Lung tumorigenesis induced by human vascular endothelial growth factor (hVEGF)-A165 overexpression in transgenic mice and amelioration of tumor formation by miR-16

Tung, Yu Tang; Huang, Pin Wu; Chou, Yu Ching; Lai, Cheng Wei; Wang, Hsiu Po; Ho, Heng Chien; Yen, Chih-Ching; Tu, Chih Yen; Tsai, Tsung-Neng; Yeh, Dah Cherng; Wang, Jiun-Long; Chong, Kowit-Yu; Chen, Chuan-Mu

doi:10.18632/oncotarget.3390

Cited by 26 publications

(16 citation statements)

References 40 publications

(43 reference statements)

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“…Numerous studies have indicated that miR-16 family members regulate cell cycle-associated genes, as well as promote tumorigenesis and metastasis (30,31). Hence, miR-16 family members have been considered as potential biomarkers in cancer diagnosis (32).…”

Section: Discussionmentioning

confidence: 99%

Decreased microRNA-181a and -16 expression levels in the labial salivary glands of Sjï¿½gren syndrome patients

Wang

Zhang

et al. 2017

Exp Ther Med

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Abstract. Sjögren syndrome (SS) is characterized by dysfunction of the exocrine glands, particularly the salivary and lacrimal glands. Thus, labial salivary gland biopsy is useful method for diagnosing SS. The aim of the present study was to investigate the microRNA (miRNA or miR) profile of labial salivary glands obtained from SS patients and to examine the correlation of miR-181a and -16 levels with the pathological grade in SS. miRNA expression in labial salivary gland tissues was profiled in 3 female patients with primary SS and 3 female patients with non-SS sicca syndrome using microarray analysis. In addition, a literature search and miRNA target gene prediction were performed to collect miRNAs involved in SS pathogenesis. Subsequent to integrating all database results, miR-181a and -16 were identified to be associated with the Ro/SS-associated antigen A and La/SS-associated antigen B during SS pathogenesis. Therefore, these miRNAs were selected for further verification in labial salivary gland tissues of 28 patients with SS and 18 non-SS sicca syndrome control individuals by quantitative reverse transcription-quantitative polymerase chain reaction. Compared with the control group, 76 miRNAs were upregulated and 51 were downregulated in the labial salivary gland of SS patients according to microarray results. In particular, miR-181a and -16 expression levels in the labial salivary gland of SS patients were decreased in comparison with those in the controls. Furthermore, the decreased expression levels of these miRNAs were associated with the labial salivary pathological focus scores. In conclusion, the present study examined the miRNA profiles in the labial salivary glands of SS patients and detected decreased miR-181a and -16 expression levels compared with the control individuals. Finally, the decreased levels of miR-181a and -16 were associated with the salivary gland pathological focus scores, suggesting that miR-181a and -16 may serve a role in the pathogenesis of SS.

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Section: Discussionmentioning

confidence: 99%

Decreased microRNA-181a and -16 expression levels in the labial salivary glands of Sjï¿½gren syndrome patients

Wang

Zhang

et al. 2017

Exp Ther Med

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“…The animals were given free access to regular rodent chow (a standard laboratory diet) and water ad libitum . 15, 16 After 2 weeks, the C57BL/6 wild-type (WT) mice were randomly divided into the following six treatment groups ( n =8): (1) normal: H 2 O drinking water; (2) Mock: H 2 O+30% fructose corn syrup; (3) KL: low-dose kefir peptides powder (50 mg kg −1 )+30% fructose; (4) KM: medium-dose kefir peptides powder (100 mg kg −1 )+30% fructose; (5) KH: high-dose kefir peptides powder (150 mg kg −1 )+30% fructose; and (6) CFM: commercial fermented milk (100 mg kg −1 ; LP-33, Uni-President Co., Tainan, Taiwan)+30% fructose. The kefir peptides powder was dissolved in deionized distilled water and orally administered daily for eight weeks.…”

Section: Methodsmentioning

confidence: 99%

Kefir peptides prevent high-fructose corn syrup-induced non-alcoholic fatty liver disease in a murine model by modulation of inflammation and the JAK2 signaling pathway

