The PPARβ/CERK/C1P signaling pathway is a potential mechanism by which antimony exposure promotes prostate cancer cell proliferation.

Prostate cancer (PCa) is the most common malignant tumor in males. Antimony (Sb) is a widespread industrial heavy metal pollutant listed as a Class IIB carcinogen by the International Agency for Research on Cancer (IARC). Previous work found that antimony exposure can promote the proliferation of prostate cancer cells, but the relevant molecular mechanisms have not been fully explored.

Transcriptomics analysis revealed that TAZ regulates the proliferation of KIRC cells through mitophagy.

Transcriptional Co-Activator with PDZ-Binding Motif (TAZ, also known as WWTR1) is a downstream effector of the Hippo pathway, involved in the regulation of organ regeneration and cell differentiation in processes such as development and regeneration. TAZ has been shown to play a tumor-promoting role in various cancers. Currently, many studies focus on the role of TAZ in the process of mitophagy.

The Present and Future of Artificial Intelligence in Urological Cancer.

Artificial intelligence has drawn more and more attention for both research and application in the field of medicine. It has considerable potential for urological cancer detection, therapy, and prognosis prediction due to its ability to choose features in data to complete a particular task autonomously. Although the clinical application of AI is still immature and faces drawbacks such as insufficient data and a lack of prospective clinical trials, AI will play an essential role in individualization and the whole management of cancers as research progresses.

Low-dose antimony exposure promotes prostate cancer proliferation by inhibiting ferroptosis via activation of the Nrf2-SLC7A11-GPX4 pathway.

Antimony (Sb) is a typical environmental pollutant. With the development of industrialization, antimony is widely used in daily life and enters the human body through the food chain, water source, air pollution, and other channels. The risk of antimony exposure has emerged as one of the public's major health concerns.

Antimony exposure promotes bladder tumor cell growth by inhibiting PINK1-Parkin-mediated mitophagy.

Antimony is one of the heavier pnictogens and is widely found in human food chains, water sources, and as an air pollutant. Recent years have seen steadily increasing concentrations of antimony in the ecological environment; critically, several studies have indicated that antimony might pose a tumorigenic risk factor in several cancers. Therefore, antimony toxicity has attracted increasing research attention, with the molecular mechanisms underlying suspected antimony-mediated tumor transformation of greatest interest.