Vibrio is a genus of ubiquitous bacteria found in a wide variety of aquatic and marine habitats; of the >100 described Vibrio spp., ~12 cause infections in humans. Vibrio cholerae can cause cholera, a severe diarrhoeal disease that can be quickly fatal if untreated and is typically transmitted via contaminated water and person-to-person contact. Non-cholera Vibrio spp. (for example, Vibrio parahaemolyticus, Vibrio alginolyticus and Vibrio vulnificus) cause vibriosis - infections normally acquired through exposure to sea water or through consumption of raw or undercooked contaminated seafood. Non-cholera bacteria can lead to several clinical manifestations, most commonly mild, self-limiting gastroenteritis, with the exception of V. vulnificus, an opportunistic pathogen with a high mortality that causes wound infections that can rapidly lead to septicaemia. Treatment for Vibrio spp. infection largely depends on the causative pathogen: for example, rehydration therapy for V. cholerae infection and debridement of infected tissues for V. vulnificus-associated wound infections, with antibiotic therapy for severe cholera and systemic infections. Although cholera is preventable and effective oral cholera vaccines are available, outbreaks can be triggered by natural or man-made events that contaminate drinking water or compromise access to safe water and sanitation. The incidence of vibriosis is rising, perhaps owing in part to the spread of Vibrio spp. favoured by climate change and rising sea water temperature.

Vibrio spp. infections.

Cyclooxygenase-2 (COX-2) is frequently expressed in many types of cancers exerting a pleiotropic and multifaceted role in genesis or promotion of carcinogenesis and cancer cell resistance to chemo- and radiotherapy. COX-2 is released by cancer-associated fibroblasts (CAFs), macrophage type 2 (M2) cells, and cancer cells to the tumor microenvironment (TME). COX-2 induces cancer stem cell (CSC)-like activity, and promotes apoptotic resistance, proliferation, angiogenesis, inflammation, invasion, and metastasis of cancer cells. COX-2 mediated hypoxia within the TME along with its positive interactions with YAP1 and antiapoptotic mediators are all in favor of cancer cell resistance to chemotherapeutic drugs. COX-2 exerts most of the functions through its metabolite prostaglandin E2. In some and limited situations, COX-2 may act as an antitumor enzyme. Multiple signals are contributed to the functions of COX-2 on cancer cells or its regulation. Members of mitogen-activated protein kinase (MAPK) family, epidermal growth factor receptor (EGFR), and nuclear factor-κβ are main upstream modulators for COX-2 in cancer cells. COX-2 also has interactions with a number of hormones within the body. Inhibition of COX-2 provides a high possibility to exert therapeutic outcomes in cancer. Administration of COX-2 inhibitors in a preoperative setting could reduce the risk of metastasis in cancer patients. COX-2 inhibition also sensitizes cancer cells to treatments like radio- and chemotherapy. Chemotherapeutic agents adversely induce COX-2 activity. Therefore, choosing an appropriate chemotherapy drugs along with adjustment of the type and does for COX-2 inhibitors based on the type of cancer would be an effective adjuvant strategy for targeting cancer.

Cyclooxygenase-2 in cancer: A review.

Consensus recommendations for the diagnosis and clinical management of Rosai-Dorfman-Destombes disease

Apigenin is a common dietary flavonoid that is abundantly present in many fruits, vegetables and Chinese medicinal herbs and serves multiple physiological functions, such as strong anti-inflammatory, antioxidant, antibacterial and antiviral activities and blood pressure reduction. Therefore, apigenin has been used as a traditional medicine for centuries. Recently, apigenin has been widely investigated for its anti-cancer activities and low toxicity. Apigenin was reported to suppress various human cancers in vitro and in vivo by multiple biological effects, such as triggering cell apoptosis and autophagy, inducing cell cycle arrest, suppressing cell migration and invasion, and stimulating an immune response. In this review, we focus on the most recent advances in the anti-cancer effects of apigenin and their underlying mechanisms, and we summarize the signaling pathways modulated by apigenin, including the PI3K/AKT, MAPK/ERK, JAK/STAT, NF-κB and Wnt/β-catenin pathways. We also discuss combinatorial strategies to enhance the anti-cancer effect of apigenin on various cancers and its use as an adjuvant chemotherapeutic agent to overcome cancer drug resistance or to alleviate other adverse effects of chemotherapy. The functions of apigenin against cancer stem cells are also summarized and discussed. These data demonstrate that apigenin is a promising reagent for cancer therapy. Apigenin appears to have the potential to be developed either as a dietary supplement or as an adjuvant chemotherapeutic agent for cancer therapy.

/pdf/apigenin-in-cancer-therapy-anti-cancer-effects-and-2y6by2r305.pdf

Apigenin in cancer therapy: anti-cancer effects and mechanisms of action

Radioresistance is a major factor leading to the failure of radiotherapy and poor prognosis in tumor patients. Following the application of radiotherapy, the activity of various metabolic pathways considerably changes, which may result in the development of resistance to radiation. Here, we discussed the relationships between radioresistance and mitochondrial and glucose metabolic pathways, aiming to elucidate the interplay between the tumor cell metabolism and radiotherapy resistance. In this review, we additionally summarized the potential therapeutic targets in the metabolic pathways. The aim of this review was to provide a theoretical basis and relevant references, which may lead to the improvement of the sensitivity of radiotherapy and prolong the survival of cancer patients.

/pdf/role-of-metabolism-in-cancer-cell-radioresistance-and-4s49140xzk.pdf

Role of metabolism in cancer cell radioresistance and radiosensitization methods.

