Heat shock protein 20 suppresses breast carcinogenesis by inhibiting the MAPK and AKT signaling pathways.

Heat shock protein (HSP) 20 belongs to the small HSP family and exhibits diverse functions, including tumor suppression, in addition to being a molecular chaperon, which is the classical property of HSPs. The present study aimed to examine the association between HSP20 expression and breast cancer (BC) progression in patients, and to explore the possible role of HSP20 in malignant phenotypes of BC cells. A series of experiments, including reverse transcription-quantitative PCR, western blotting, Cell Counting Kit-8 and flow cytometry, were performed. Data from Gene Expression Omnibus and Kaplan-Meier Plotter revealed that HSP20 expression was significantly downregulated in BC tissues, and patients with BC with lower HSP20 expression exhibited poorer recurrence-free survival. The data revealed that HSP20 was closely associated with the pathological tumor stage (P=0.015) and pathological tumor node metastasis (P=0.031) of patients with BC. Additionally, HSP20 expression was markedly decreased in BC cell lines. Exogenous overexpression of HSP20 inhibited proliferation and accelerated apoptosis of BC cells. These cells exhibited decreased migration and invasion when HSP20 was overexpressed. Furthermore, HSP20 overexpression suppressed the MAPK and AKT signaling pathways, as evidenced by the reduced phosphorylation levels of AKT, ERK, JNK and p38. Knockdown of HSP20 exerted the opposite effects. Notably, the AKT agonist, SC79, and the ERK agonist, LM22B-10, reversed the decrease in cell proliferation and migration induced by HSP20 overexpression. Overall, the data suggest that the decreased expression of HSP20 in BC tissues may be associated with disease progression. HSP20 also attenuated the malignant phenotype of BC cells and the inhibition of MAPK and AKT signaling may be associated with this effect. Therefore, HSP20 may be a potential prognostic marker or a candidate therapeutic target for BC.

Complications after appendectomy in patients with treated appendicitis: results from a retrospective study.

BACKGROUND: This study was designed to provide additional insights into the incidence of appendectomy complications in patients with appendicitis. METHODS: A total of 619 patients who underwent appendectomy for appendicitis between 2014 and 2020 were recruited. Preoperative patient data and details of postoperative complications were collected. Comparisons between simple and complex appendicitis were obtained via univariate and multivariate analyses of the outcomes. RESULTS: Simple and complex appendicitis was diagnosed in 192 and 427 patients, respectively. Twenty-eight patients with simple appendicitis developed complications, and 14 of these were infectious complications. In patients with complex appendicitis, 65 patients developed complications, and 55 of these were infectious complications. Infectious complications were identified as the largest proportion of complications. The significant risk factor for infectious complications in simple appendicitis was American Society of Anesthesiologists (ASA) grade [odds ratio (OR) =7.843, 95% confidence interval (CI): 1.987-30.955, P=0.003]. ASA grade (OR =1.992, P=0.032) and positive bacterial culture (OR =4.019, 95% CI: 1.809-8.933, P=0.001) were significantly related to infectious complication in complex appendicitis. CONCLUSIONS: This study showed that appendectomy is not always a routine operation with few complications. There was a relatively high rate of complications in patients with appendicitis, which were mostly infectious complications. A higher ASA grade correlated with infectious complication. In some cases of complex appendicitis, patients with positive bacterial culture may have had a greater risk of infectious complications.

Increased EXT1 gene copy number correlates with increased mRNA level predicts short disease-free survival in hepatocellular carcinoma without vascular invasion.

Exostosin-1 (EXT1) has been demonstrated to participate in the progression of many cancers. However, it has not been previously described in patients with hepatocellular carcinoma (HCC) without vascular invasion. In this study, we got the accurate data of EXT1 mRNA Z-score from the CBio data portal of The Cancer Genome Atlas (TCGA), which was used to express the level of EXT1 gene expression. We analyzed the EXT1 gene expression between HCC and normal liver tissue and compared the clinical significance of tumor tissue's EXT1 gene expression of HCC patients without vascular invasion based on data from TCGA database. The association between EXT1 gene expression and disease-free survival (DFS) was further analyzed. EXT1 gene copy number was also analyzed in this study. Univariate and multivariate analyses showed that high EXT1 gene expression group was significantly poorer than that of the low EXT1 gene expression group (P = .004). In addition, EXT1 gene expression was positively associated with α-fetoprotein (AFP), which is a well-known marker for HCC. There was a significant positive correlation between EXT1 copy number and upregulated EXT1 gene (P < .0001). In conclusion, upregulation of EXT1 could be an important indicator to the short DFS of HCC patients without vascular invasion. EXT1 gene copy number amplification is one of the mechanisms underlying the upregulation of EXT1.