Objective To investigate the influence of cyclooxygenase-2 (COX-2) knock-down on cell proliferation and apoptosis in gastric cancer cell line SGC7901.Methods The mRNA levels of COX-2 in SGC7901 and gastric epithelium cells (GES) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) assays.The influence of COX-2 on the proliferation and apoptosis of cell line SGC7901 was evaluated with methyl thiazolyl tetrazolium (MTT) and fluorescence-activated cell sorter (FACS) assay.Results qRT-PCR assay indicated that the mRNA level of COX-2 in SGC7901 was significantly higher than that in GES (P ＜ 0.01).MTT and FACS assays showed that the proliferation was reversed by COX-2 knock-down in SGC7901 cells.Up-regulated Bax and down-regulated Bcl-2 can inhibit the expression of COX-2.Conclusions COX-2 could contribute to the proliferation of gastric cancer cell line SGC7901.

Objective:To evaluate the effectiveness of contrast-enhanced ultrasound in the differential diagnosis of atypical adenomyosis and fibroids using a decision tree model.Methods:The data of cases with difficulty in differentiating atypical adenomyosis from fibroids on conventional ultrasound examination at Shengjing Hospital of China Medical University from April 2021 to April 2022 were selected and analyzed. Ninety-five patients with contrast-enhanced ultrasound examination were finally selected, including 64 patients in the pathologically confirmed adenomyosis group and 31 patients in the fibroids group. The data from the qualitative analysis and the quantitative analysis of the time-intensity curve (TIC) curve were collected separately, including the temporal variability of contrast entry into the lesion, i.e.the difference between the time when the contrast agent started to enter the lesion and the time when the contrast agent finally filled the lesion completely. Indicators were first screened for inclusion in the decision tree model by univariate and multifactorial analyses, and decision tree models based on qualitative analysis indicators, and qualitative and TIC-based analyses were developed to further assess the diagnostic efficacy of both models.Results:Through the univariate analysis, it showed that the qualitative analysis indicators of lesion onset enhancement pattern, enhancement intensity, intra-lesion contrast distribution, and post-contrast lesion border were of statistical significance (all P<0.05) between the two groups. The differences in contrast arrive time (AT), contrast time to peak (TTP), |ΔAT|, and |ΔTTP| in the TIC curve analysis indexes were statistically significant between the two groups (all P<0.05). The difference in lesion temporal phase variability was statistically significant between the two groups ( P<0.05). After further screening by multifactorial analysis, the accuracy and misdiagnosis rates were 87.40% and (17.90±3.90)% in the qualitative analysis-based decision tree model respectively, and 90.50% and (21.10±4.20) % in the qualitative and TIC curve-based analysis decision tree model respectively. The ROC curves were plotted according to the two groups of models, and the areas under the curves were 0.915 and 0.931 respectively. Conclusions:A decision tree model based on ultrasonographic image analysis has diagnostic value for the differential diagnosis of atypical adenomyosis and uterine fibroids.

Objective:To investigate the efficacy of postmastectomy radiotherapy (PMRT) for human epidermal growth factor receptor 2 (HER2)-positive T 1-2N 1M 0 breast cancer in the context of HER2-targeted therapy. Methods:This study collected the clinical data of 105 female patients with HER2-positive T 1-2N 1M 0 breast cancer who underwent modified radical mastectomy in the First Affiliated Hospital of Bengbu Medical College from January 2013 to December 2019. Then, the clinical outcomes of these patients were observed, and the prognostic factors and the efficacy of PMRT were analyzed. Results:The median follow-up time was 50 months (ranging from 14 to 107 months), and the 5-year overall survival (OS), local-regional recurrence-free survival(LRFS), and disease-free survival (DFS) were 81.6%, 91.9%, and 76.2%, respectively. The multivariate analysis indicated that independent prognostic factors for OS and DFS include the age, pathologic grade, and tumor size; the independent risk factors for LRFS include positive lymph node ratio (LNR) and hormone receptor (HR) status; and the independent prognostic factor for DFS was PMRT (HR: 2.85, 95% CI: 1.10-8.80, P < 0.05). The subgroup analysis suggested that PMRT significantly improved the OS of various high-risk subgroups ( χ2=4.01-9.18, P < 0.05). However, the further stratified analysis indicated that PMRT only increased the OS of the patients who did not receive HER2-targeted therapy in various high-risk subgroups ( χ2=4.50-6.70, P < 0.05), while there was no statistical difference before and after PMRT for the individuals who received targeted treatment ( P > 0.05). Conclusions:PMRT is an independent prognostic factor for the DFS of patients with HER2-positive T 1-2N 1M 0 breast cancer who underwent modified radical mastectomy. PMRT can improve the OS of high-risk patients with ages < 45 years old, pathologic grade Ⅲ, tumor diameter ≥ 3 cm, LNR > 10%, and HR (-) who received no HER2-targeted therapy. However, the efficacy may be compromised to some extent in the context of the application of HER2-targeted therapy.

The mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway is widely activated by a variety of extracellular stimuli, and its dysregulation is associated with the proliferation, invasion, and migration of cancer cells. ERK1/2 is located at the distal end of this pathway and rarely undergoes mutations, making it an attractive target for anticancer drug development. Currently, an increasing number of ERK1/2 inhibitors have been designed and synthesized for antitumor therapy, among which representative compounds have entered clinical trials. When ERK1/2 signal transduction is eliminated, ERK5 may provide a bypass route to rescue proliferation, and weaken the potency of ERK1/2 inhibitors. Therefore, drug research targeting ERK5 or based on the compensatory mechanism of ERK5 for ERK1/2 opens up a new way for oncotherapy. This review provides an overview of the physiological and biological functions of ERKs, focuses on the structure-activity relationships of small molecule inhibitors targeting ERKs, with a view to providing guidance for future drug design and optimization, and discusses the potential therapeutic strategies to overcome drug resistance.