The role of circular RNA in cancer is emerging. A newly reported circular RNA HIPK3 (circHIPK3) is critical in cell proliferation of various cancer types, although its role in non-small cell lung cancer (NSCLC), has yet to be elucidated. Our results provided evidence that silencing of circHIPK3 significantly impaired cell proliferation, migration, invasion and induced macroautophagy/autophagy. Mechanistically, we uncovered that autophagy was induced upon loss of circHIPK3 via the MIR124-3p-STAT3-PRKAA/AMPKa axis in STK11 mutant lung cancer cell lines (A549 and H838). STAT3 abrogation as well as transfection with a MIR124-3p mimic, recapitulated the induction of autophagy. We also demonstrated antagonistic regulation on autophagy between circHIPK3 and linear HIPK3 (linHIPK3). We therefore propose that the ratio between circHIPK3 and linHIPK3 (C:L ratio) may reflect autophagy levels in cancer cells. We observed that a high C:L ratio (>0.49) was an indicator of poor survival, especially in advanced-stage NSCLC patients. These results support that circHIPK3 is a key autophagy regulator in a subset of lung cancer and has potential clinical use as a prognostic factor. The circular RNA HIPK3 (circHIPK3) functions as an oncogene and autophagy regulator may potential use as a prognostic marker and therapeutic target in lung cancer.

The long noncoding RNA (lncRNA) has previously been identified as a prognostic marker in hepatocellular carcinoma. Here, we performed a comprehensive analysis of lncRNA expression profiles from RNA-Seq data and report that plays a similar role in lung cancer. Analysis of 918 lung cancer and normal lung tissues and lung cancer cell lines revealed that was significantly downregulated in lung cancer; this decreased expression was associated with poor patient survival. bound and stabilized the YBX1 protein. Silencing of triggered both cell survival and cell death signaling through dysregulation of the oncogenes YBX1, MET, and p21. In this network, p21 played an oncogenic role by promoting cell proliferation and antiapoptosis in lung cancers. played a tumor-suppressive role as indicated by inhibition of multiple cell cycle-related genes in human primary lung tumors. These data show that has potential as a new diagnostic and prognostic marker and as a therapeutic target for lung cancer. The lncRNA functions as a tumor suppressor, with potential use a diagnostic/prognostic marker and therapeutic target in lung cancer..

BackgroundHepatocellular carcinoma (HCC) is the fifth most common cancer and the third cause of cancer-related deaths, worldwide. It is essential to develop an effective prognostic biomarker and determine the mechanisms underlying HCC invasion and metastasis.AimsThis study aimed to investigate the expression of Golgi glycoprotein73 (GP73) and Epithelial-mesenchymal transition (EMT) molecules such as E-cadherin and Vimentin in HCC. We also evaluated the prognostic value of GP73 in HCC.MethodsImmunohistochemistry (IHC) was used to determine the expression of GP73 and EMT molecules in 75 HCC specimens and the corresponding paracarcinomatous liver (PCL) tissues. Spearman’s correlation test was used to analyze the correlation of GP73 and EMT molecules. Clinicopathological features of the HCC patients were also analyzed. Univariate survival analysis was performed by the Kaplan–Meier method and differences among the groups were analyzed by the Log-rank test.ResultsGP73 expression in HCC was higher compared with PCL tissues (χ 2  = 73.60, P < 0.05). EMT molecules were also detected in HCC and PCL tissues. GP73 was negatively correlated with E-cadherin (r = − 0.49, P < 0.05), but positively correlated with Vimentin (r = 0.46, P < 0.05) in HCC. GP73 was correlated with the clinicopathological features including Edmondson grade, vascular invasion and TNM stage (P < 0.05), which was also associated with overall survival (OS) (P < 0.05).ConclusionsGP73 was negatively with E-cadherin and positively correlated with Vimentin. It might be associated with aggressive behavior of HCC and had influence on patients’ OS. Further research is needed to determine the potential of GP73.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/29 vs/1504046946108618; http://med.motic.com/MoticGallery/Slide?id=3b6a037e-f60e-4c68-9106-41e790de9431&user=2C69F0D6-A478-4A2B-ABF0-BB36763E8025; http://med.motic.com/MoticGallery/Slide?id=a25b5b32-b613-47b0-9f8b-e1e67a95d1bf&user=2C69F0D6-A478-4A2B-ABF0-BB36763E8025.

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The aim of the present study was to investigate the molecular responses involved in radiation-induced liver damage (RILD). Sprague-Dawley rats (6-weeks-old) were irradiated once at a dose of 20 Gy to the right upper quadrant of the abdomen. The rats were then sacrificed 3 days and 1, 2, 4, 8 and 12 weeks after irradiation and rats, which were not exposed to irradiation were used as controls. Weight measurements and blood was obtained from the rats and liver tissues were collected for histological and apoptotic analysis. Immunohistochemistry, reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were performed to measure the expression levels of mRNAs and proteins, respectively. The serum levels of alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase were increased significantly in the RILD rats. Histological investigation revealed the proliferation of collagen and the formation of fibrotic tissue 12 weeks after irradiation. Apoptotic cells were observed predominantly 2 and 4 weeks after irradiation. The immunohistochemistry, RT-qPCR and western blot analysis all revealed the same pattern of changes in the expression levels of the molecules assessed. The expression levels of transforming growth factor-β1 (TGF-β1), nuclear factor (NF)-κB65, mothers against decapentaplegic homolog 3 (Smad3) and Smad7 and connective tissue growth factor were increased during the recovery period following irradiation up to 12 weeks. The expression levels of tumor necrosis factor-α, Smad7 and Smad4 were only increased during the early phase (first 4 weeks) of recovery following irradiation. In the RILD rat model, the molecular responses indicated that the TGF-β1/Smads and NF-κB65 signaling pathways are involved in the mechanism of RILD recovery.