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Ectopic expression of circ‑0004904 promoted autophagy, but inhibited migration and proliferation of HTR8 cells compared with those in the negative control group. Silencing of circ‑0004904 inhibited autophagy, and induced migration and proliferation in JEG3 cells compared with those in the negative control group. In addition, circ‑0004904 regulated the levels of ATG12 via interaction with miR‑570. Furthermore, circ‑0004904 regulated the FUS/VEGF axis in HTR8 and JEG3 cells. In conclusion, circ‑0004904 was abnormally expressed in the plasma and placental tissues of patients with preeclampsia. In addition, circ‑0004904 was involved in the regulation of proliferation, invasion and autophagy in HTR8 and JEG3 cells. Thus, circ‑0004904 may be used as a potential diagnostic biomarker and therapeutic target for preeclampsia.Radiation is one of the main methods for the treatment of colorectal cancer (CRC) before or after surgery. However, radiotherapy tolerance of patients with CRC is often a major concern. Interferon regulatory factor 1 (IRF1) is a member of the IRF family and is involved in the development of multiple diseases, including tumors. The present study investigated the role of IRF1 in the development and radiation sensitivity of CRC. Immunohistochemistry was performed to examine the expression levels of IRF1 in tissue samples from patients with CRC, as well as in nude mice. MTT, 5‑ethynyl‑20‑deoxyuridine, colony formation, cell cycle alteration and apoptosis assays were performed in CRC cell lines. Western blotting and immunofluorescence were used to detect the expression levels of a series of proteins. RNA sequencing was applied to identify genes whose expression was upregulated by IRF1 overexpression. Xenograft nude mouse models and hematoxylin and eosin staining were used to validate the present findings in vivo. It was revealed that the expression levels of IRF1 were significantly lower in CRC tissues than in adjacent tissues. IRF1 upregulation inhibited cell proliferation and colony formation, caused G1 cell arrest, promoted cell apoptosis, and enhanced the sensitivity of CRC cells to X‑ray irradiation. The role of IRF1 in promoting the radiosensitivity of CRC was further demonstrated in nude mice with CRC xenografts. In addition, RNA sequencing revealed that overexpression of IRF1 in CRC cells significantly increased the expression levels of interferon‑induced protein family members interferon α inducible protein 6, interferon induced transmembrane protein 1 and interferon induced protein 35 (fold change >2.0). In summary, the present study demonstrated that the upregulation of IRF1 inhibited the progression and promoted the radiosensitivity of CRC, likely by regulating interferon‑induced proteins.Subsequently to the publication of the above paper, the authors have retrospectively realized that they used the human normal liver cell, line L‑02, for the experiments reported in this study instead of the intended hepatocellular cell line, Huh‑7. Consequently, the results and conclusions reported in this article must be considered to lack reliability. Therefore, the authors have requested that the article be retracted from the publication. The authors apologize to the Editor and to the readership for any inconvenience caused. [the original article was published in Oncology Reports 42 1125‑1132, 2019; DOI 10.3892/or.2019.7213].Cancers of the urinary tract, as well as those of the female and male reproductive systems, account for a large percentage of malignancies worldwide. Mortality is frequently affected by late diagnosis or therapeutic difficulties. The Sonic Hedgehog (SHH) pathway is an evolutionary conserved molecular cascade, which is mainly associated with the development of the central nervous system in fetal life. The present review aimed to provide an in‑depth summary of the SHH signaling pathway, including the characterization of its major components, the mechanism of its upstream regulation and non‑canonical activation, as well as its interactions with other cellular pathways. In addition, the three possible mechanisms of the cellular SHH cascade in cancer tissue are discussed. PD98059 The aim of the present review was to summarize significant findings with regards to the expression of the SHH pathway components in kidney, bladder, ovarian, cervical and prostate cancer. Reports associated with common deficits and de‑regulations of the SHH pathway were summarized, despite the differences in molecular and histological patterns among these malignancies. However, currently, neither are SHH pathway elements included in panels of prognostic/therapeutic molecular patterns in any of the discussed cancers, nor have the drugs targeting SMO or GLIs been approved for therapy. The findings of the present review may support future studies on the treatment of and/or molecular targets for gynecological and genitourinary cancers.Lung cancer has become the leading cause of cancer‑associated mortality worldwide. However, the underlying mechanisms of lung cancer remain poorly understood. DnaJ heat shock protein family (HSP40) member C12 (DNAJC12) is a type III member belonging to the HSP40/DNAJ family. The role of DNAJC12 in numerous types of cancer has been previously reported; however, the effect of DNAJC12 in lung cancer remains unknown. The results of the present study indicated that DNAJC12 may be involved in lung cancer proliferation and migration by regulating the β‑catenin signaling pathway. Data generated in the present study and from The Cancer Genome Atlas revealed that the DNAJC12 expression levels were significantly upregulated in lung cancer tissues compared with non‑cancer lung tissues. The expression of DNAJC12 was subsequently knocked down in A549 and NCI‑H1975 lung cancer cells using lentiviral transfections and further experiments demonstrated that the knockdown of DNAJC12 inhibited the proliferation, colony formation, migration and invasion of lung cancer cells. The results of flow cytometric assays also revealed that the knockdown of DNAJC12 induced the apoptosis of lung cancer cells. In addition, the effects of DNAJC12 knockdown on the in vivo growth of lung cancer cells were observed. Signaling pathway analysis revealed that the knockdown of DNAJC12 expression suppressed the phosphorylation of p65 NF‑κB, downregulated the expression levels and inhibited the subsequent activation of β‑catenin, and downregulated the expression levels of vimentin. Rescue experiments demonstrated that the overexpression of β‑catenin, but not that of NF‑κB or vimentin, reversed the effects of DNAJC12 knockdown on the proliferation and invasion of lung cancer cells. On the whole, the findings of the present study suggest that DNAJC12 may play a crucial role in lung cancer tumorigenesis by regulating the expression and activation of β‑catenin. Therefore, DNAJC12 may represent a novel target for the treatment of lung cancer.