Peptide-Drug Conjugate Targeting Keratin 1 Inhibits Triple-Negative Breast Cancer in Mice.

Selective delivery of chemotherapy to the tumor site while sparing healthy cells and tissues is an attractive approach for cancer treatment. Carriers such as peptides can facilitate selective tumor targeting and payload delivery. Peptides with specific affinity for the overexpressed cell-surface receptors in cancer cells are conjugated to chemotherapy to afford peptide-drug conjugates (PDCs) that show selective uptake by cancer cells.

RIPK1 Mediates TNF-Induced Intestinal Crypt Apoptosis During Chronic NF-κB Activation.

Background And Aims: Tumor necrosis factor (TNF) is a major pathogenic effector and a therapeutic target in inflammatory bowel disease (IBD), yet the basis for TNF-induced intestinal epithelial cell (IEC) death is unknown, because TNF does not kill normal IECs. Here, we investigated how chronic nuclear factor (NF)- κB activation, which occurs in human IBD, promotes TNF-dependent IEC death in mice.

Methods: Human IBD specimens were stained for p65 and cleaved caspase-3.

Dysregulation of Intestinal Epithelial Cell RIPK Pathways Promotes Chronic Inflammation in the IBD Gut.

Crohn's disease (CD) and ulcerative colitis (UC) are common intestinal bowel diseases (IBD) characterized by intestinal epithelial injury including extensive epithelial cell death, mucosal erosion, ulceration, and crypt abscess formation. Several factors including activated signaling pathways, microbial dysbiosis, and immune deregulation contribute to disease progression. Although most research efforts to date have focused on immune cells, it is becoming increasingly clear that intestinal epithelial cells (IEC) are important players in IBD pathogenesis.