Storgaard Berntsen (officehemp0)

Lentiviral‑mediated knockdown of miR‑29c resulted in increased the expression levels of COL1α1, COL3α1, α‑SMA and TGF‑β1, while lentiviral‑mediated miR‑29c overexpression significantly suppressed the expression levels of these fibrosis‑related genes. Taken together, these results demonstrated that miR‑29c was significantly associated with silica‑induced pulmonary fibrosis and the expression levels of COL1α1, COL3α1, TGF‑β1 and α‑SMA are under the regulation of miR‑29c to different extents. This study therefore identified possible candidate molecular targets for preventing or delaying the occurrence and progression of silicosis.The tumor microenvironment composed of a mixture of stromal cells and their secretions has a marked impact on cancer progression. In particular, soluble factors and metabolites contribute to malignancy through the dysregulation of autophagy in cancer cells. The present study investigated the effects of ovarian cancer‑associated fibroblasts (OVCAFs) with their secretory substances on the autophagy and migration of ovarian cancer cells. The conditioned‑medium (CM) of OVCAFs isolated from fresh human ovarian cancer tissues was analyzed for the levels of 27 common cytokines/chemokines using a cytokine array. Autophagy in cancer cells was assessed by determining the expression of the vacuolar form of LC3 by western blot analysis and immunofluorescence. Cancer cell migration was assessed by Transwell migration assay. Interleukin (IL)‑8 was found to be the most highly upregulated cytokine among the cytokines/chemokines found in the OVCAF‑CM. The role of IL‑8 in ovarian cancer cell migration and its mechanistic link with autophagy was investigated. Recombinant human IL‑8 (rhIL‑8) stimulated the migration of SKOV3 and Kuramochi ovarian cancer cells, and concurrently downregulated basal autophagy, in concentration‑dependent manner. Compared to the CM of control counterpart normal fibroblasts isolated from benign ovaries (OVNF‑CM), the CM from 3 OVCAF isolates (namely, OVCAF‑9, ‑20 and ‑43) exerted effects similar to rhIL‑8 on both cancer cell lines. The pharmacological induction of autophagy with rapamycin or metformin attenuated the pro‑migratory effects of IL‑8. Neutralizing anti‑IL‑8 antibody counteracted the inhibitory effect of OVCAF‑CM on basal autophagy. On the whole, the present study highlights the involvement of IL‑8 released by CAFs in the ovarian tumor microenvironment in promoting cancer cell migration through the suppression of autophagy.Recent studies have revealed that long noncoding RNAs (lncRNAs) are closely associated with colorectal cancer (CRC); however, the role of the lncRNA RPLP0P2 in CRC remains largely unknown. In the present study, RNA expression profiles of CRC were collected from The Cancer Genome Atlas database and the prognosis of CRC with respect to RPLP0P2 was assessed. Subsequently, RPLP0P2 expression was knocked down in the human CRC cell line RKO using a short hairpin RNA (shRNA) lentivirus, and the biological behaviors of the cells, such as proliferation, migration, cell cycle progression and apoptosis, were examined. The results demonstrated that the expression levels of RPLP0P2 were higher in CRC tissue compared with those in normal tissue, and RPLP0P2 was associated with prognosis. RPLP0P2 knockdown significantly decreased cell colony formation, migration and invasion, and arrested CRC cells in the S phase to G2/M phase transition. Furthermore, apoptosis was significantly increased in CRC cells infected with the RPLP0P2 shRNA lentivirus compared with in the control group. In conclusion, RPLP0P2 may promote proliferation, invasion and migration, and inhibit apoptosis of CRC cells, suggesting that RPLP0P2 may function as an oncogene in CRC.The present study aimed to investigate the function of the single nucleotide polymorphism (SNP) rs41291957 in the prognosis of intracerebral hemorrhage (ICH). In addition, the molecular mechanisms underlying the role of microRNA (miR)‑143,