Loss of Tyrosine Phosphatase Delta Promotes Gastric Cancer Progression via Signal Transducer and Activator of Transcription 3 Pathways.

BACKGROUND: The protein tyrosine phosphatase delta (PTPRD) is a tumor suppressor, and its role in gastric cancer (GC) remains poorly understood. METHODS: The expressions of PTPRD were determined based on public data. In addition, the mRNA expressions of PTPRD in the GC samples, and the expressions of PTPRD in the GC cell lines including HGC27, SGC790, and BGC823, and gastric epithelial cell line GES-1 were determined by western blotting and quantitative real-time PCR. Furthermore, PTPRD siRNA was transfected into the HGC27 cell line, and then, cell proliferation, migration, and invasion were evaluated. The activity of signal transducer and activator of transcription 3 (STAT3) pathways in HGC27 cells transfected with PTPRD siRNA was determined by western blotting. RESULTS: PTPRD deletion was found in the GC patients, and this deletion was found to be correlated with poor prognosis in the GC patients. Expression of PTPRD was significantly downregulated in gastric carcinoma specimens and tumor cell lines when compared with those in normal controls. PTPRD also plays a key role in the GC cells proliferation, invasion, and migration. Silencing PTPRD expression by siRNA dramatically promoted GC cells proliferation, invasion, and migration. Mechanism study demonstrated that phosphorylation of STAT3 was inhibited by silencing PTPRD expression and the according changes including inhibition of cell migration and invasion were observed. CONCLUSION: This study supports PTPRD as a tumor suppressor and could be served as a marker for prognostic of GC. Silencing PTPRD could be a potential therapeutic in GC.

[Protective effects of sulforaphane on the oxidative damage of kidney mitochondria complex in obese rats induced by high-fat diet].

OBJECTIVE: To realize the oxidative damage of kidney mitochondrial complex in obese rats induced by high-fat diet and investigate the protective effects of sulforaphane against the damage. METHODS: Eighty-eight adult male SD rats were used, after 1 week adaptability feeding, 8 rats were selected as control group and given low-fat diet. The other 80 rats were given high-fat diet. After 2 weeks, the 32 diet-induced obesity models were choosen whose weight gain was higher than 40%. The 32 rats were randomly divided into 4 groups, i.e. high fat group, high fat+sulforaphane low dose group, high fat+sulforaphane middle dose group and high fat+sulforaphane high dose group. The rats in the sulforaphane low, middle and high dose groups were orally administered with sulforaphane 5, 10 and 20 mg/kg, all the 4 groups were kept feeding high-fat diet for 5 weeks. All rats were sacrificed and their kidneys were removed to assay the index of oxidative damages. RESULTS: The content of ROS (0.26 ± 0.04) and MDA((0.87 ± 0.05) U/mg) in the hight-fat group were significantly higher than those in the control group((0.20 ± 0.02),(0.57 ± 0.08) U/mg)(t values were -3.02 and -4.72, P < 0.05). The activity of T-AOC((0.43 ± 0.04) U/mg) and MMP (12.09 ± 1.56) were lower than the control group ((0.48 ± 0.04 U/mg, (16.08 ± 3.12) )(t values were 2.06 and 2.28, P < 0.05). Gavage intervention with sulforaphane, the MDA amount ((0.67 ± 0.05), (0.55 ± 0.05), (0.56 ± 0.07) U/mg) in the sulforaphane low, middle and high dose groups were lower than the hight-fat group ((0.87 ± 0.05) U/mg (t values were 3.65, 5.71 and 5.60. P < 0.05). The activity of T-AOC ((0.49 ± 0.05), (0.55 ± 0.05), (0.54 ± 0.04) U/mg), T-SOD ((61.07 ± 2.79), (55.95 ± 2.39), (60.26 ± 6.02) U/mg) and the level of MMP ((17.17 ± 2.52), (18.24 ± 2.54), (18.21 ± 3.65)) were higher than in the high-fat group ((0.43 ± 0.04) U/mg,(47.22 ± 2.43) U/mg,(12.09 ± 1.56)) (tT-AOC values were -2.36, -4.83 and -4.30; tT-SOD values were -6.37, -4.71 and -5.99; tMMP values were -2.90, -3.52 and -3.50, P < 0.05). The activity of GSH-Px in the sulforaphane low and middle dose groups ((69.12 ± 8.63), (64.43 ± 6.58) U/mg) were higher than those in the high-fat group((53.03 ± 5.70) U/mg)(t values were -3.82 and -2.71, P < 0.05). But there were no significant difference between the high dose group ((60.02 ± 7.05) U/mg) and the high-fat group (t = -1.66, P > 0.05). CONCLUSION: High-fat diet can induce the mitochondrial oxidative dysfunction in kidney, and sulforaphane shows protective effect on the kidney mitochondrial complex from oxidative damage in obese rats induced by high-fat diet.

Clinical and CT Imaging Differences Between Gastric Schwannoma and Gastric Leiomyoma.

OBJECTIVE: To determine whether computed tomography (CT) imaging features can be used to differentiate gastric schwannoma (GS) from gastric leiomyoma (GL) and to develop a nomogram as a predictive model. STUDY DESIGN: Retrospective study. Place and Duration of the Study: Department of Medical Imaging, Affiliated Hospital of Jining Medical University, Jining, Shandong, China, from July 2009 to June 2022. METHODOLOGY: Clinical and imaging data of 43 patients with GS and 57 patients with GL were analysed retrospectively. The independent factors for differentiating GS and GL were obtained by the logistic regression analysis. Receiver operating characteristic curve (ROC) was plotted, area under curve (AUC) and calibration tests were used to evaluate the diagnostic efficiency of the model. RESULTS: The GS group had more females and was older than the GL group (p <0.05). There were statistical differences between the two groups in tumour location, growth mode, LD/SD ratio, necrosis, ulcers, the presence of tumour-associated lymph nodes, enhancement degree, and the HU (Hounsfield units) values of tumour in the venous phase and delayed phase (p <0.05). Logistic regression analysis showed that tumour location, growth mode, LD/SD (long and short diameters) ratio, and the presence of tumour-associated lymph nodes were independent factors in differentiating GS from GL, and a nomogram model was established accordingly. When the model threshold was >0.319, the AUC was 0.987 (95% confidence interval [CI] 0.941~0.999). The sensitivity and specificity were 97.7% and 94.7%, respectively. CONCLUSION: The proposed nomogram model based on CT imaging features can be used to differentiate GS from GL. KEY WORDS: Gastric leiomyoma, Gastric schwannoma, Computed tomography, Diagnosis.