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Abstract Background The role of annexin II in the development and progression of gastric cancer was explored. Methods Real-time PCR was conducted to detect annexin II and S100A6 mRNA expression. Protein expressions of annexin II and S100A6 were also examined by immunohistochemistry in 436 clinicopathologically characterized gastric cancer cases. Results The expression of annexin II and S100A6 mRNA differ significantly among gastric tumor tissue and matched non-cancerous gastric mucosa. Protein levels of annexin II and S100A6 were up-regulated in gastric cancer compared with adjacent non-cancerous tissues. High expression of annexin II correlated with age, location of tumor, size of tumor, differentiation, histological type, depth of invasion, vessel invasion, lymph node metastasis, distant metastasis and Tumor, Node, Metastasis (TNM) stage, and also with expression of S100A6. Further multivariate analysis suggested that expression of annexin II and S100A6 were independent prognostic indicators for gastric cancer. Cumulative five-year survival rates of patients with high expression of both annexin II and S100A6 was significantly lower than those with low expression of both. Conclusion Expression of annexin II in gastric cancer was significantly associated with depth of invasion, lymph node metastasis and distant metastasis, TNM stage, high S100A6 expression, and poor prognosis. Annexin II and S100A6 proteins could be useful prognostic marker to predict tumor progression and prognosis in gastric cancer.

Secondary resistance is a major limitation in the efficacy of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor treatment of lung cancer. Previous studies have shown that expression of the long non‑coding RNA HOX transcript antisense RNA (HOTAIR) is upregulated in lung cancer, which is correlated with metastasis and poor prognosis. However, the precise role of HOTAIR and its effects on gefitinib resistance in human lung adenocarcinoma are not known. To address this issue, in the present study we established a gefitinib‑resistant (R)PC‑9 human lung adenocarcinoma cell line and examined cell viability with the 3‑(4,5‑dimethylthiazol‑2‑yl)‑5‑(3‑carboxymethoxyphenyl)‑2‑ (4‑sulfophenyl)‑2H‑tetrazolium assay. We found that gefitinib concentrations <10 μM inhibited the viability of PC‑9 but not RPC‑9 cells in a dose‑dependent manner. Lentivirus‑mediated HOTAIR RNA interference induced cell apoptosis and S‑phase arrest, as determined by terminal deoxynucleotidyl transferase‑mediated dUTP nick end labeling and flow cytometry. Consistent with these observations, HOTAIR suppression was associated with tumor shrinkage and restoration of gefitinib sensitivity in RPC‑9 xenograft mice. Immunohistochemical analyses and western blot revealed that HOTAIR silencing resulted in the upregulation of B cell lymphoma 2‑associated X protein (Bax), Caspase‑3 and transforming growth factor α (TGF‑α) and downregulation of EGFR and B cell lymphoma 2 (Bcl‑2) levels. These results indicate that HOTAIR normally prevents the activation of Bax/Caspase‑3 while inducing TGF‑α/EGFR signaling. Thus, targeting HOTAIR may be a novel therapeutic strategy for treating gefitinib‑resistant lung adenocarcinoma. [ABSTRACT FROM AUTHOR]

Spring water is an important direct drinking water resource. Enterococcus faecalis is a significant opportunistic pathogen from environment that causes human neonatal sepsis and urinary tract infections. Our study investigated the prevalence, virulence genes, antimicrobial resistance, and molecular characterization of E. faecalis from spring water in Guangdong, China. A total of 285 spring water samples were collected from January 2017 to January 2018, in which 47 (16.49%) samples were contaminated by E. faecalis. Antimicrobial susceptibility result showed that many isolates were resistant to tetracycline (93.6%), gentamicin (29.8%), and ciprofloxacin (25.5%). The virulence gene test revealed the positive rate of gelE, asa1, ace, and cylA were 100, 82.3, 76.6, and 70.2%, respectively. Enterobacterial repetitive intergenic consensus‐polymerase chain reaction and multilocus sequence typing classified 47 isolates into 12 and 5 clusters, respectively, which revealed the genetic relatedness and diversity. This finding illustrated the presence of virulence genes and provided understanding on the spread of antibiotic‐resistant and genetic diversity isolates. It can help us gradually increase our knowledge of microbiological risk management in E. faecalis from spring water. Practical applications: Investigating the prevalence of Enterococcus faecalis isolates from spring water could increase this microbial safety ondrinking water. In our research, antibiotic susceptibility, virulence genes, serotypingand molecular characteristic were selected to thorough comparison among Enterococcus faecalis isolates. Spring water is common in China as drinking water, then understanding the dissemination and monitoring the prevalence of this microorganism is necessary to improve the drinking water safety. [ABSTRACT FROM AUTHOR]

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin., Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1., Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects., Conclusions: These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC., Competing Interests: No potential conflict of interest relevant to this article was reported., (Copyright © 2024. Korean Gastric Cancer Association.)

