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      Fusobacterium nucleatum Promotes Metastasis in Colorectal Cancer by Activating Autophagy Signaling via the Upregulation of CARD3 Expression

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          Abstract

          Aims: We aimed to measure the abundance of Fusobacterium nucleatum ( F. nucleatum) in colorectal cancer (CRC) tissues from patients and to uncover the function of this bacterium in colorectal tumor metastasis.

          Methods: We collected metastatic and non-metastatic CRC tissues to analyze F. nucleatum abundance. Cells were incubated with F. nucleatum or chloroquine (CQ) or were transfected with CARD3-targeting siRNA; the expression of mRNAs and proteins was then measured. CRC cells stably transfected with shRNA-luc were mixed with F. nucleatum and intravenously injected into BALB/cJ mice. APC Min/+, CARD3 -/-and CARD3 wt C57BL mice were given F. nucleatum; some mice were given azoxymethane (AOM) and dextran sodium sulfate (DSS).

          Results: F. nucleatum was abundant in CRC tissues from patients with metastasis. F. nucleatum infection increased CRC cell motility and upregulated the expression of CARD3, LC3-II, Beclin1 and Vimentin, and downregulated the expression of E-cadherin and P62 in CRC cells. These effects were attenuated by treatment with CQ, siCARD3 or both. APC Min/+ mice gavaged with F. nucleatum developed more aggressive tumors than control mice. After AOM/DSS administration, the colorectums of CARD3 -/- mice had fewer tumors than those of control mice. Tumors from CARD3 -/- mice had lower levels of LC3-II and Beclin1 and higher levels of P62 than those from control mice. BALB/cJ mice injected with both CT26-luc cells and F. nucleatum formed more metastases than control mice. CQ treatment, CARD3 knockdown or both reduced the ability of CT26-luc cells to form metastases in vivo.

          Conclusions: F. nucleatum is enriched in CRC tissues from patients with metastasis. F. nucleatum orchestrates CARD3 and autophagy to control CRC metastasis. Measuring and targeting F. nucleatum and its associated pathways will yield approaches for the prevention and treatment of CRC metastasis.

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          FLASH: fast length adjustment of short reads to improve genome assemblies.

          T. Magoc, S. L. Salzberg (2013)
          Next-generation sequencing technologies generate very large numbers of short reads. Even with very deep genome coverage, short read lengths cause problems in de novo assemblies. The use of paired-end libraries with a fragment size shorter than twice the read length provides an opportunity to generate much longer reads by overlapping and merging read pairs before assembling a genome. We present FLASH, a fast computational tool to extend the length of short reads by overlapping paired-end reads from fragment libraries that are sufficiently short. We tested the correctness of the tool on one million simulated read pairs, and we then applied it as a pre-processor for genome assemblies of Illumina reads from the bacterium Staphylococcus aureus and human chromosome 14. FLASH correctly extended and merged reads >99% of the time on simulated reads with an error rate of <1%. With adequately set parameters, FLASH correctly merged reads over 90% of the time even when the reads contained up to 5% errors. When FLASH was used to extend reads prior to assembly, the resulting assemblies had substantially greater N50 lengths for both contigs and scaffolds. The FLASH system is implemented in C and is freely available as open-source code at http://www.cbcb.umd.edu/software/flash. t.magoc@gmail.com.
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            Microbial genomic analysis reveals the essential role of inflammation in bacteria-induced colorectal cancer

            Janelle Arthur, Raad Gharaibeh, Marcus Mühlbauer … (2014)
            Enterobacteria, especially Escherichia coli, are abundant in patients with inflammatory bowel disease or colorectal cancer (CRC). However, it is unclear whether cancer is promoted by inflammation-induced expansion of E. coli and/or changes in expression of specific microbial genes. Here we use longitudinal (2, 12 and 20 weeks) 16S rRNA sequencing of luminal microbiota from ex-germ free mice to show that inflamed Il10 −/− mice maintain a higher abundance of Enterobacteriaceae than healthy wild-type mice. Experiments with mono-colonized Il10 −/− mice reveal that host inflammation is necessary for E. coli cancer-promoting activity. RNA-sequence analysis indicates significant changes in E. coli gene catalogue in Il10 −/− mice, with changes mostly driven by adaptation to the intestinal environment. Expression of specific genes present in the tumor-promoting E. coli pks island are modulated by inflammation/CRC development. Thus, progression of inflammation in Il10 −/− mice supports Enterobacteriaceae and alters a small subset of microbial genes important for tumor development.
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              Listeria hijacks host mitophagy through a novel mitophagy receptor to evade killing

              Yifan Zhang, Yikun Yao, Xiaoxu Qiu … (2019)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Theranostics
                Journal ID (iso-abbrev): Theranostics
                Journal ID (publisher-id): thno
                Title: Theranostics
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1838-7640
                Publication date Collection: 2020
                Publication date (Electronic): 1 January 2020
                Volume: 10
                Issue: 1
                Pages: 323-339
                Affiliations
                [1 ]Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
                [2 ]Key Laboratory of Hubei Province for Digestive System Disease, Wuhan, Hubei Province, China.
                [3 ]Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, China.
                [4 ]Department of Gastroenterology, The Affiliated Hospitalof North Sichuan Medical College, Road Wenhua 63#, Region Shunqing, Nanchong City 637000, China.
                [5 ]Center for Epigenetics & Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX77030, USA.
                Author notes
                ✉ Corresponding author: Weiguo Dong, MD and PhD, Department of Gastroenterology, Key Laboratory of Hubei Province for Digestive System Disease, Renmin Hospital of Wuhan University, Jiefang Road 238, Wuhan 430060, China. E-mail, dongweiguo@ 123456whu.edu.cn , Tel., +86 13986167388.

                # These authors contributed equally to this work.

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: thnov10p0323
                DOI: 10.7150/thno.38870
                PMC ID: 6929621
                PubMed ID: 31903123
                SO-VID: 7acfe0e0-444c-4e47-8560-ebcbfd7c5d99
                Copyright © © The author(s)
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                History
                Date received : 30 July 2019
                Date accepted : 25 September 2019
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Molecular medicine
                Keywords: microbe,gene regulation,gene targeting,colorectal cancer
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: microbe, gene regulation, gene targeting, colorectal cancer

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