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      The long noncoding RNA CTA‐941F9.9 is frequently downregulated and may serve as a biomarker for carcinogenesis in colorectal cancer

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          Abstract

          Background

          Long noncoding RNAs (lncRNAs) participate in the carcinogenesis of many different cancers. This study aimed to detect expression of lncRNA CTA‐941F9.9 in colorectal cancer tissues compared with matched nontumorous adjacent tissues (NATs). Moreover, we investigated whether this molecule is able to influence carcinogenesis in colorectal cancer (CRC).

          Methods

          Colorectal cancer tissues and NATs from two cohorts of patients were examined. Quantitative PCR was performed to quantify levels of CTA‐941F9.9 expression in these samples. The association between CTA‐941F9.9 expression and clinicopathological features, including receiver operating characteristic (ROC) curves, was also analyzed to evaluate the diagnostic value of CTA‐941F9.9 in CRC. Potential effects of lncRNA CTA‐941F9.9 on CRC cells were assessed via autophagy, transwell assay, CCK8 assays, and flow cytometry.

          Results

          Our experimental results showed lncRNA CTA‐941F9.9 to be significantly downregulated in CRC tissues in both cohorts, with areas under the ROC curve (AUC) of 0.802 and 0.876. However, no significant correlations between CTA‐941F9.9 expression levels and clinicopathological characteristics or patient outcomes were observed. We also found that CTA‐941F9.9 promotes autophagy in CRC cell lines but no significant function of CTA‐941F9.9 in regulating cancer cell proliferation or migration.

          Conclusions

          LncRNA CTA‐941F9.9 is frequently downregulated in CRC compared with NATs and might play an important role in CRC carcinogenesis.

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          Most cited references31

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          Reducing mortality from colorectal cancer by screening for fecal occult blood. Minnesota Colon Cancer Control Study.

          Jack Mandel, John Bond, Timothy R Church … (1993)
          Although tests for occult blood in the feces are widely used to screen for colorectal cancers, there is no conclusive evidence that they reduce mortality from this cause. We evaluated a fecal occult-blood test in a randomized trial and documented its effectiveness. We randomly assigned 46,551 participants 50 to 80 years of age to screening for colorectal cancer once a year, to screening every two years, or to a control group. Participants who were screened submitted six guaiac-impregnated paper slides with two smears from each of three consecutive stools. About 83 percent of the slides were rehydrated. Participants who tested positive underwent a diagnostic evaluation that included colonoscopy. Vital status was ascertained for all study participants during 13 years of follow-up. A committee determined causes of death. A single pathologist determined the stage of each tissue specimen. Differences in mortality from colorectal cancer, the primary study end point, were monitored with the sequential log-rank statistic. The 13-year cumulative mortality per 1000 from colorectal cancer was 5.88 in the annually screened group (95 percent confidence interval, 4.61 to 7.15), 8.33 in the biennially screened group (95 percent confidence interval, 6.82 to 9.84), and 8.83 in the control group (95 percent confidence interval, 7.26 to 10.40). The rate in the annually screened group, but not in the biennially screened group, was significantly lower than that in the control group. Reduced mortality in the annually screened group was accompanied by improved survival in those with colorectal cancer and a shift to detection at an earlier stage of cancer. Annual fecal occult-blood testing with rehydration of the samples decreased the 13-year cumulative mortality from colorectal cancer by 33 percent.
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            LC3 conjugation system in mammalian autophagy

            Isei Tanida, Takashi Ueno, Eiki Kominami (2004)
            Autophagy is the bulk degradation of proteins and organelles, a process essential for cellular maintenance, cell viability, differentiation and development in mammals. Autophagy has significant associations with neurodegenerative diseases, cardiomyopathies, cancer, programmed cell death, and bacterial and viral infections. During autophagy, a cup-shaped structure, the preautophagosome, engulfs cytosolic components, including organelles, and closes, forming an autophagosome, which subsequently fuses with a lysosome, leading to the proteolytic degradation of internal components of the autophagosome by lysosomal lytic enzymes. During the formation of mammalian autophagosomes, two ubiquitylation-like modifications are required, Atg12-conjugation and LC3-modification. LC3 is an autophagosomal ortholog of yeast Atg8. A lipidated form of LC3, LC3-II, has been shown to be an autophagosomal marker in mammals, and has been used to study autophagy in neurodegenerative and neuromuscular diseases, tumorigenesis, and bacterial and viral infections. The other Atg8 homologues, GABARAP and GATE-16, are also modified by the same mechanism. In non-starved rats, the tissue distribution of LC3-II differs from those of the lipidated forms of GABARAP and GATE-16, GABARAP-II and GATE-16-II, suggesting that there is a functional divergence among these three modified proteins. Delipidation of LC3-II and GABARAP-II is mediated by hAtg4B. We review the molecular mechanism of LC3-modification, the crosstalk between LC3-modification and mammalian Atg12-conjugation, and the cycle of LC3-lipidation and delipidation mediated by hAtg4B, as well as recent findings concerning the other two Atg8 homologues, GABARAP and GATE-16. We also highlight recent findings regarding the pathobiology of LC3-modification, including its role in microbial infection, cancer and neuromuscular diseases.
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              The Atg16L complex specifies the site of LC3 lipidation for membrane biogenesis in autophagy.

