A vicinal oxygen chelate protein facilitates viral infection by triggering the unfolded protein response in Nicotiana benthamiana.

Vicinal oxygen chelate (VOC) proteins are members of an enzyme superfamily with dioxygenase or non-dioxygenase activities. However, the biological functions of VOC proteins in plants are poorly understood. Here, we show that a VOC in Nicotiana benthamiana (NbVOC1) facilitates viral infection. NbVOC1 was significantly induced by infection by beet necrotic yellow vein virus (BNYVV). Transient overexpression of NbVOC1 or its homolog from Beta vulgaris (BvVOC1) enhanced BNYVV infection in N. benthamiana, which required the nuclear localization of VOC1. Consistent with this result, overexpressing NbVOC1 facilitated BNYVV infection, whereas, knockdown and knockout of NbVOC1 inhibited BNYVV infection in transgenic N. benthamiana plants. NbVOC1 interacts with the basic leucine zipper transcription factors bZIP17/28, which enhances their self-interaction and DNA binding to the promoters of unfolded protein response (UPR)-related genes. We propose that bZIP17/28 directly binds to the NbVOC1 promoter and induces its transcription, forming a positive feedback loop to induce the UPR and facilitating BNYVV infection. Collectively, our results demonstrate that NbVOC1 positively regulates the UPR that enhances viral infection in plants.

[Retracted] Actin­binding protein anillin promotes the progression of hepatocellular carcinoma in vitro and in mice.

[This retracts the article DOI: 10.3892/etm.2021.9885.].

[Retracted] KIF2C promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo.

[This retracts the article DOI: 10.3892/etm.2021.10528.].

KIF2C promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo.

Hepatocellular carcinoma (HCC) is one of the most common malignancies with high mortality and morbidity rates. In recent years, HCC targeted therapy has gained increasing attention. Due to the heterogeneity and high metastasis of HCC, more effective therapeutic targets are needed. Kinesin family member 2C (KIF2C), also known as mitotic centromere-associated kinesin, is a microtubule-based motor protein which is involved in a variety of important cellular processes, such as mitosis. The effects of KIF2C on cancer progression and development have been widely studied; however, its potential effects on HCC remains unclear. In the present study, high expression of KIF2C in human HCC tissues was demonstrated using The Cancer Genome Atlas database and immunohistochemistry assays. KIF2C expression was associated with HCC prognosis, including overall survival and disease-free survival. KIF2C expression was also associated with clinical pathological characteristics including the number of tumor nodes (P=0.015) and tumor size (P=0.009). KIF2C knockdown inhibited the proliferation of HCC cells in vitro, confirmed by MTT and colony formation assays, and suppressed tumor growth in mice which was confirmed by a xenograft mouse model. Together, the results suggested that KIF2C may serve as a promising therapeutic target for the treatment of HCC.

RNA-Seq Reveals Function of Bta-miR-149-5p in the Regulation of Bovine Adipocyte Differentiation.

Intramuscular fat is a real challenge for the experts of animal science to improve meat quality traits. Research on the mechanism of adipogenesis provides invaluable information for the improvement of meat quality traits. This study investigated the effect of bta-miR-149-5p and its underlying mechanism on lipid metabolism in bovine adipocytes. Bovine adipocytes were differentiated and transfected with bta-miR-149-5p mimics or its negative control (NC). A total of 115 DEGs including 72 upregulated and 43 downregulated genes were identified in bovine adipocytes. The unigenes and GO term biological processes were the most annotated unigene contributor parts at 80.08%, followed by cellular component at 13.4% and molecular function at 6.7%. The KEGG pathways regulated by the DEGs were PI3K-Akt signaling pathway, calcium signaling pathway, pathways in cancer, MAPK signaling pathway, lipid metabolism/metabolic pathway, PPAR signaling pathway, AMPK signaling pathway, TGF-beta signaling pathway, cAMP signaling pathway, cholesterol metabolism, Wnt signaling pathway, and FoxO signaling pathway. In addition to this, the most important reactome enrichment pathways were R-BTA-373813 receptor CXCR2 binding ligands CXCL1 to 7, R-BTA-373791 receptor CXCR1 binding CXCL6 and CXCL8 ligands, R-BTA-210991 basigin interactions, R-BTA-380108 chemokine receptors binding chemokines, R-BTA-445704 calcium binding caldesmon, and R-BTA-5669034 TNFs binding their physiological receptors. Furthermore, the expression trend of the DEGs in these pathways were also exploited. Moreover, the bta-miR-149-5p significantly (p < 0.01) downregulated the mRNA levels of adipogenic marker genes such as CCND2, KLF6, ACSL1, Cdk2, SCD, SIK2, and ZEB1 in bovine adipocytes. In conclusion, our results suggest that bta-miR-149-5p regulates lipid metabolism in bovine adipocytes. The results of this study provide a basis for studying the function and molecular mechanism of the bta-miR-149-5p in regulating bovine adipogenesis.

Actin-binding protein anillin promotes the progression of hepatocellular carcinoma in vitro and in mice.

Hepatocellular carcinoma (HCC) is a common type of tumor with high mortality worldwide. Investigations associated with the molecular etiology of HCC and screening novel therapeutic targets are still urgently in need. Anillin (ANLN), as a type of evolutionarily conserved actin-binding protein, is involved in multiple cellular processes. ANLN widely affected the progression and metastasis of several types of cancer, and its overexpression was frequently demonstrated in previous studies. The present study demonstrated high expression of ANLN in human HCC tissues, which was also associated the prognosis of patients with HCC. The associations between ANLN expression and the clinicopathological features were determined, including the number of tumor nodes (P=0.011) and tumor size (P=0.003) of patients with HCC. It was found that ANLN promoted cell proliferation, invasion and migration of HCC cells in vitro, and affected tumor growth in vivo. Therefore, ANLN is suggested as a promising therapeutic target for the treatment of HCC.

KLF15 promotes transcription of KLF3 gene in bovine adipocytes.

The Krüppel-like factors (KLF) family plays an important role in adipogenesis, which is subject to internal hierarchical regulation. KLF3 is a member of KLF family, mainly responsible for adipocyte differentiation and fat deposition. However, the transcriptional regulation of bovine KLF3 gene and its relationship with KLF15 gene remains unclear during bovine adipogenesis. Here, we report that the expression pattern of KLF3 and KLF15 genes during bovine adipogenesis, when KLF15 gene was overexpressed through adenoviral vector (Ad-KLF15) in bovine adipocytes the expression level of KLF3 gene was increased, similarly when KLF15 was down regulated through siRNA the expression level of KLF3 was also reduced. To explore the transcriptional regulation of bovine KLF3 gene and its relationship with KLF15, serial deletion constructs of the 5'flanking region of bovine KLF3gene revealed through dual-luciferase reporter assay that the core promoter is located in -264 to -76 regions. The most proximal GGGG element in the promoter of the bovine KLF3 gene (located in -264 to -76 regions) is required for promotion by KLF15. Electrophoretic mobility shift (EMSA) and chromatin immunoprecipitation (ChIP) assays further confirmed that KLF15 gene binds to the KLF3 gene core promoter region in bovine adipocytes. These findings conclude that KLF15 promotes the transcriptional activity of KLF3 in bovine adipocytes. This mechanism to provides a new direction for further study of adipogenesis by internal regulation of members within KLF family.