Objective: To study the expression of tumor associated vascular insulin receptor (TVIR) in colorectal cancer with or without metabolic syndrome (MS) and its relationship with the pathological features of colorectal cancer., Methods: The expression of TVIR in 220 colorectal cancer specimens was detected by tissue microarray and immunohistochemistry. The relationships between the expression of TVIR and the pathological features (pathological subtypes, histological grade, invasion depth, lymph node metastasis and TNM stage) of colorectal cancer with/without MS were analyzed., Results: The insulin receptor expression was observed in colorectal cancer tissue or border area between cancer and normal tissue, but not in normal intestinal tissue. The high-expression rates of TVIR in MS group was remarkably lower than that of non-MS group (21.6%vs. 41.0%, P < 0.05). TVIR high expression was significantly associated with tumor deep invasion, lymph node metastasis and high TNM stage ( P <0.05 or P <0.01). Univariate logistic regression analysis showed high-expression of TVIR to be significantly associated with risk of deep invasion ( OR =2.21, 95% CI : 1.10-4.44, P <0.05), lymph node metastasis ( OR =2.21, 95% CI : 1.26-3.86, P <0.01) and high TNM stage ( OR =2.08, 95% CI : 1.19-3.63, P <0.05). Such associations can be observed in patients without MS, but not in patients with MS., Conclusions: s: High-expression of TVIR is associated with aggressive pathological features such as invasion, lymph node metastasis and high TNM stage of colorectal cancer, especially for those patients without MS. TVIR could be a useful biological marker for prognosis of colorectal cancer.

Cyclooxygenase-2 (COX2) and tumor-associated macrophages (TAMs) are associated with invasion, angiogenesis, and poor prognosis in many human cancers. However, the role of TAMs in human gastric cancer (GC) remains elusive. In the present study, we first measured COX2 expression and TAM infiltration in human GC tissues using double immunohistochemical staining. Then, we indirectly cocultured M2-polarized macrophages derived from human THP-1 cells with GC cells as an in vitro model. Transwell assays, siRNA transfection, treatment with a COX2 inhibitor and Western blotting were used to investigate the relationship among TAMs, invasion and COX2 expression as well as the underlying molecular mechanism. Double IHC staining showed that TAMs were aggregated near GC tumor nests and had high COX2 expression; moreover, the number of TAMs that infiltrated the tumor nest was correlated with the depth of invasion, COX2 expression and poor prognosis in human GC. In an in vitro assay, after treatment with phorbol myristate acetate (PMA), the THP-1 cells differentiated into M2 macrophages and induced COX2/MMP9-dependent invasiveness in GC cells. Pretreatment of GC cells with COX2 siRNA or a COX2 inhibitor (Celecoxib) can negate these promoting effects. The results of this study and those of our previous studies indicate that coculture with M2-polarized macrophages can induce the COX2-dependent release of matrix metalloproteinase-9 (MMP9), which subsequently increases the invasiveness of GC cells. Our data may provide a basis for targeting TAMs or for polarizing TAMs through immune regulation to halt GC progression, which could soon become a nonsurgical treatment for human gastric cancer., Competing Interests: None., (AJTR Copyright © 2019.)

