological impacts remain poorly understood. This study used zebrafish to elucidate the hepatotoxicity induced by LaO NPs through oxidative stress, apoptosis, and metabolic dysregulation. Exposure to LaO NPs triggered reactive oxygen species (ROS) overload in the liver of larvae, provoking oxidative damage and hepatocyte apoptosis.

The effect and mechanisms of nano cerium dioxide (Nano-CeO) on cardiovascular development in zebrafish (Danio rerio).

The widespread application of nano-cerium dioxide (Nano-CeO) in agriculture, industry, and other fields has led to an increasing amount of it being released into the environment and becoming a pollutant with potential biological hazards. However, studies on the effects of ceria on cardiovascular development were limited. This study aims to detect the cardiovascular toxicity of Nano-CeO, focusing on its impact on zebrafish hematopoietic function and cardiac development, and to explore its potential molecular mechanisms.

PPARβ/δ-ANGPTL4 axis mediates the promotion of mono-2-ethylhexyl phthalic acid on MYCN-amplified neuroblastoma development.

Di-2-ethylhexyl phthalic acid (DEHP) is one of the most widely used plasticizers in the industry, which can improve the flexibility and durability of plastics. It is prone to migrate from various daily plastic products through wear and leaching into the surrounding environment and decompose into the more toxic metabolite mono-2-ethylhexyl phthalic acid (MEHP) after entering the human body. However, the impacts and mechanisms of MEHP on neuroblastoma are unclear.

CDKN2B-AS1 mediates proliferation and migration of vascular smooth muscle cells induced by insulin.

Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the intimal hyperplasia in type 2 diabetes mellitus (T2DM) patients after percutaneous coronary intervention. We aimed to investigate the role of lncRNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in VSMC proliferation and migration, as well as the underlying mechanism. T2DM model mice with carotid balloon injury were used in vivo and mouse aortic vascular smooth muscle cells (MOVAS) stimulated by insulin were used in vitro to assess the role of CDKN2B-AS1 in VSMC proliferation and migration following vascular injury in T2DM state.

lncRNA KCNQ1OT1 Suppresses the Inflammation and Proliferation of Vascular Smooth Muscle Cells through IκBa in Intimal Hyperplasia.

Inflammation and proliferation of vascular smooth muscle cells (VSMCs) are the key events in intimal hyperplasia. This study aimed to explore the mechanism by which long non-coding RNA (lncRNA) KCNQ1OT1 affects VSMC inflammation and proliferation in this context. A vein graft (VG) model was established in mice to introduce intimal hyperplasia.

DNA damage response--a double-edged sword in cancer prevention and cancer therapy.

Genomic stability depends on an efficient DNA damage repair system to keep the chromosomes intact. Unrepaired DNA damage not only causes cell cycle arrest, apoptosis, but also accumulates genome mutations. DNA damage response (DDR) exhibits a critical function on the protection against human cancer, as indicated by the high predisposition to cancer of individuals with germ-line mutations in DDR genes.

Melanoma differentiation associated gene-7/interleukin-24 induces caspase-3 denitrosylation to facilitate the activation of cancer cell apoptosis.

Melanoma differentiation-associated gene-7 (mda-7)/interleukin-24 (IL-24) induces caspase-3 cleavage and subsequent activation via the intrinsic or extrinsic pathway to result in cancer cell-selective apoptosis, but whether mda-7/IL-24 may directly regulate caspase-3 through the post-translational modification remains unknown. Here, we reported that tumor-selective replicating adenovirus ZD55-IL-24 led to caspase-3 denitrosylation and subsequent activation, indicating that caspase-3 denitrosylation played a crucial role in ZD55-IL-24-induced cancer cell apoptosis. To confirm the relationship between caspase-3 denitrosylation and its activation in response to ZD55-IL-24, we treated carcinoma cells with the different nitric oxide (NO) regulators to modulate caspase-3 denitrosylation level, then observed the corresponding caspase-3 cleavage.

Expression, purification, and characterization of RGD-mda-7, a His-tagged mda-7/IL-24 mutant protein.

