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miR-199a-3p may play an important role in tumour inhibition. The aim of the present study was to determine any link between miR-199a-3p expression in thyroid tissues and clinicopathologic features, as well as to assess potential usefulness of miR-199a-3p in prediction for invasion and metastasis of papillary thyroid carcinoma (PTC).A total of 188 tissue samples (136 PTCs, 52 normal thyroid tissue) were collected. We measured the levels of miR-199a-3p with quantitative reverse-transcriptase PCR (RT-qPCR) in all subjects. In addition, the correlation between the expression levels of miR-199a-3p and clinicopathological factors was explored.qRT-PCR indicated that the expression levels of miR-199a-3p was 7.1 (95% CI, 3.9-12.4) in PTCs, which was significantly lower than that of in the normal thyroid tissues 31.4 (95% CI, 15.4-44.3) (p = 0.002). Receiver operating characteristic curve (ROC) analyses revealed that miR-199a-3p could be promising biomarkers for PTC, with relatively high area under the curve (AUC) values was 0.87 (95% CI, 0.66-0.90; p = 0.001). Low miR-199a-3p expression levels were linked to TNM stage (p = 0.026), extra-thyroidal extension (p = 0.02), lymph node (LN) metastasis (p = 0.036), distant metastasis (p = 0.002) and recurrence of LN metastasis (p = 0.03).Our data suggest that downregulation of miR-199a-3p in thyroid tissues is linked to invasion and metastasis of PTC and may be a potential target for therapeutic intervention.

BACKGROUND We investigated whether the plant-derived agent triptolide (TPL) could effectively inhibit the growth and invasion of human hepatocellular carcinoma (HCC) cells. MATERIAL AND METHODS MHCC-97H cells were treated with various concentration of TPL for various times. To detect the effect of NF-κB on TPL-induced signal pathways, MHCC-97H cells were transfected with p65 siRNA or p65 cDNA, then treated with TPL. We detected cell survival and apoptosis by MTT, soft-agar colony formation assay, flow cytometry, and TUNEL assay. Cell migration and invasion was determined by Matrigel invasion and a wound-healing assay. NF-κB activity was detected by electrophoretic mobility shift assay (EMSA); MMP-9 activity was detected by ELISA. Western blot and real-time PCR (RT-PCR) assays were used to detect p65 and MMP-9 protein and mRNA expression. A subcutaneously implanted tumor model of MHCC-97H cells in nude mice was used to assess the effects of TPL on tumorigenesis in vivo. RESULTS We showed that TPL treatment significantly suppressed growth and induced apoptosis of MHCC-97H cells in a dose- and time-dependent manner in vitro. Furthermore, TPL treatment inhibited invasion in vitro and inhibited the growth and lung metastasis of MHCC-97H cells in vivo. NF-κB and MMP-9 were inactivated with TPL treatment. Overexpression of p65 restored MMP-9 activity and inhibited the TPL anti-tumor effect on MHCC-97H cells. Knockdown of p65 blocked MMP-9 activation and enhanced TPL-induced cell apoptosis and survival inhibition, and TPL inhibition of migration and invasion in vitro. CONCLUSIONS TPL treatment inhibited MHCC-97H cell growth, invasion, and metastasis in vitro and vivo, suggesting that TPL could be developed as a potential therapeutic agent for the treatment of HCC.

Following the publication of this article, we realize that an error was made with the second author's (Yanlei Sun's) address: This should have been written as "Department of General Surgery, Cancer Hospital of Linyi, Linyi, Shandong 276001", not as "Department of General Surgery, Central Hospital of Linyi, Linyi, Shandong 276400". Therefore, the author affiliations and addresses in this paper should have appeared as follows: SHICHANG CUI1, YANLEI SUN2, YANG LIU3, CHENGBIAO LIU1, JINBAO WANG1, GUANG HAO1 and QIDONG SUN1 1Department of General Surgery, Central Hospital of Linyi, Linyi, Shandong 276400; 2Department of General Surgery, Cancer Hospital of Linyi, Linyi, Shandong 276001; 3Department of Obstetrics and Gynecology, Central Hospital of Linyi, Linyi, Shandong 276400, P.R. China. The authors regret this error in the affiliation, and apologize for any inconvenience caused. [the original article was published in the Molecular Medicine Reports 16: 9494-9502, 2017; DOI: 10.3892/mmr.2017.7828].

A variety of microRNAs (miRs) have been demonstrated to be associated with the development and malignant progression of human cancer; however, the regulatory mechanism of miR‑137 underlying hepatocellular carcinoma (HCC) growth and metastasis still remains to be fully revealed. In the present study, reverse transcription‑quantitative polymerase chain reaction and western blot were used to examine mRNA and protein expression. MTT assay, wound healing assay and Transwell assay were performed to determine cell proliferation, migration and invasion. Luciferase reporter assay was conducted to confirm the targeting relationship. miR‑137 was significantly downregulated in HCC tissues compared to adjacent normal tissues. Low expression of miR‑137 was significantly associated with lymph node metastasis, vein invasion, advanced clinical stage and poor prognosis in HCC. In addition, miR‑137 was also downregulated in several liver cancer cell lines compared with normal liver epithelial cells. Overexpression of miR‑137 led to a significant reduction in cell proliferation, migration and invasion of HepG2 cells. Enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) was further identified as a direct target gene of miR‑137, and the protein expression of EZH2 was negatively regulated by miR‑137 in HepG2 cells. Additionally, EZH2 was significantly upregulated in HCC tissues and liver cancer cell lines. Furthermore, overexpression of EZH2 significantly eliminated the inhibitory effects of miR‑137 on the malignant phenotypes of HepG2 cells. Therefore, the findings suggest that miR‑137 may have a suppressive role in HCC growth and metastasis via targeting EZH2.