BACKGROUNDCircular RNAs (circRNAs) are considered to be highly stable due to the closed structure, which are predominately correlated with the development and progression of a wide variety of cancers. Colon cancer is one of the most common malignancies worldwide. A recent study demonstrated the upregulated expression of circPIP5K1A in non-small cell lung cancer. However, few studies have investigated the relationship between circ_0014130 level and colon cancer. Therefore, elucidating the underlying mechanisms of circPIP5K1A’s role may help with the identification of novel diagnostic and therapeutic targets for colon cancer.AIMTo investigate the status of circPIP5K1A in colon cancers and its effects on the modulation of cancer development.METHODSThe expression level of circPIP5K1A in tissue and serum samples from colon cancer patients, as well as human colonic cancer cell lines was detected by real-time quantitative reverse transcription-polymerase chain reaction. Following the transfection of specifically synthesized small interfering RNA (siRNA) into colon cell lines, we used Hoechst staining assay to measure the ratio of cell death in the absence of circPIP5K1A. Moreover, we also used the Transwell assay to assess the migratory function of colon cells overexpressing circPIP5K1A. Additionally, we employed a series of bioinformatics prediction programs to predict the potential of circPIP5K1A-targeted miRNAs and mRNAs. The miR-1273a vector was constructed, and then transfected with or without circPIP5K1A vector into colon cancer cells. Afterwards, the expression of activator protein 1 (AP-1), interferon regulating factor 4 (IRF-4), caudal type homeobox 2 (CDX-2), and zinc finger of the cerebellum 1 (Zic-1) was detected by western blotting.RESULTSCircPIP5K1A was significantly upregulated in colon cancer tissue relative to their adjacent normal tissues. Knockdown of circPIP5K1A in colon cancer cells impaired cell viability and suppressed cell invasion and migration, while enforced expression of circPIP5K1A exhibited the opposite effects on cell migration. Bioinformatics prediction program predicted that the association of circPIP5K1A with miR-1273a, as well as AP-1, IRF-4, CDX-2, and Zic-1. Subsequent studies showed that overexpression of circPIP5K1A augmented the expression of AP-1 but attenuated the expression of IRF-4, CDX-2, and Zic-1. Reciprocally, overexpression of miR-1273a abrogated the oncogenic function of circPIP5K1A in colon cancers.CONCLUSIONOverall, our data demonstrate the oncogenic role of circPIP5K1A-miR-1273a axis in regulation of colon cancer development, which provides a novel insights into colon cancer pathogenesis.
Puccinia striiformis f. sp. tritici (Pst), the causal agent of stripe rust, is an obligate biotrophic pathogen responsible for severe wheat disease epidemics worldwide. Pst and other rust fungi are acknowledged to deliver many effector proteins to the host, but little is known about the effectors’ functions. Here, we report a candidate effector Pst_8713 isolated based on the genome data of CY32 and the expression of Pst_8713 is highly induced during the early infection stage. The Pst_8713 gene shows a low level of intra-species polymorphism. It has a functional N-terminal signal peptide and its product was found in the host cytoplasm and nucleus. Co-infiltrations in Nicotiana benthamiana demonsrated that Pst_8713 was capable of suppressing cell death triggered by mouse pro-apoptotic protein-BAX or Phytophthora infestans PAMP-INF1. Overexpression of Pst_8713 in plants suppressed pattern-triggered immunity (PTI) -associated callose deposition and expression of PTI-associated marker genes and promoted bacterial growth in planta. Effector-triggered immunity (ETI) induced by an avirulent Pst isolate was weakened when we overexpressed Pst_8713 in wheat leaves which accompanied by reduction of reactive oxygen species (ROS) accumulation and hypersensitive response (HR). In addition, the host induced gene silencing (HIGS) experiment showed that knockdown of Pst_8713 weakened the virulence of Pst by producing fewer uredinia. These results indicated that candidate effector Pst_8713 is involved in plant defense suppression and contributes to enhancing the Pst virulence.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.