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Gastric cancer is the second leading cancer-related mortality worldwide and more effective treatment strategies are urgently needed to combat the disease. Using lipoteichoic acid (LTA) and miR-27b-3p agomir, we aimed to assess the efficacy of this combination of therapies in treating gastric cancer.

The RNA levels of miR-27b-3p, FOXO3, MET, KRAS, vascular endothelial growth factor C (VEGFC), TSC1, and P65 were analyzed by quantified-PCR (Q-PCR) and the cell viability of AGS cells was analyzed by MTT. Confirm Luciferase reporter assays were used to explore the putative miR-27b-3p binding sites and Western blot analyzed the protein level of GAPDH, VEGFC, P65, AKT, and phosphorylated-AKT (p-AKT). The level of P65 in both the cytoplasm and nucleus of AGS cells was visualized by immunofluorescence assay. Subcutaneous xenograft models of gastric cancer were established, and mice were treated with miR-27b-3p agomir, LTA, or both. Hematoxylin-eosin staining and Ki-67 immunohistochemistry analysis of tumor tissues were then performed.

The results showed that the decreased expression of miR-27b-3p in gastric cancer cell lines inhibited the viability of AGS cells, and VEGFC was confirmed as the target of miR-27b-3p. In addition, ectopic expression of miR-27b-3p significantly inhibited the AKT pathway in AGS and N87 cells, and LTA suppressed the proliferation of gastric cancer cells by inhibiting the NF-κB pathway. In an established xenograft model, both miR-27b-3p agomir alone and LTA treatment alone inhibited tumor growth and treatment which combined the two showed an even stronger inhibitory effect.

Taken together, the combined use of LTA and miR-27b-3p agomir exhibited a synergistic effect in the treatment of gastric cancer.

Taken together, the combined use of LTA and miR-27b-3p agomir exhibited a synergistic effect in the treatment of gastric cancer.

Gastric cancer (GC) is a common malignant tumor with a high incidence in China. The use of immune checkpoint inhibitors has become the focus of tumor immunotherapy in recent years. This study was to investigate the clinicopathological and prognostic significance of programmed death ligant-1 (PD-L1) expression in GC.

We searched the PubMed, ScienceNet, EMbase, CNKI, and Wanfang databases for retrospective cohort studies on the clinicopathology and prognosis of PD-L1 expression in GC published between January 2010 and April 2020. The literature was first selected to extract data according to the inclusion and exclusion criteria, then a meta-analysis performed using Stata15.0 software. Publication bias and sensitivity analysis were carried out for the included studies.

A total of 3,218 patients in 15 studies were included in the meta-analysis. The positive expression of PD-L1 was related to a decrease in the 3-year survival rate (HR =1.32, 95% CI 1.02-1.49, P=0.028) and 5-year survival rate (HR =1.39, 95% CI 1.14-1.69, P=0.001). The difference in PD-L1 expression was related to lymph node metastasis (OR =1.73, 95% CI 1.18-2.54, P<0.001), but not to tumor stage (OR =1.28, 95% CI 0.81-2.02, P=0.292).

The results show that PD-L1 is related to the prognosis of GC. Its high expression decreases the 3- and 5-year survival rates and promotes lymph node metastasis, but does not reflect tumor stage. The results may provide a theoretical basis for the choice of clinical immunotherapy in GC patients.

The results show that PD-L1 is related to the prognosis of GC. Its high expression decreases the 3- and 5-year survival rates and promotes lymph node metastasis, but does not reflect tumor stage. The results may provide a theoretical basis for the choice of clinical immunotherapy in GC patients.

Radiation-induced gastrointestinal syndrome (GIS) often occurs after therapeutic or accidental exposure to high doses of radiation. Unfortunately, there are still no effective medical treatments for GIS. N-Myc downstream regulated gene 2 (NDRG2), is a tumor suppressor gene and promotes cell apoptosis and differentiation. The aim of our study was to identify the role of NDRG2 in the progression of GIS and explore the potential mechanism.

We generated Ndrg2

mice, lacking NDRG2 specifically in the intestinal epithelium. Survival analysis was performed to validate the effect of NDRG2 on GIS, and other common indicators (body weight loss and diarrhea) were used for the assessment of GIS. Enzyme-linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) were conducted to obtain the expression of pro-inflammatory interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α). TUNNEL and western blotting were further adopted to determine the relationship between NDRG2 an.

These findings all indicated that NDRG2 deficiency in the intestine protects mice against radiation-induced GIS mainly through promoting proliferation and suppressing apoptosis of epithelial cells.

As the population ages, the number of elderly patients with colorectal cancer is increasing year by year. However, older people have rarely been the focus of studies on colorectal cancer. Therefore, in the present study, we aimed to carry out a retrospective analysis of this patient subgroup.

A retrospective study of clinical data of patients aged over 80 years who died from colorectal cancer in our hospital between 1993 and 2020 was performed. Logistic regression, the Kaplan-Meier method, and a multivariate Cox proportional hazards model were used to analyze the overall survival and treatment outcomes of the patients.

A total of 87 patients were included in the study. The overall median survival was 45 months. In most patients, the primary lesion was located in the right colon. One-quarter of the patients refused to accept any treatment. selleck kinase inhibitor Patients with stage IV tumors, who accounted for the largest proportion of the study population, displayed a higher rate of abandoning treatment than did patients of other stages. Almost all patients with stages II and III accepted surgery. Patients who underwent surgery to treat their colorectal cancer had longer survival than those who did not.

Old age should not be a reason for giving up treatment for colorectal cancer. The treatment of colorectal cancer patients aged 80 years and above requires individualized evaluation and more aggressive treatment to achieve greater benefits.

Old age should not be a reason for giving up treatment for colorectal cancer. The treatment of colorectal cancer patients aged 80 years and above requires individualized evaluation and more aggressive treatment to achieve greater benefits.