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Oral squamous cell carcinoma (OSCC) is a common tumor in the world. Despite the rapid development of medical care, OSCC is also accompanied by high incidence and mortality every year. Therefore, it is still necessary to continuously develop new methods or find new targets to treat OSCC. Previous research showed that scavenger receptor class A member 5 (SCARA5) was one of the potential biomarkers of OSCC, and its expression is significantly low in OSCC. This study aimed to explore the role and related molecular mechanisms of SCARA5 in OSCC. In this study, we found that the SCARA5 expression was lower in CAL-27 and SCC-9 cells than that in human normal oral epithelial keratinocytes. SCARA5 overexpression significantly inhibited cell proliferation and induced apoptosis of CAL-27 and SCC-9 cells. In addition, SCARA5 repressed OSCC cell epithelial–mesenchymal transformation (EMT), evidenced by increased E-cadherin expression and reduced N-cadherin expression. Finally, we found that SCARA5 could suppress STAT3, PI3K, and AKT phosphorylation. Therefore, SCARA5 was related to STAT3 and PI3K/AKT signaling pathways in OSCC. In conclusion, SCARA5 inhibited the proliferation and EMT and induced the apoptosis of OSCC cells through the inhibition of STAT3 and PI3K/AKT signaling pathways, thereby exerting a tumor suppressor effect.

The spatiotemporal heterogeneity of rice canopy leaves at different leaf positions is very important for non-destructive monitoring under Cadmium (Cd) stress, and is one of the key problems that need to be solved urgently in modern agriculture. This study aims to explore the temporal and spatial heterogeneity of chlorophyll content and fluorescence in rice canopy leaves under different Cd stress concentrations. The responses of the relative chlorophyll content (SPAD) and Chlorophyll fluorescence (ChlF) parameters to Cd stress in the tillering, heading, and filling stages were analyzed through pot experiments with three Cd concentrations: 0.20 mg·kg−1 (CK), 0.60 mg·kg−1 (Cd1), and 1.60 mg·kg−1 (Cd2). Results showed that the canopy leaf SPAD value increased with increasing Cd concentration. Compared with CK, the leaf SPAD value in the Cd1 and Cd2 treatments were 1.91–3.45% and 5.52–12.01% lower, respectively. The SPAD value of the lower leaves was higher in the tillering stage, while the SPAD value of the upper leaves was higher in the heading and filling stages. The non-photochemical quenching coefficient (NPQ) of the third leaf (D3), the initial fluorescence yield (Fo) of the second leaf (D2), and the maximum photochemical efficiency (Fv/Fm) of photosystem II (PSII) in the tillering stage; the NPQ, Fo, and Fv/Fm of the D3 in the heading stage; and the NPQ, Fo, Fv/Fm, and Fv/Fm of the D2 in the filling stage were more sensitive to Cd stress than the other leaves and ChlF parameters. [ABSTRACT FROM AUTHOR]

Aim: Casein kinase 2 interacting protein-1 (CKIP-1) is a recently discovered intracellular regulator of bone formation, muscle cell differentiation, and tumor cell proliferation. Our study aims to identify the inhibition of BMP2-Smad1/5 signaling by CKIP-1 in odontoblastic differentiation of human dental pulp stem cells (DPSCs). Materials and Methods: DPSCs infected CKIP-1 siRNA or transfected CKIP-1 full-length plasmid were cultured in odontoblastic differentiation medium or added noggin (200 ng/mL) for 21 days. We examined the effects of CKIP-1 on odontoblastic differentiation, mineralized nodules formation, and interaction by western blot, real-time polymerase chain reaction (RT-PCR), alkaline phosphatase (ALP) staining, alizarin red S staining, and immunoprecipitation. Results: Firstly, we have demonstrated that CKIP-1 expression markedly decreased time-dependently along with cell odontoblastic differentiation. Indeed, the silence of CKIP-1 upregulated odontoblastic differentiation via BMP2-Smad1/5 signaling, while CKIP-1 over-expression had a negative effect on odontoblastic differentiation of DPSCs. Furthermore, CKIP-1 could interact with Neuropilin-1 (NRP1). Conclusions: This work provides data that advocates a novel perception on odontoblastic differentiation of DPSCs. Therefore, inhibiting the expression of CKIP-1 may be of great significance to the development of dental caries. [ABSTRACT FROM AUTHOR]