Circ_0056618 enhances PRRG4 expression by competitively binding to miR-411-5p to promote the malignant progression of colorectal cancer.

The purpose of this paper was to explore the role of circ_0056618 and associated mechanisms in colorectal cancer (CRC). The expression of circ_0056618, proline rich and Gla domain 4 (PRRG4) mRNA and miR-411-5p was measured by quantitative real-time PCR (qPCR).The protein levels of PRRG4 and epithelial-mesenchymal transition (EMT)-related markers were detected by western blot. Cell proliferation was assessed by cell counting kit-8, EdU, and colony formation assays. Cell migration and invasion were assessed by transwell assay. Cell apoptosis was detected by flow cytometry assay. The putative relationship between miR-411-5p and circ_0056618 or PRRG4 was verified by dual-luciferase reporter assay. The effects of circ_0056618 on tumor growth in vivo were determined by animal study. Circ_0056618 and PRRG4 was upregulated, while miR-411-5p was downregulated in CRC tumor tissues and cells. Circ_0056618 knockdown or PRRG4 knockdown inhibited CRC cell proliferation, migration/invasion, EMT, and survival. Circ_0056618 positively modulated PRRG4 expression by targeting miR-411-5p. MiR-411-5p absence or PRRG4 overexpression could rescue circ_0056618 knockdown-induced inhibition on proliferation, migration/invasion, and EMT in CRC cells. Animal assay showed circ_0056618 knockdown impeded tumor growth in vivo. Circ_0056618 promoted CRC growth and development by upregulating PRRG4 expression via competitively targeting miR-411-5p.

Silencing of FoxM1 blocks growth, migration and invasion of papillary thyroid carcinoma cells.

The aim of the present study was to investigate the effect of Forkhead box transcription factor M1 (FoxM1)-silencing on the growth, migration and invasion of K1 human papillary thyroid carcinoma (PTC) cells. The effect of FoxM1-small interfering RNA (siRNA) in K1 cells was detected by western blot analysis. FoxM1-siRNA and control siRNA were transfected into K1 cells using Lipofectamine® 2000 (transfection group, T) and the non-meaning sequence group (NM). K1 cells exposed to PBS solution comprised the blank control group (CON). Cell proliferation ability was detected using an MTT assay. Cell migration and invasion was detected by the single cell scratch test and Transwell invasion assay, respectively. Western blot analysis indicated that FoxM1 siRNA downregulated the expression of FoxM1 protein. Cell proliferation, migration and invasion were significantly lower in the T group compared with the NM and CON groups (P<0.05). These results indicated that silencing of FoxM1 expression could block growth, invasion and migration of K1 cells. This study may provide a novel target gene for targeted therapy of PTC.

miR-138-5p acts as a tumor suppressor by targeting hTERT in human colorectal cancer.

Colorectal cancer (CRC) is the second most common cancer in the world. The incidence of this cancer is increasing in the developing countries. Mechanism of CRC tumorigenesis has been widely studied at the molecular levels, and has been recently proposed microRNAs as novel players in CRC. It has been reported that microRNA-138-5p (miR-138-5p) play key roles in different kinds of human cancers. However, the roles and underlying molecular mechanisms of miR-138-5p in CRC have not been adequately elucidated. Thus, the aim of the present study was to investigate the roles and possible regulatory mechanisms of miR-138-5p in CRC. In this study, we demonstrated that miR-138-5p was significantly down-regulated in CRC tissue samples and cell lines. Functional analyses indicated that the overexpression of miR-138-5p significantly delayed cell proliferation, reduced colony formation and increased apoptosis in CRC cell lines. Moreover, human telomerase reverse transcriptase (hTERT), an important oncogene in the management of tumors, was confirmed as a direct target of miR-138-5p in CRC cells. We also found that the hTERT expression was increased in CRC tissues and was inversely correlated with miR-138-5p. Further study showed that the restoration of hTERT expression by an overexpressing plasmid could reverse the effects of miR-138-5p on proliferation and apoptosis of CRC cells. Taken together, these data defines a major suppresses proliferation and promotes apoptosis role for miR-138-5p, a microRNA functions as a tumor suppressor in CRC, by directly targeting hTERT, which would be provide a new strategy for future CRC therapies.

Ligustrazine alleviates acute pancreatitis by accelerating acinar cell apoptosis at early phase via the suppression of p38 and Erk MAPK pathways.

OBJECTIVE: This study aimed to investigate the role of ligustrazine on apoptosis and inflammatory reaction in acute pancreatitis. METHODS: Rats and acinar cells were treated with caerulein to induce acute pancreatitis models. Cell models were treated with saline, p38 inhibitor, Erk inhibitor and ligustrazine. Then, the levels of TNF-α, IL-1ß and IL-6 were determined by ELISA assay, the protein levels of p38, Erk1/2, p53 and cleaved caspase3 were determined by western blotting, and apoptosis were measured by flow cytometry. Rat models were treated with saline and ligustrazine. Plasma amylase and pancreatic myeloperoxidase activity and the levels of TNF-α, IL-1ß and IL-6 in rats were determined. The protein levels of p38, Erk1/2, p53 and cleaved caspase3 in pancreas tissues were determined by western blotting, and pancreas tissues were also performed TUNEL staining to observe apoptosis status. RESULTS: Ligustrazine downregulated the levels of TNF-α, IL-1ß, IL-6. The protein levels of p38 and Erk were reduced by p38 inhibitor, Erk inhibitor and ligustrazine, while the levels of p53 and cleaved caspase 3 were upregulated. Apoptosis of AP acinar cells and cells in AP rat models was promoted after treated with ligustrazine. Plasma amylase and pancreatic myeloperoxidase activity in AP rat models were reduced by ligustrazine. CONCLUSION: Ligustrazine alleviates acute pancreatitis by accelerating acinar cell apoptosis at early phase via the suppression on p38 and Erk MAPK pathways. It is capable of attenuating the severity of acute pancreatitis and may have a therapeutic effect on patients with acute pancreatitis.

[Determination of major and minor components in standard talc samples by ICP-AES].

The standard talc sample was fused with Na2CO3 and Na2B4O7 and then the fused disc was dissolved with HCl solution. SiO2, MgO, Al2O3, Fe3O2 and CaO in talc samples were determined simultaneously by ICP-AES. The optimum analytical line with high sensitivity and low spectral interference were carefully chosen. The sources and properties of the interference were discussed. The recoveries for these elements were 98.8%-104.4%, with precision of 0.12%-2.4% RSD (n = 6). The results of major and minor components in talc samples by this method were in agreement with those provided by the standard method.