RESUMEN
Background. A correlation has been noted between diabetes mellitus (DM) and changes in the oral cavity. The present study aimed to estimate, compare, and correlate serum and salivary glucose and IgA levels and salivary candidal carriage in diabetic and non-diabetic individuals. Methods. Eighty-eight subjects were categorized into three groups: group 1 (controlled DM; n=27), group 2 (uncontrolled DM; n=32) and group 3 (non-diabetics; n=29). Serum and salivary glucose levels were estimated by glucose oxidase/peroxidase method, serum and salivary IgA by a diagnostic kit, and candidal colonization by inoculating samples into Sabouraud dextrose agar plate. Statistical analyses were carried out by one-way ANOVA, post hoc Tukey tests, and Pearson's correlation coefficient. Results. Significant elevation of serum IgA levels was observed in group 2 compared to group 3 and significant decreases in salivary IgA levels in groups 1 and 2. The candidal carriage was significantly higher in group 2 compared to group 3. Serum glucose and salivary IgA levels showed a significant correlation in group 1. There was a positive correlation between serum/ salivary glucose and serum/salivary IgA levels in group 2. In addition, there was a significant correlation between serum glucose and serum IgA levels in group 3. Conclusion. Saliva could be a potential, non-invasive diagnostic tool to estimate glucose levels. The evaluation of salivary components, like IgA, might be useful in diagnosing and managing oral manifestations in diabetic individuals. Elevated salivary glucose levels contribute to elevated candidal carriage, making individuals susceptible to oral candidiasis.
RESUMEN
Protein phosphatases play a crucial role in cell cycle progression, cell survival, cellular signaling, and genomic integrity. The protein phosphatase 1 (PP1) regulatory subunit SDS22 plays a significant role in cell cycle progression. A recent study showed that SDS22 plays a vital role in epithelial integrity and tumor suppression in Drosophila. However, its tumor suppressive activity remains obscure in the mammalian system. Here, for the first time, we show that SDS22 inhibits the growth of breast cancer cells through induction of apoptosis. SDS22 negatively regulates the AKT kinase signaling pathway through PP1. SDS22 associates predominantly with AKT and dephosphorylates the phospho Thr308 and phospho Ser473 through PP1 and hence abrogates the cell migration, invasion, and tumor growth. Thus, our study deciphers the long-standing question of how PP1 negatively regulates the AKT signaling pathway. Further, we observed a significant converse correlation in the expression levels of SDS22 and phospho form of AKT with reduced levels of SDS22 in the higher grades of cancer. Overall, our results suggest that SDS22 could be a putative tumor suppressor and replenishment of SDS22 would be an important strategy to restrict the tumor progression.