No abstract

The presence of a live cell cohabiting within another cell has fascinated scientists for many decades. Far from being a spurious event, many have attempted to uncover the molecular mechanism underlying this phenomenon. In this study, we observed anchorage-dependent MCF-7 cells internalizing neighboring epithelial cells (entosis) after siRNA-mediated silencing of the Metallothionein-2A (MT-2A) gene. MTs belong to a family of low-molecular weight proteins, which bind metal ions endogenously and its over-expression has been reported in a variety of cancers that include breast, prostate, and colon. We provide microscopic evidence at light and ultrastructural levels of the occurrence of entosis after altering MT expression in a subpopulation of MCF-7 breast cancer cells by silencing the MT-2A gene. Our results demonstrate that adheren junctions may play important roles in the formation of cell-in-cell cytostructure after MT-2A gene downregulation and the entotic process does not appear to involve genes associated with autophagy. Interiorized cells often underwent lysosomal degradation within the cytoplasmic body of the engulfing cell. It would appear that a subset of breast cancer cells could die via entosis after MT-2A gene silencing. Anat Rec, 293:1685Rec, 293: -1691

Integrin binding to ligand plays essential roles in the differentiation and function of mammalian cells. beta2 integrins in leukocytes are needed for migration to sites of inflammation and in lymph nodes as well as for cellular events such as phagocytosis and the formation of the conjugates between T cells and antigen-presenting cells. In T cells, integrin adhesion is activated primarily by the antigen-receptor (TCR complex) and chemokines in a process known as 'inside-out' signalling. Great progress has been made in identifying mutations that are responsible for leukocyte adhesion deficiency (LAD) syndromes, a disorder that presents with an impaired ability to clear pathogens and recurrent life-threatening infections. LAD mutations have been identified with defects in integrins, fucosylation and in the new intracellular mediator kindlin-3. Here, we review the key players in the 'inside-out' and 'outside-in' signalling pathways that will serve as new potential targets in the design of novel therapeutics to treat various immunodeficiencies.

Hibiscus chlorotic ringspot virus (HCRSV), a Carmovirus, occurs worldwide and induces chlorotic ringspots on leaves, stunting and flower distortion in Hibiscus species, including kenaf. The HCRSV capsid has T = 3 icosahedral symmetry and contains 180 copies of the coat protein. A virus yield of 48-70 mg per 100 g of infected kenaf leaves was achieved with an improved purification scheme involving sucrose-cushion and sucrose density-gradient centrifugation. The virus was crystallized using PEG 8000 and 2,3-butanediol as co-precipitants. The crystals belonged to the cubic space group P23, with unit-cell parameter a = 392 A, and diffracted X-rays to at least 4.5 A resolution.

Keloids are proliferative growths of dermal collagen, usually resulting from excessive tissue response during wound healing. There is evidence that keratinocytes may promote keloidogenesis via epithelial-mesenchymal interactions. Metallothioneins (MTs) are known to be involved in the fundamental cellular processes of growth and apoptosis. In this study, we evaluated the expression of MT isoforms in normal and keloid keratinocytes. The expression patterns of ten functional MT isoforms were assessed using real-time RT-PCR in primary cultures of normal and keloid keratinocytes. The MT-2A isoform was the most abundant MT isoform in both normal and keloid keratinocytes while the MT-1B isoform was absent. There was a significant increase in the mRNA expression of four MT isoforms, viz. MT-1A, 1E, 1F and 2A in keloid keratinocytes as compared to normal keratinocytes. Up-regulation of MT-1A, 1E, 1F and 2A isoforms may play a part in the development of keloids by paracrine signaling.