Chen

Tsai

et al. 2016

Nutr & Diabetes

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Objective:In recent years, people have changed their eating habits, and high-fructose-containing bubble tea has become very popular. High-fructose intake has been suggested to be a key factor that induces non-alcoholic fatty liver disease (NAFLD). Kefir, a fermented milk product composed of microbial symbionts, has demonstrated numerous biological activities, including antibacterial, antioxidant and immunostimulating effects. The present study aims to evaluate the effects of kefir peptides on high-fructose-induced hepatic steatosis and the possible molecular mechanism.Results:An animal model of 30% high-fructose-induced NAFLD in C57BL/6J mice was established. The experiment is divided into the following six groups: (1) normal: H2O drinking water; (2) mock: H2O+30% fructose; (3) KL: low-dose kefir peptides (50 mg kg−1)+30% fructose; (4) KM: medium-dose kefir peptides (100 mg kg−1)+30% fructose; (5) KH: high-dose kefir peptides (150 mg kg−1)+30% fructose; and (6) CFM: commercial fermented milk (100 mg kg−1)+30% fructose. The results show that kefir peptides improve fatty liver syndrome by decreasing body weight, serum alanine aminotransferase, triglycerides, insulin and hepatic triglycerides, cholesterol, and free fatty acids as well as the inflammatory cytokines (TNF-α, IL-6 and IL-1β) that had been elevated in fructose-induced NAFLD mice. In addition, kefir peptides markedly increased phosphorylation of AMPK to downregulate its targeted enzymes, ACC (acetyl-CoA carboxylase) and SREBP-1c (sterol regulatory element-binding protein 1), and inhibited de novo lipogenesis. Furthermore, kefir peptides activated JAK2 to stimulate STAT3 phosphorylation, which can translocate to the nucleus, and upregulated several genes, including the CPT1 (carnitine palmitoyltransferase-1) involved in fatty acid oxidation.Conclusion:Our data have demonstrated that kefir peptides can improve the symptoms of NAFLD, including body weight, energy intake, inflammatory reaction and the formation of fatty liver by activating JAK2 signal transduction through the JAK2/STAT3 and JAK2/AMPK pathways in the high-fructose-induced fatty liver animal model. Therefore, kefir peptides may have the potential for clinical application for the prevention or treatment of clinical metabolic syndrome.

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“…VEGF is located at chromosome 6p12, and it comprises a coding region with eight exons and seven introns ( 1 ). The VEGF gene family includes VEGF-A, -B, -C, -D and -E ( 13 , 26 – 28 ). Among these factors, VEGF-A is considered the most important in regulating tumor angiogenesis.…”

Section: Case Reportmentioning

confidence: 99%

“…There are three types of VEGF receptor (VEGFR) found on the cell surface: VEGFR-1, −2, and −3 ( 13 ). In particular, VEGF-A binds with VEGFR-1 and VEGFR-2, which leads to signal transduction ( 28 , 29 ). VEGF-C and -D regulate lymphatic vessel endothelium and promote lymphangiogenesis and invasion of tumor cells in patients with NPC via binding with VEGFR-3 ( 30 ).…”

Section: Case Reportmentioning

confidence: 99%

Addition of bevacizumab to systemic therapy for locally advanced and metastatic nasopharyngeal carcinoma

et al. 2018

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Radiotherapy is a vital treatment option for patients with nasopharyngeal carcinoma (NPC). Concurrent cisplatin-based radiochemotherapy with or without adjuvant chemotherapy had acquired good clinical effects with good local control rates. However, a number of patients present with metastasis following systemic regimens or initial diagnosis of locally advanced NPC, which cause difficulty for subsequent therapy. Therefore, there is an urgent requirement to discover novel targeted therapies. The present report describes one case of a patient with NPC and multiple metastases. The patient was treated with systemic therapy in combination with bevacizumab, palliative radiotherapy and chemotherapy following treatment with cetuximab and concurrent chemoradiotherapy in 2015. Following the addition of bevacizumab, metastases were reduced or disappeared after >2 months, and the duration of progression-free survival was 7 months. Bevacizumab is a monoclonal antibody that targets VEGF, and it is associated with angiogenesis, which causes the growth, invasion and progression of tumors. In previous studies, bevacizumab has been approved for the treatment of several types of malignant cancer and it has been able to effectively improve prognosis. In the present review, the effect of adding bevacizumab to systemic therapy for the treatment of NPC was analyzed, with a particular focus on advanced and metastatic diseases. A growing number of phase I/II clinical trials involving bevacizumab for NPC have been conducted with clinical outcomes showing improved rates of overall survival and progression-free survival as well as improvements in the quality of life of patients. However, severe or deadly toxicities can also result from combination treatment with bevacizumab. In the future, bevacizumab may become a common addition to systemic therapy for the treatment of locally advanced and metastatic NPC.

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Lung tumorigenesis induced by human vascular endothelial growth factor (hVEGF)-A165 overexpression in transgenic mice and amelioration of tumor formation by miR-16

Cited by 26 publications

References 40 publications

Decreased microRNA-181a and -16 expression levels in the labial salivary glands of Sjï¿½gren syndrome patients

Decreased microRNA-181a and -16 expression levels in the labial salivary glands of Sjï¿½gren syndrome patients

Kefir peptides prevent high-fructose corn syrup-induced non-alcoholic fatty liver disease in a murine model by modulation of inflammation and the JAK2 signaling pathway

Addition of bevacizumab to systemic therapy for locally advanced and metastatic nasopharyngeal carcinoma

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