Circulating plasma miR222-3P status and its potential diagnostic performance in prostate cancer.

BACKGROUND: Although studies suggest that miR222-3p is dysregulated in prostate cancer (PC) cells and tissues, the possible changes in the level of miR222-3p in the plasma samples of PC patients remained unclear. The present study aimed to evaluate the diagnostic value of the plasma miR222-3p expression level as a potential biomarker in PC, benign prostatic hyperplasia (BPH) and healthy people. METHODS: Blood samples were collected from 100 adult males (54 patients with PC, 27 patients with BPH and 19 healthy individuals) referred to our affiliated hospital. The expression level of miR222-3p was evaluated using a quantitative reverse transcription-polymerase chain reaction. Receiver operating characteristic curves were used to evaluate miR222-3p diagnostic accuracy for discriminating between the PC, BPH and healthy individuals. RESULTS: The expression level of miR222-3p was significantly higher in PC patients compared to healthy individuals as a fold change of 5.3 (p = 0.009), but not for BPH individuals. The diagnostic value of the plasma miR222-3p for discrimination of the PC patients from healthy individuals was reasonable [cut-off value (fold change relative to miR16-5p) = 1.69, area under the curve = 0.73, sensitivity = 0.75 and specificity = 0.74]. CONCLUSIONS: Circulating plasma miR-222-3p significantly upregulated in PC patients, but not in BPH ones. Besides these preliminary results showed that miR222-3p has the potential to discriminate PC patients from healthy ones. Addittional studies with a larger sample size are required to confirm these data.

Novel insights into the interaction between long non-coding RNAs and microRNAs in glioma.

Glioma is the most common brain tumor of the central nervous system. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified to play a vital role in the initiation and progression of glioma, including tumor cell proliferation, survival, apoptosis, invasion, and therapy resistance. New documents emerged, which indicated that the interaction between long non-coding RNAs and miRNAs contributes to the tumorigenesis and pathogenesis of glioma. LncRNAs can act as competing for endogenous RNA (ceRNA), and molecular sponge/deregulator in regulating miRNAs. These interactions stimulate different molecular signaling pathways in glioma, including the lncRNAs/miRNAs/Wnt/ß-catenin molecular signaling pathway, the lncRNAs/miRNAs/PI3K/AKT/mTOR molecular signaling pathway, the lncRNAs-miRNAs/MAPK kinase molecular signaling pathway, and the lncRNAs/miRNAs/NF-κB molecular signaling pathway. In this paper, the basic roles and molecular interactions of the lncRNAs and miRNAs pathway glioma were summarized to better understand the pathogenesis and tumorigenesis of glioma.

Evaluation of the plasma level of long non-coding RNA PCAT1 in prostatic hyperplasia and newly diagnosed prostate cancer patients.

BACKGROUND: Prostate cancer (PCa) is generally detected by prostate-specific antigen (PSA) as one of the most widely applied tumor markers over decades for its high sensitivity. Nevertheless, it causes overtreatment or an unnecessary biopsy because of its limited specificity. PCa-associated ncRNA transcript 1 (PCAT1), the newly identified long non-coding RNA (lncRNA) has been reported to associate with the progress of PCa. In vitro studies proposed that PCAT-1 may be an appealing candidate for diagnostic accuracy improvement with regard to its notable overexpression in PCa cells. The present study aimed to evaluate the diagnostic potential of the plasma PCAT1 expression levels in PCa patients in comparison to benign prostatic hyperplasia (BPH) patients and healthy controls. METHODS: The plasma lncRNA PCAT1 level was measured by a real-time quantitative reverse transcriptase-polymerase chain reaction in 40 men newly diagnosed with PCa, 20 patients with BPH and 20 healthy subjects. The results were analyzed statistically using SPSS, version 25 (IBM Corp., Armonk, NY, USA). RESULTS: The expression of PCAT1 was significantly higher in healthy subjects compared to BPH patients (p = 0.03). The diagnostic accuracy of the plasma lncRNA PCAT-1 for discrimination of the healthy subjects than BPH patients was reasonable (area under the receiver operating characteristic curve = 0.799; sensitivity = 71%; specificity = 74%; negative predictive value = 74%; positive predictive value = 71%). CONCLUSIONS: It appears that the plasma levels of PCAT1 expression have reasonable diagnostic accuracy for the discrimination of healthy individuals compared to those with BPH, although no significant difference of PCAT1 expression levels was observed in comparisons between the PCa with BPH and normal groups.

RAS/MAPK signaling functions in oxidative stress, DNA damage response and cancer progression.

Mitogen-activated protein kinase (MAPK) signaling pathways organize a great constitution network that regulates several physiological processes, like cell growth, differentiation, and apoptotic cell death. Due to the crucial importance of this signaling pathway, dysregulation of the MAPK signaling cascades is involved in the pathogenesis of various human cancer types. Oxidative stress and DNA damage are two important factors which in common lead to carcinogenesis through dysregulation of this signaling pathway. Reactive oxygen species (ROS) are a common subproduct of oxidative energy metabolism and are considered to be a significant physiological modulator of several intracellular signaling pathways including the MAPK pathway. Studies demonstrated that the MAP kinases extracellular signal-regulated kinase (ERK) 1/2 and p38 were activated in response to oxidative stress. In addition, DNA damage is a partly common circumstance in cell life and may result in mutation, cancer, and even cell death. Recently, accumulating evidence illustrated that the MEK/ERK pathway is associated with the suitable performance of cellular DNA damage response (DDR), the main pathway of tumor suppression. During DDR, the MEK/ERK pathway is regularly activated, which contributes to the appropriate activation of DDR checkpoints to inhibit cell division. Therefore, the aim of this review is to comprehensively discuss the critical function of MAPK signaling in oxidative stress, DNA damage, and cancer progression.