Objective To evaluate the value of 3.0T magnetic resonance multi-b value diffusion-weighted imaging (DWI) in evaluating the efficacy of chemotherapy for patients with central lung squamous cell carcinoma and atelectasis. Methods Twenty patients with lung squamous cell carcinoma were examined by magnetic resonance imaging (MRI) (including T1WI, T2WI and multi-b value DWI) before chemotherapy, 2 cycles of chemotherapy and 4 cycles of chemotherapy. The images, the tumor volume and changes of apparent diffusion coefficient (ADC) were analyzed. Results In the patients with central lung cancer and atelectasis, the tumor and atelectasis could be distinguished on MRI examination before radiotherapy. It was more easily identified on T2WI images after radiotherapy. In the 20 patients, the ADC values in the effective group (partial remission or complete remission) and the invalid group were increased, but the differences of ADC values in the effective group before chemotherapy, 2 cycles and 4 cycles of chemotherapy were statistically significant [b=800 s/mm2:(1.09 ± 0.52) × 10-6 mm2/s, (1.22 ± 0.59) × 10-6 mm2/s, (1.24 ± 0.52) × 10-6 mm2/s, F = 31.19, P < 0.001]. There was no significant difference in ADC values between before and after chemotherapy (b = 800 s/mm2: (1.10 ± 0.49) × 10-6 mm2/s, (1.16 ± 0.60) × 10-6 mm2/s, (1.20 ± 0.72) × 10-6 mm2/s, F=2.86, P=0.089]. When b=800 s/mm2, the ADC curve slope in the effective group was more stable, better linearity. Conclusions The MRI technique can accurately distinguish the tumor from atelectasis before and after chemotherapy. The change of ADC value after chemotherapy is earlier than that of morphological change. The change rate of b value can better evaluate the curative effect of chemotherapy.

Escherichia coli ; genetics ; metabolism ; Escherichia coli Proteins ; genetics ; Gene Knockout Techniques ; Hydrogen-Ion Concentration ; Peptide Initiation Factors ; genetics ; Polyribosomes ; metabolism ; Protein Biosynthesis ; Stress, Physiological

Objective: To investigate the expression and functional role of FK506 binding protein 10 (FKBP10) in oral squamous cell carcinoma (OSCC), and to provide a research basis for the estimated prognosis and targeted therapy of OSCC. Methods: A total of 284 OSCC samples and 19 normal samples were selected from the Cancer Genome Atlas (TCGA) database, and diagnostic analysis was performed to determine mRNA expression. Survival analysis for FKBP10 and OSCC was conducted on a gene expression profile interaction analysis website. Real-time fluorescence quantitative PCR and Western Blot were used to detect the mRNA and protein expression of FKBP10 in four OSCC cell lines and SAS and SCC9 cells transfected with siRNA. The cell proliferation ability of FKBP10-silenced cells was detected using the CCK8 method, and the cell cycle distribution and apoptosis were detected by flow cytometry. Cell migration and invasion ability were detected through wound healing and invasion experiments. The expression changes of total protein and phosphatidylinositol 3-kinase (PI3K)-serine/threonine kinase (AKT) after FKBP10 silencing were analyzed by proteomics and Western Blot. Results: According to the analysis of gene expression levels, the mRNA expression level of FKBP10 in OSCC was significantly higher than that in normal tissues (P < 0.001). In terms of diagnosis, the expression level of FKBP10 has unique diagnostic value for OSCC (P < 0.05). The survival analysis of FKBP10 and OSCC showed that a high expression of FKBP10 led to a decrease in patient survival and poor prognosis (P < 0.05). The expression of FKBP10 mRNA and protein in OSCC cell lines was higher than that in normal oral keratinocytes (P < 0.001). Silencing FKBP10 can reduce the proliferation, invasion, and migration ability of SAS and SCC9 (P < 0.001), and also block their cell cycle in the G0/G1 phase (P < 0.001), with a significant increase in apoptosis (P < 0.05). Protein mass spectrometry and Western blot analysis revealed that FKBP10 silencing significantly downregulated the expression of multiple proteins in the RAP1 signaling pathway, mainly RAP guanine nucleotide exchange factor 1 (RAPGEF1) (P < 0.05) and the phosphorylation of PI3K-AKT proteins (P < 0.05). Conclusion FKBP10 is highly expressed in OSCC, leading to poor prognosis for patients. Downregulated FKBP10 expression can inhibit the proliferation, migration, and invasion ability of OSCC cells, hinder cell cycle progression, and promote apoptosis via the RAP1-PI3K-AKT axis. FKBP10 is a potential therapeutic target and prognostic biomarker for OSCC.