Effects of AIF-1 inflammatory factors on the regulation of proliferation of breast cancer cells.

The purpose of this study was to explore the effect of Allograft Inflammatory Factor 1 (AIF-1) on the regulation of proliferation of breast cancer cells. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), cell culture and counting, and mass spectrometry were performed. The biologically active high-purity recombinant protein rhAIF-1 was obtained by optimizing the rhAIF-1 protein purification system, and MDA-MB-231 and MDA-MB-361 breast cancer cell lines were used. After adding to the culture medium, rhAIF-1 was found to promote cell proliferation in dose-dependent and time-dependent manners. The purified protein rhAIF-1 was marked with rhodamine and incubated with the cells. Confocal imaging analysis revealed that the foreign protein was localized in the cytoplasm, and rhAIF-1 was unevenly distributed in the cytoplasm. Although AIF-1 accumulates around the nucleus, it can not enter the nucleus, suggesting that other factors might be involved in the regulation of cell proliferation. In order to find the possible interacting protein of rhAIF-1, protein immunoprecipitation technique and mass spectrometry were employed, and it was indicated that ADAM28m was the possible interacting protein of rhAIF-1. The interaction between rhAIF-1 and ADAM28m was validated by immunoprecipitation along with Western blotting. It was found that rhAIF-1 could precipitate ADAM28m protein by immunoprecipitation. The results indicated that IF-1 participates in the development of breast cancer by interacting with ADAM28m and activating downstream signaling pathways. It was concluded that AIF-1 provides a new idea for the molecular mechanism of breast cancer cell proliferation and acts as a new target for the prevention and treatment of breast cancer in the future.

Proliferation and migration of hepatocellular carcinoma are accelerated by LINC01287 via the miR-559/TCF12 axis.

OBJECTIVE: To uncover the role of LINC01287 in the progression of hepatocellular carcinoma (HCC) and the indicated molecular mechanism. PATIENTS AND METHODS: Relative levels of LINC01287 and miR-559 in 32 pairs of HCC tissues and normal ones, as well as HCC cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Receiver operating characteristic (ROC) curves and Kaplan-Meier curves were depicted for assessing the diagnostic and prognostic potentials of LINC01287 in HCC, respectively. Proliferative and migratory capacities in HCC cells influenced by LINC01287 were assessed by cell counting kit-8 (CCK-8) and transwell assay, respectively. The regulatory loop LINC01287/miR-559/TCF12 was ascertained by Dual-Luciferase reporter assay. The involvement of the regulatory loop in the progression of HCC was examined via rescue experiments. RESULTS: LINC01287 was upregulated in HCC tissues and cell lines, whereas miR-559 was downregulated. LINC01287 displayed certain diagnostic and prognostic potentials in HCC. Knockdown of LINC01287 could inhibit proliferative and migratory capacities in HCC cells. The regulatory loop LINC01287/miR-559/TCF12 was responsible for the aggravation of HCC. CONCLUSIONS: LINC01287 drives proliferative and migratory capacities in HCC via targeting the miR-559/TCF12 axis.

Hepatic coccidiosis in the goat.

Coccidial oocysts were seen in the bile from five goats infected with coccidia either naturally or artificially. The oocysts measured on average 21.3 by 18.3 microns and resembled those of Eimeria ninakohlyakimovae. Livers and gall bladders of infected animals showed various degrees of histopathological changes. In the worst case, bile had a thick consistency and contained blood and necrotic debris. Apart from those in the bile, oocysts were seen in liver smears and in the centrilobular vein in two histological sections. Forms resembling meronts and measuring on average 200 by 147 microns were seen in sections of bile duct.