              Naonobu Fujita, Takashi Itoh, Hiroko Omori … (2008)
              Two ubiquitin-like molecules, Atg12 and LC3/Atg8, are involved in autophagosome biogenesis. Atg12 is conjugated to Atg5 and forms an approximately 800-kDa protein complex with Atg16L (referred to as Atg16L complex). LC3/Atg8 is conjugated to phosphatidylethanolamine and is associated with autophagosome formation, perhaps by enabling membrane elongation. Although the Atg16L complex is required for efficient LC3 lipidation, its role is unknown. Here, we show that overexpression of Atg12 or Atg16L inhibits autophagosome formation. Mechanistically, the site of LC3 lipidation is determined by the membrane localization of the Atg16L complex as well as the interaction of Atg12 with Atg3, the E2 enzyme for the LC3 lipidation process. Forced localization of Atg16L to the plasma membrane enabled ectopic LC3 lipidation at that site. We propose that the Atg16L complex is a new type of E3-like enzyme that functions as a scaffold for LC3 lipidation by dynamically localizing to the putative source membranes for autophagosome formation.
              Article 0 comments Cited 349 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Zhenning Wang:
                ORCID: https://orcid.org/0000-0003-0557-3097
                josieon826@sina.cn
                Yongxi Song:
                ORCID: https://orcid.org/0000-0002-5736-9453
                songyongxi840309@126.com
                Journal
                Journal ID (nlm-ta): J Clin Lab Anal
                Journal ID (iso-abbrev): J. Clin. Lab. Anal
                Journal ID (doi): 10.1002/(ISSN)1098-2825
                Journal ID (publisher-id): JCLA
                Title: Journal of Clinical Laboratory Analysis
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0887-8013
                ISSN (Electronic): 1098-2825
                Publication date (Electronic): 25 July 2019
                Publication date Collection: November 2019
                Volume: 33
                Issue: 9 ( doiID: 10.1002/jcla.v33.9 )
                Electronic Location Identifier: e22986
                Affiliations
                [ 1 ] Department of Surgical Oncology and General Surgery The First Hospital of China Medical University Shenyang China
                Author notes
                [*] [* ] Correspondence

                Zhenning Wang and Yongxi Song, Department of Surgical Oncology and General Surgery, The First Hospital of China Medical University, 155 North Nanjing Street, Heping District, Shenyang 110001, China.

                Email: josieon826@ 123456sina.cn (Z.W.); songyongxi840309@ 123456126.com (Y.S.)

                Author information
                https://orcid.org/0000-0003-0557-3097
                https://orcid.org/0000-0002-5736-9453
                Article
                Publisher ID: JCLA22986
                DOI: 10.1002/jcla.22986
                PMC ID: 6868415
                PubMed ID: 31343781
                SO-VID: c4e21609-5f03-4e27-b3f6-26a67f3ec877
                Copyright © © 2019 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals, Inc.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 11 March 2019
                Date revision received : 02 July 2019
                Date accepted : 03 July 2019
                Page count
                Figures: 9, Tables: 2, Pages: 11, Words: 5624
                Funding
                Funded by: Natural Science Foundation of Liaoning Province
                Award ID: 20180550582
                Funded by: National Nature Science Foundation‐Outstanding Youth Foundation Training Project of China Medical University
                Award ID: YQ20160001
                Funded by: Project of Science and Technology of Shenyang
                Award ID: 18-014-4-07
                Categories
                Subject: Research Article
                Subject: Research Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id jcla22986
                cover-date November 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.7.2 mode:remove_FC converted:21.11.2019

                ScienceOpen disciplines: Clinical chemistry
                Keywords: biomarker,carcinogenesis,colorectal cancer,cta‐941f9.9,long noncoding rnas
                Data availability:
                ScienceOpen disciplines: Clinical chemistry
                Keywords: biomarker, carcinogenesis, colorectal cancer, cta‐941f9.9, long noncoding rnas

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