Triclosan (TCS) is used as an antimicrobial agent and has been widely dispersed and detected in the environment and organisms including human samples. Methyl-triclosan (MTCS) is the predominant bacterial TCS metabolite. At present, the toxicological effects and mechanism of TCS and MTCS are still not fully understood. In this study, the cytotoxic effects of TCS and MTCS in HepG2 cells were investigated in terms of cell proliferation, comet assay, cell cycle, and apoptosis. In addition, the expressions of related proteins were detected with western blotting analysis. The results showed that TCS could significantly inhibit cell proliferation, while MTCS had no obvious effect on cell growth. Both TCS and MTCS caused oxidative injury associated with HO-1 induction and increased DNA strand breaks, which consequently initiated the damage repair process via up-regulation of DNA-PKcs. In addition, TCS blocked the HepG2 cells in S and G2/M phases of cell cycle through down-regulation of cyclin A2 and CDK; while MTCS induced cell cycle arrest at the S phase through up-regulation of cyclin A2 and CDK. Furthermore, TCS activated p53 mediated apoptosis in HepG2 cells in a caspase-independent manner, while MTCS induced apoptosis was dependent on caspase. Moreover, TCS exposure exhibited more severe toxicity in HepG2 cells as compared with MTCS exposure, indicating that the replacement of the ionizable proton in TCS by the methyl group in MTCS is correlated with the cellular toxicity and the molecular mechanism.

/pdf/comparison-of-hepatotoxicity-and-mechanisms-induced-by-59go6x7279.pdf

Comparison of hepatotoxicity and mechanisms induced by triclosan (TCS) and methyl-triclosan (MTCS) in human liver hepatocellular HepG2 cells.

In our daily life, people are inevitably exposed to potentially hazardous chemical contaminants. More and more evidences indicate that environmental endocrine-disrupting chemicals (EDCs) negatively affect human reproductive health and are related to many diseases including infertility. Environmental reproductive health focuses on exposure to ubiquitous and persistent EDCs. This chapter mainly discusses the effects of EDCs on the outcome of human in vitro fertilization (IVF), including oocyte quality, fertilization, embryo quality, implantation, and live births. It may be useful for doctors to advise IVF patients to avoid these adverse environmental factors as much as possible. In addition, it is important for clinical embryologists to bear in mind that adverse IVF outcome may result from such undesirable environmental exposure, and quality management and quality control in the IVF laboratory should be strengthened.

Effects of Environmental EDCs on Oocyte Quality, Embryo Development, and the Outcome in Human IVF Process.

Colon cancer (CRC) is a prevalent malignancy that exhibits distinct differences in incidence, prognosis, and treatment responses between males and females. These disparities have long been attributed to hormonal differences, particularly the influence of oestrogen signalling. This review aims to provide a comprehensive analysis of recent advances in our understanding of the molecular mechanisms underlying sex differences in colon cancer and the protective role of membrane and nuclear oestrogen signalling in CRC development, progression, and therapeutic interventions. We discuss the epidemiological and molecular evidence supporting sex differences in colon cancer, followed by an exploration of the impact of oestrogen in CRC through various genomic and nongenomic signalling pathways involving membrane and nuclear oestrogen receptors. Furthermore, we examine the interplay between oestrogen receptors and other signalling pathways, in particular the Wnt/β-catenin proliferative pathway and hypoxia in shaping biological sex differences and oestrogen protective actions in colon cancer. Lastly, we highlight the potential therapeutic implications of targeting oestrogen signalling in the management of colon cancer and propose future research directions to address the current gaps in our understanding of this complex phenomenon.

Sex Differences in Colon Cancer: Genomic and Nongenomic Signalling of Oestrogen

OBJECTIVE
We aimed to determine the role of Troponin T1 (TNNT1) in paclitaxel (PTX) resistance and tumor progression in breast cancer (BC).