Increased expression of HOXB7 has been reported to correlate with the progression in many cancers. However, the specific mechanism by which it promotes the evolution of gastric cancer (GC) is poorly understood.In this study, we sought to investigate the role of HOXB7 in GC by assessing HOXB7 expression in patient tissue and its correlation to clinical characteristics. We found that GC tissues showed increased expression of HOXB7 and that the HOXB7 expression was significantly associated with Lauren classification, invasion depth, lymphatic metastasis and poor prognosis, and could serve as an independent prognostic factor. To further investigate the role of HOXB7 in GC, we generated stable GC cell lines and both over-expressed and knocked down HOXB7 expression. Over-expression of HOXB7 in GC cell lines enhanced cell proliferation, colony formation, migration and invasion ability, whereas the opposite trends were observed upon reduction of HOXB7 expression by knockdown. These findings were further supported by our in vivo studies which show that HOXB7 expression can affect the GC cells' subcutaneous growth and lung metastases. A Phospho-MAPK Array Kit was used to explore the possible mechanism of HOXB7-induced cell proliferation and invasion. We found that the AKT signaling pathway and the two members of the MAPK pathway, were involved in those promoting effects. In conclusion, our results showed that increased expression of HOXB7 might play an important role in promoting GC proliferation, migration and invasion by inducing both AKT and MAPK pathways, thus resulting in progression of, and poor prognosis in GC patients.

Background/aim: Intestinal tuberculosis (ITB) and Crohn's disease (CD) are important differential diagnoses that can be difficult to distinguish. Polymerase chain reaction (PCR) for Mycobacterium tuberculosis (MTB) is an efficient and promising tool. This meta-analysis was performed to systematically and objectively assess the potential diagnostic accuracy and clinical value of PCR for MTB in distinguishing ITB from CD., Materials and Methods: We searched PubMed, Embase, Web of Science, Science Direct, and the Cochrane Library for eligible studies, and nine articles with 12 groups of data were identified. The included studies were subjected to quality assessment using the revised Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) tool., Results: The summary estimates were as follows: sensitivity 0.47 (95% CI: 0.42-0.51); specificity 0.95 (95% CI: 0.93-0.97); the positive likelihood ratio (PLR) 10.68 (95% CI: 6.98-16.35); the negative likelihood ratio (NLR) 0.49 (95% CI: 0.33-0.71); and diagnostic odds ratio (DOR) 21.92 (95% CI: 13.17-36.48). The area under the curve (AUC) was 0.9311, with a Q* value of 0.8664. Heterogeneity was found in the NLR. The heterogeneity of the studies was evaluated by meta-regression analysis and subgroup analysis., Conclusions: The current evidence suggests that PCR for MTB is a promising and highly specific diagnostic method to distinguish ITB from CD. However, physicians should also keep in mind that negative results cannot exclude ITB for its low sensitivity. Additional prospective studies are needed to further evaluate the diagnostic accuracy of PCR.

Objective: To explore the NEK-6 expression in gastric cancer tissue and its relationship with clinicopathological features., Methods: Fluorescent quantification PCR and Western blotting were used to examine the NEK-6 expression in 36 samples of fresh gastric cancer tissues and para-cancer gastric mucosal tissues, human gastric cancer cell lines(BGC-823, MKN-28, SGC-7901, MGC-803, HGC-27, AGS), and human normal gastric epithelial cell line (GES-1). Gastric cancer cell lines with the highest expression level were selected to perform the invasion and migration tests, and the effect of down-regulated NEK-6 expression by siRNA transfection on above invasion and migration tests were observed. Meanwhile NEK-6 expression in 94 paraffin samples of gastric cancer tissues was examined by immunohistochemistry and its positivity was compared among different clinicopathologic features., Results: Fluorescent quantification PCR revealed gastric cancer tissues had significantly higher NEK-6 expression than para-cancer tissues(0.002 80±0.001 36 vs. 0.001 91±0.001 48, P<0.05), NEK-6 expression was up-regulated in 31 gastric cancer tissues (86.1%), and human gastric cancer cell lines had significantly higher NEK-6 expression than GES-1 cells, among whom BGC-823 and AGS cell lines were the highest. Invasion and migration tests showed that as compared to negative siRNA control group, ability of invasion and migration in BGC-823 and AGS cells after siRNA transfection was obviously decreased. In 94 paraffin samples, positive expression rate of NEK-6 was 60.6%(57/94), and NEK-6 expression was significantly associated with gastric cancer distant metastasis, lymph nodes metastasis and TNM staging(all P<0.05)., Conclusions: NEK-6 expression is up-regulated in gastric cancer tissues, which is significantly associated with distant metastasis, lymph nodes metastasis and TNM staging. Down-regulation of NEK-6 expression can inhibit the ability of invasion and migration in gastric cancer cells.