miRNA analysis in pancreatic cancer: the Dartmouth experience

Abreu, Francine B. de; Li, Xiaoying; Tsongalis, Gregory J.

doi:10.1515/cclm-2017-0046

Cited by 53 publications

(39 citation statements)

References 37 publications

(50 reference statements)

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“…Therefore, finding effective methods for treating Pca is important. Previous studies have found abnormal expression of miRNAs in Pca, and that this correlates with the development, differentiation, invasion and metastasis of Pca (36,37). The results of the present study revealed that the expression level of miR-539 in cancerous tissues from Pca patients was markedly lower than that in adjacent tissues and Pca cell lines, suggesting that miR-539 may be associated with the occurrence and progression of Pca.…”

Section: Discussionsupporting

confidence: 46%

miR‑539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1

et al. 2020

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MicroRNA (miR)-539 has inhibitory effects on certain types of cancer, but its role in pancreatic cancer (Pca) remains unclear. The present study investigated the effects of miR-539 on Pca, and aimed to determine possible therapeutic targets for the treatment of Pca. The expression of miR-539 in Pca tissues, paired normal adjacent tissues and Pca cell lines (cAPAN-2, BxPc3, cFPAc1, SW1990 and PANc1), and human non-cancerous pancreatic cells (hTRET-HPNE) was determined and compared. The effects of upregulation and downregulation of miR-539 on proliferation, apoptosis, cell cycle, invasion, migration and epithelial-mesenchymal transition (EMT) of Pca cells were investigated. Additionally, the target gene of miR-539 was predicted and its effects on Pca cells were further investigated. The results revealed low expression of miR-539 in Pca tissues and cell lines. Additionally, increasing miR-539 expression inhibited the proliferation, migration, invasion and EMT of Pca cells and induced apoptosis by blocking G1 phase of the cell cycle, while reducing miR-539 expression had the opposite results. Furthermore, specificity protein 1 (SP1) was found to be the target gene of miR-539. SP1 promoted the proliferation, migration, invasion and EMT transformation of Pca cells, but these effects were reversed by high expression of miR-539. Additionally, miR-539 suppressed the proliferation, metastasis, invasion and EMT transformation of Pca cells through targeting SP1. Therefore, miR-539 overexpression may contribute toward development of novel therapeutic strategies for Pca in the future.

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Section: Discussionsupporting

confidence: 46%

miR‑539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1

et al. 2020

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“…microRNAs (miRNAs) are small non-coding RNAs that regulate protein expression. They are identified as regulatory molecules and biomarkers in virtually all cancer types, and in pancreatic cancer, several miRNAs could turn out to be valuable biomarkers [22][23][24][25][26]. Despite an extensive bibliographic revision, there is, to our knowledge, no literature on miRNA and risk of VTE in PDAC or DECC patients.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs and Neutrophil Activation Markers Predict Venous Thrombosis in Pancreatic Ductal Adenocarcinoma and Distal Extrahepatic Cholangiocarcinoma

Oto

Navarro

Larsen

et al. 2020

IJMS

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Cancer-associated venous thrombosis (VTE) increases mortality and morbidity. However, limited tools are available to identify high risk patients. Upon activation, neutrophils release their content through different mechanisms, thereby prompting thrombosis. We explored plasma microRNAs (miRNAs) and neutrophil activation markers to predict VTE in pancreatic ductal adenocarcinoma (PDAC) and distal extrahepatic cholangiocarcinoma (DECC). Twenty-six PDAC and 6 DECC patients recruited at cancer diagnosis, were examined for deep vein thrombosis and pulmonary embolisms, and were then followed-up with clinical examinations, blood collections, and biCUS. Ten patients developed VTE and were compared with 22 age- and sex-matched controls. miRNA expression levels were measured at diagnosis and right before VTE, and neutrophil activation markers (cell-free DNA, nucleosomes, calprotectin, and myeloperoxidase) were measured in every sample obtained during follow-up. We obtained a profile of 7 miRNAs able to estimate the risk of future VTE at diagnosis (AUC = 0.95; 95% Confidence Interval (CI) (0.987, 1)) with targets involved in the pancreatic cancer and complement and coagulation cascades pathways. Seven miRNAs were up- or down-regulated before VTE compared with diagnosis. We obtained a predictive model of VTE with calprotectin as predictor (AUC = 0.77; 95% CI (0.57, 0.95)). This is the first study that addresses the ability of plasma miRNAs and neutrophil activation markers to predict VTE in PDAC and DECC.

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“…Potentially curable localised tumours are confirmed in less than 20% of cases. Elderly persons suffer from pancreatic cancer more often than younger ones [ 1 - 3 ].…”

Section: Introductionmentioning

confidence: 99%

Disorders noticed during development of pancreatic cancer: potential opportunities for early and effective diagnostics and therapy

Bałan

Zygmanowska

Radomska-Leśniewska

2017

cejoi

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Pancreatic cancer, with a total five-year survival rate below 5%, represents a disease with a high level of malignancy. Some of the pancreatic cancer bad prognosis factors are nutrition disorders. Malnutrition, neither recognized nor properly referred to by the healthcare system, leads to well-documented negative health consequences in hospitalized patients including their impaired immunity, delayed post-surgery wound healing, a high risk of infectious complications, morbidity and mortality. There are numerous factors contributing to the development of pancreatic cancer, including telomerases, inflammation, angiogenesis, epigenetics and genetics factors, miRNA, pancreatic cancer stem cells. On the basis of molecular analyses, it has been established that precursor injuries may trigger pancreatic cancer when added to genetic alterations. Perhaps, combination of few presently used methods, like signal transduction modulated by K-ras, STAT3 activation, HMGB1 releasing, presence of oxidative stress and free radicals secretion, genes for proangiogenic growth factors activation or tissue-specific miRNA genes expression – will solve the problem of inadequate diagnostics.

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miRNA analysis in pancreatic cancer: the Dartmouth experience

Cited by 53 publications

References 37 publications

miR‑539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1

miR‑539 suppresses the proliferation, migration, invasion and epithelial mesenchymal transition of pancreatic cancer cells through targeting SP1

MicroRNAs and Neutrophil Activation Markers Predict Venous Thrombosis in Pancreatic Ductal Adenocarcinoma and Distal Extrahepatic Cholangiocarcinoma

Disorders noticed during development of pancreatic cancer: potential opportunities for early and effective diagnostics and therapy

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