METHODS
Differentially expressed genes were obtained from the GSE4298 and GSE90564 datasets. Hub genes were isolated from protein-protein interaction networks and further validated by real-time quantitative polymerase chain reaction. The effect of TNNT1 on PTX resistance was determined using cell counting kit-8, 5-ethynyl-2'-deoxyuridine, wound healing, transwell, flow cytometry assays, and subcutaneous xenografted tumor model. Western blotting was used to detect proteins associated with PTX resistance, apoptosis, migration, invasion, and other key pathways. Hematoxylin-eosin and immunohistochemical staining were used to evaluate the role of TNNT1 in tumors.


RESULTS
After comprehensive bioinformatic analysis, we identified CCND1, IGF1, SFN, INHBA, TNNT1, and TNFSF11 as hub genes for PTX resistance in BC. TNNT1 plays a key role in BC and is upregulated in PTX-resistant BC cells. TNNT1 silencing inhibited PTX resistance, proliferation, migration, and invasion while promoting apoptosis of PTX-resistant BC cells. Tumor xenograft experiments revealed that TNNT1 silencing suppresses PTX resistance and tumor development in vivo. In addition, TNNT1 silencing inhibited the expression of proteins in the rat sarcoma virus (RAS)/rapidly accelerated fibrosarcoma1 (RAF1) pathway in vivo. Treatment with a RAS/RAF1 pathway activator reversed the inhibitory effect of TNNT1 silencing on proliferation, migration, and invasion while promoting apoptosis of PTX resistance BC cells.


CONCLUSION
Silencing of TNNT1 suppresses PTX resistance and BC progression by inhibiting the RAS/RAF1 pathway, which is a promising biomarker and therapeutic target for drug resistance in BC.

Troponin T1 silencing inhibits paclitaxel resistance and the development of breast cancer via suppressing rat sarcoma virus/rapidly accelerated fibrosarcoma 1 pathway.

Bioactive components in prunella vulgaris for treating Hashimoto’s disease via regulation of innate immune response in human thyrocytes

Testosterone promotes the migration, invasion and EMT process of papillary thyroid carcinoma by up-regulating Tnnt1.

Triclosan (TCS) is widely used as broad-spectrum antibacterial agent. However, it may threaten the health of human offspring if the mother is exposed to TCS during pregnancy. The present study aimed to identify potential mechanisms behind the toxic effect of TCS on the offspring of Caenorhabditis elegans (C. elegans), using this nematode as a suitable animal model. The results of the current study demonstrated that the locomotory behavior and reproductive capacity of C. elegans offspring was severely affected by prenatal exposure to different concentrations of TCS. A high‑throughput gene microarray was performed to investigate molecular alterations in C. elegans offspring following TCS exposure during pregnancy. Microarray results indicated that 113 genes were differentially expressed following TCS treatment compared with the control group. Gene ontology analysis demonstrated that these dysregulated genes were primarily associated with neuron development, muscular strength and reproduction. Pathway analysis results demonstrated that differentially expressed genes participated in several signaling pathways, including arginine, proline, and purine metabolism, progesterone‑mediated oocyte maturation and neuroactive ligand‑receptor interaction. Finally, 7 TCS toxicity-associated genes were confirmed by reverse transcription‑quantitative polymerase chain reaction. The present study indicates that TCS exposure during pregnancy may disturb the locomotory behavior and reproductive capacity of C. elegans offspring, primarily through 7 TCS toxicity‑associated genes, which merits further study from an environmental health perspective.

/pdf/potential-genetic-damage-to-nematode-offspring-following-4gsk5wqxda.pdf

Potential genetic damage to nematode offspring following exposure to triclosan during pregnancy

Primary human thyrocytes maintained the function of thyroid hormone production and secretion in vitro

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Testosterone promotes the migration, invasion and EMT process of papillary thyroid carcinoma by up-regulating Tnnt1.

Potential genetic damage to nematode offspring following exposure to triclosan during pregnancy

Primary human thyrocytes maintained the function of thyroid hormone production and secretion in vitro