RGD peptide (Arg-Gly-Asp tripeptide) binds to integrin αVβ(3) and αVβ(5), which is selectively expressed in tumor neovasculature and on the surface of some tumor cells. Some studies showed that coupling the RGD peptides to anticancer drugs yielded compounds with increased efficiency against tumors and lowered toxicity to normal tissues. The melanoma differentiation-associated gene-7/interleukin-24 gene (mda-7/IL-24) is a novel tumor-suppressor/cytokine gene that exhibits potent tumor-suppressive activity without damaging normal cells.

MDA-7/IL-24 induces Bcl-2 denitrosylation and ubiquitin-degradation involved in cancer cell apoptosis.

MDA-7/IL-24 was involved in the specific cancer apoptosis through suppression of Bcl-2 expression, which is a key apoptosis regulatory protein of the mitochondrial death pathway. However, the underlying mechanisms of this regulation are unclear. We report here that tumor-selective replicating adenovirus ZD55-IL-24 leads to Bcl-2 S-denitrosylation and concomitant ubiquitination, which take part in the 26S proteasome degradation.

Potent antitumor effect elicited by RGD-mda-7, an mda-7/IL-24 mutant, via targeting the integrin receptor of tumor cells.

The melanoma differentiation-associated gene-7/interleukin-24 gene (mda-7/IL-24) is a novel tumor-suppressor/cytokine gene that exhibits potent tumor-suppressive activity without damaging normal cells. To enhance the antitumor effect, an mda-7/IL-24 mutant, RGD-mda-7, which includes the cell adhesive sequence 164Arg-165Gly-166Asp (RGD motif), was constructed and evaluated for bioactivity. RGD peptide binds to integrins α(V)β(3) and α(V)β(5), which are selectively expressed in tumor neovasculature and in the surface of some tumor cells.

A critical role of Sp1 transcription factor in regulating the human Ki-67 gene expression.

Ki-67 plays a crucial role in cell proliferation as well as maintenance or regulation of cell division. The mechanism governing the Ki-67 gene expression remains unknown. Thus, we cloned the core promoter of the human Ki-67 gene and further investigated its transcriptional regulation.

Identification of HLA-A*0201-restricted cytotoxic T lymphocyte epitope from proliferating cell nuclear antigen.

Peptide-based immunotherapy strategies appear promising as an approach to successfully induce an antitumor immune response and prolong survival in patients with various cancers. Protein antigens and their specific epitopes are formulation targets for anti-tumor vaccines. Bioinformatical approaches to predict major histocompatibility complex binding peptides can facilitate the resource-consuming effort of T cell epitope identification.

[Mechanistic study of nimesulide on enhancing gammadeltaT cell-mediated killing of gastric cancer cells].

Aim: To explore the effect of nimesulide on human gammadeltaT cell function.

Methods: gammadeltaT cells were cultured routinely, collected on the 9th day, and then induced with nimesulide at indicated concentrations (0.25 micromol/L, 0.

Potent antitumor efficacy of interleukin-18 delivered by conditionally replicative adenovirus vector in renal cell carcinoma-bearing nude mice via inhibition of angiogenesis.

It has been demonstrated that interleukin 18 (IL-18) exerts antitumor activity. In this study, we investigated whether oncolytic adenovirus-mediated gene transfer of IL-18 could induce strong antitumor activity. A tumor-selective replicating adenovirus expressing IL-18 (ZD55-IL-18) was constructed by insertion of an IL-18 expression cassette into the ZD55 vector, which is based on deletion of the adenoviral E1B 55-kDa gene.

Inhibition of renal cancer cell growth by oncolytic adenovirus armed short hairpin RNA targeting hTERT gene.

RNA interference (RNAi) has been proved to be a powerful tool for gene knockdown purpose and holds a great promise for the treatment of cancer. Our previous study demonstrated that the reduction of hTERT expression by means of chemically synthesized siRNAs and shRNAs expressed from plasmid resulted in proliferation inhibition in human renal carcinoma cells. In this study, we constructed a novel oncolytic adenovirus-based shRNA expression system, ZD55-hTERT, and to explore ZD55-hTERT-mediated RNAi for hTERT gene silencing.