Determination of the Levels of Expression of Sarcolectin and Calcyclin and of the Percentages of Apoptotic But Not Proliferating Cells to Enable Distinction Between Recurrent and Nonrecurrent Cholesteatomas

Abstract

The present data emphasize the existence of distinct subgroups of cholesteatomas identifiable at both cell kinetic and differentiation levels. Some of the biological variables used here to identify distinct biological subgroups of cholesteatomas in turn enabled some biological variables to be identified, so making it possible to classify the cholesteatomas in terms of recurrence versus nonrecurrence.

Expression of S100A6 in Cardiac Myocytes Limits Apoptosis Induced by Tumor Necrosis Factor-α

“…Taken together, the above data indicate that the same TNF-␣ pathway that initiates and sustains the apoptotic response in cardiac myocytes and is subject to negative modulation by S100A6 also induces S100A6. In agreement with our observation that S100A6 is an anti-apoptotic gene, in a cholesteatoma cell line, high levels of S100A6 were associated with the lowest levels of apoptosis (11). However, several recent publications have shown that exogenously administered S100A6 at micromolar concentrations induces glioblastoma cell apoptosis by interacting with the receptor for advanced glycation end products (47), and exogenously introduced S100A6 to a human liver cell line (Hep3B and HepG2) potentiated apoptotic response of the calcium ionophore A23187 (48).…”

“…S100A6 (calcyclin), a 10-kDa protein belonging to the S100 subfamily of EF-hand, calcium-binding proteins (1)(2)(3), is expressed in diverse tissues, including smooth muscle, brain, lung, kidney, and heart (4 -5), and has been linked with cell cycle progression (6 -8), cytoskeleton rearrangement (9), exocytosis (10), and cell survival (11). Stimuli, including growth factors (12), inflammatory cytokines (13), vasopressin (14), phorbol esters (15), and cadmium ions (16), have been reported to induce an increase in S100A6 mRNA and/or protein levels.…”

Possible Involvement of Keratinocyte Growth Factor and Its Receptor in Enhanced Epithelial-Cell Proliferation and Acquired Recurrence of Middle-Ear Cholesteatoma

“…More importantly, expression of both KGF and KGFR correlated with recurrence within 18 months after operation. To our knowledge, there is no information on the molecular mechanisms that could affect cell kinetics in cholesteatoma, apart from the study of Choufani et al (1999), who demonstrated major differences between recurrent and nonrecurrent cholesteatomas with respect to the extent of apoptosis, distribution of apoptotic cells, and percentage of calcyclin-positive cells. Taken together, the present results suggest that the interaction between KGF and KGFR may be involved in the recurrence of cholesteatoma.…”

Proteomic Analyses of Proteins Differentially Expressed in Recurrent and Primary Pterygia

“…PA28 is associated with the processing of p53 [21], and is also homologous to a Ki-antigen that contains the "KEKE" motif [22]. In addition, sarcolectin (S7), which is co-expressed with p53 and co-localized with Ki-67 in leiomyoma [23], was also down-regulated. These findings suggest that PA28 and sarcolectin are associated with p53 and Ki-ras-dependent signaling pathway for cell cycle regulation, and they may also have an effect on the recurrency of a pterygium.…”