Optimizing autophagy modulation for enhanced TRAIL-mediated therapy: Unveiling the superiority of late-stage inhibition over early-stage inhibition to overcome therapy resistance in cancer.

Autophagy is a vital mechanism that eliminates large cytoplasmic components via lysosomal degradation to maintain cellular homeostasis. The role of autophagy in cancer treatment has been studied extensively. Autophagy primarily prevents tumour initiation by maintaining genomic stability and preventing cellular inflammation.

Zoonotic linkage and environmental contamination of Methicillin-resistant (MRSA) in dairy farms: A one health perspective.

Methicillin-Resistant (MRSA) is a ubiquitous public health challenge, with its prevalence in human, animal, and environmental interfaces posing significant concerns. This study aimed to characterize and detect the zoonotic linkages of MRSA within the cow-environment-human interfaces in dairy farms to address the One Health perspective. A comprehensive investigation, involving 636 samples (an equal number of raw milk and cow nasal swab samples, along with varying numbers of human nasal swab and environmental samples), revealed an overall MRSA prevalence of 13.

An Antidepressant Drug Increased TRAIL Receptor-2 Expression and Sensitized Lung Cancer Cells to TRAIL-induced Apoptosis.

Background: TRAIL has emerged as a promising therapeutic target due to its ability to selectively induce apoptosis in cancer cells while sparing normal cells. Autophagy, a highly regulated cellular recycling mechanism, is known to play a cell survival role by providing a required environment for the cell. Recent studies suggest that autophagy plays a significant role in increasing TRAIL resistance in certain cancer cells.

Inhibition of autophagy flux by sertraline attenuates TRAIL resistance in lung cancer via death receptor 5 upregulation.

Tumor necrosis factor‑related apoptosis‑inducing ligand (TRAIL) is a potential target for cancer therapy, owing to its ability to selectively kill cancer cells without causing significant toxicity to normal cells. However, due to the lack of death receptor expression, cancer cells can become highly resistant to TRAIL. Hence, it is vital to develop agents that restore TRAIL efficacy.