Hypoxia is an important factor in radioresistance of laryngeal carcinoma. Glucose transporter-1 (GLUT-1) is an important hypoxic marker in malignant tumors, including laryngeal carcinoma. Apigenin is a natural phytoestrogen flavonoid that has potential anticancer effects. Various studies have reported that the effects of apigenin on lowering GLUT-1 expression were involved in downregulation of the PI3K/Akt pathway. Thus, apigenin may improve the radiosensitivity of laryngeal carcinoma by suppressing the expression of GLUT-1 via the PI3K/Akt pathway. The effect of GLUT-1 and PI3K/Akt pathway-related factor expressions by apigenin or antisense oligonucleotides (AS-ODNs) on the radiosensitivity of laryngeal carcinoma in vivo was assessed. The xenograft volume, xenograft weight and apoptosis detection were performed to determine radiosensitivity. The results showed that apigenin or apigenin plus GLUT-1 AS-ODNs improved the radiosensitivity of xenografts. Apigenin or apigenin plus GLUT-1 reduced the expression of GLUT-1, Akt, and PI3K mRNA after X-ray radiation. We found similar results at the protein level. The results suggest that the effects of apigenin on inhibiting xenograft growth and enhancing xenograft radiosensitivity may be associated with suppressing the expression of GLUT-1 via the PI3K/Akt pathway. In addition, apigenin may enhance the effects of GLUT-1 AS-ODNs via the same mechanism.

/pdf/inhibiting-glut-1-expression-and-pi3k-akt-signaling-using-2dnj534nwp.pdf

Inhibiting GLUT-1 expression and PI3K/Akt signaling using apigenin improves the radiosensitivity of laryngeal carcinoma in vivo

The mechanisms underlying cancer radioresistance remain unclear. Several studies have found that increased glucose transporter‑1 (GLUT‑1) expression is associated with radioresistance. Recently, the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway was reported to be involved in the control of GLUT‑1 trafficking and activity. Activation of the PI3K/Akt pathway may itself be associated with cancer radioresistance. Thus, increasing attention has been devoted to the effects of modifying the expression of GLUT‑1 and the PI3K/Akt pathway on the increase in the radiosensitivity of cancer cells. This review discusses the importance of the association between elevated expression of GLUT‑1 and activation of the PI3K/Akt pathway in the development of radioresistance in cancer.

/pdf/roles-of-glucose-transporter-1-and-the-phosphatidylinositol-42by5esy0j.pdf

Roles of glucose transporter-1 and the phosphatidylinositol 3‑kinase/protein kinase B pathway in cancer radioresistance

Background.
Malignant cells show increased glucose uptake in vitro and in vivo, which is thought to be mediated by glucose transporters. In this study, we investigated the effect of plasmid-derived antisense RNA against the Glut-l gene on proliferation and glucose uptake in laryngeal carcinoma Hep-2 cells.

Methods.
The expression plasmids pcDNA3.1(+)-Glut-1 and pcDNA3.1(+)-anti Glut-1 were constructed. The MTT method was used to assess cell growth inhibition. The expression of Glut-1 mRNA and protein was detected by reverse transcriptase-polymerase chain reaction and Western blotting, respectively.

Results.
After transfection, Glut-1 AS clearly inhibited glucose uptake and cell growth in Hep-2 cells, and we observed a decrease in the expression of Glut-1 mRNA and protein in Hep-2 cells.

Conclusions.
Glut-1 AS decreases glucose uptake and inhibits the proliferation of Hep-2 cells. © 2009 Wiley Periodicals, Inc. Head Neck, 2009

Inhibition of cell proliferation and glucose uptake in human laryngeal carcinoma cells by antisense oligonucleotides against glucose transporter-1.

Apigenin is a natural phyto-oestrogen flavonoid, which exerts various biological effects, including anti‑oxidative, anti‑inflammatory and anticancer activities. In addition, apigenin has recently been reported to target hypoxic markers; however, there are currently no studies regarding the association between apigenin and glucose transporter‑1 (GLUT‑1) in adenoid cystic carcinoma (ACC). The present study investigated whether apigenin inhibits the proliferation of ACC cells or suppresses the expression of GLUT‑1 in ACC cells. The results of the present study demonstrated that apigenin inhibits ACC‑2 cell growth in a dose‑ and time‑dependent manner. Treatment with apigenin also induced apoptosis and G2/M‑phase arrest in a dose‑ and time‑dependent manner. Corresponding with the above results, the expression levels of GLUT‑1 were significantly decreased following treatment in a dose- and time-dependent manner. These results suggest that the inhibition of ACC-2 cell growth by apigenin may be due to the decreased expression of GLUT-1.

/pdf/apigenin-inhibits-the-proliferation-of-adenoid-cystic-1p5h6y8emi.pdf

Apigenin inhibits the proliferation of adenoid cystic carcinoma via suppression of glucose transporter-1

Background. The purpose of this study was to explore the factors associated with the recurrence of Rosai-Dorfman disease (RDD) in the nasal cavity and paranasal sinus. Methods. In this study, we conducted a review of the English- language literature published between 1969 and 2010 on the recurrence of and treatment strategies for sinonasal RDD. Results. To our knowledge, 126 cases of RDD have been reported to date. Of the 126 patients, 32 (25.4%) had no recurrence or were alive with no evidence of disease; remission occurred in only 1 patient (0.7%); 69 patients (54.8%) had a recurrent, persistent, or progressive course; and 6 patients (4.8%) died from the disease. In patients with recurrent, persistent, and progressive disease, there was no significant tendency for lymph node involvement. Conclusion. Sinonasal RDD is generally described as benign. However, recurrence and fatal outcome have been reported. Our results suggest that the initial modality may affect the recurrence of RDD. V C 2011 Wiley Periodicals, Inc. Head Neck 34: 1504-1513, 2012

Factors associated with recurrence and therapeutic strategies for sinonasal rosai–dorfman disease

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