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      Role of Metastasis Suppressor KAI1/CD82 in Different Cancers

      review-article
      Author(s): 1 , 2 , 3 , 1 , 3 , , 3 ,
      Publication date (Electronic):
      Journal: Journal of Oncology
      Publisher: Hindawi

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          Abstract

          Metastasis is one of the characteristics of malignant tumors and the main cause of death worldwide. The process of metastasis is mainly affected by tumor metastasis genes, tumor metastasis suppressor genes, tumor microenvironment, extracellular matrix degradation, and other factors. Thus, it is essential to elucidate the mechanism of metastasis and find the therapeutic targets in order to prevent the development of malignant tumors. KAI1/CD82, a member of tetraspanin superfamily of glycoproteins, has been reported as a tumor metastasis suppressor gene in various types of cancers without affecting the tumor formation. Many studies have demonstrated that low expression of KAI1/CD82 might lead to poor prognosis due to its interactions with other tetraspanins and integrins, resulting in the regulation of cell motility and invasion, cell-cell adhesion, and apoptosis. Considering its pathological and physiological significance, KAI1/CD82 could be a potential strategy for clinical predicting and preventing tumor progression and metastasis. The present review aims to discuss the role of KAI1/CD82 in metastasis for different cancers and examine its prospects as a metastasis biomarker and a therapeutic target.

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          KAI1, a metastasis suppressor gene for prostate cancer on human chromosome 11p11.2.

          J T Dong, P W Lamb, C W Rinker-Schaeffer … (1995)
          A gene from human chromosome 11p11.2 was isolated and was shown to suppress metastasis when introduced into rat AT6.1 prostate cancer cells. Expression of this gene, designated KAI1, was reduced in human cell lines derived from metastatic prostate tumors. KAI1 specifies a protein of 267 amino acids, with four hydrophobic and presumably transmembrane domains and one large extracellular hydrophilic domain with three potential N-glycosylation sites. KAI1 is evolutionarily conserved, is expressed in many human tissues, and encodes a member of a structurally distinct family of leukocyte surface glycoproteins. Decreased expression of this gene may be involved in the malignant progression of prostate and other cancers.
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            CircLONP2 enhances colorectal carcinoma invasion and metastasis through modulating the maturation and exosomal dissemination of microRNA-17

            Kai. Han, Feng-Wei Wang, Chen-Hui Cao … (2020)
            Background Metastasis causes the vast majority of colorectal carcinoma (CRC)-related deaths. However, little is known about the specific traits and underlying mechanisms of metastasis-initiating cells in primary CRC. And whether or not circular RNAs (circRNAs) take part in this particular event remain not adequately stated yet. Methods A screening method based on Transwell assay was first applied to build CRC subgroups with different metastatic potential. High throughput RNA sequencing was used to find out novel metastatic drivers in CRC metastasis-initiating step. A series of in vitro and in vivo assays were further applied to elucidate the functions and underlying molecular mechanisms of circRNAs in CRC metastasis. Results A circRNA consisting of exon 8–11 of LONP2, termed as circLONP2, was upregulated in metastasis-initiating CRC subgroups. Aberrant higher expression of circLONP2 was observed in primary CRC tissues with established metastasis, and along the invasive margin in metastatic site. High expression of circLONP2 predicted unfavorable overall survival. Functional studies revealed that circLONP2 could enhance the invasiveness of CRC cells in vitro, and targeting circLONP2 through anti-sense oligonucleotide (ASO) dramatically reduced the penetrance of metastasis to foreign organs in vivo. Mechanically, circLONP2 directly interacted with and promoted the processing of primary microRNA-17 (pri-miR-17), through recruiting DiGeorge syndrome critical region gene 8 (DGCR8) and Drosha complex in DDX1-dependent manner. Meanwhile, upregulated mature miR-17-5p could be assembled into exosomes and internalized by neighboring cells to enhance their aggressiveness. Conclusions Our data indicate that circLONP2 acts as key metastasis-initiating molecule during CRC progression through modulating the intracellular maturation and intercellular transfer of miR-17, resulting in dissemination of metastasis-initiating ability in primary site and acceleration of metastasis formation in foreign organs. circLONP2 could serve as an effective prognostic predictor and/or novel anti-metastasis therapeutic target in CRC treatment.
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              Metastasis suppressors genes in cancer.

              K. Vaidya, Joshua D Welch, Lewis Stafford (2007)
              The major problem for cancer patients is metastasis of the cancer from the primary tumor to secondary sites. Metastasis is the process by which tumor cells disseminate from the primary tumor, migrate through the basement membrane, survive in the circulatory system, invade into a secondary site, and start to proliferate. In the past, research had concentrated on the biology, taking more of a global view instead of a molecular view. More recently, the focus has been determining the molecular underpinnings, looking at genes that induce or inhibit metastasis. Metastasis suppressors, by definition, inhibit metastasis at any step of the metastatic cascade without blocking primary tumor growth. The expanding list of metastasis suppressors exist with every cellular compartment and have been shown to work by regulating signaling pathways that inhibit proliferation, cell migration and growth at the secondary site. Still, the biochemical basis of their inhibition is not completely known. Here we review the known metastasis suppressors and summarize the suspected mechanisms by which they inhibit metastasis.
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                Author and article information

                Contributors
                Qian Zhang:
                ORCID: https://orcid.org/0000-0001-7746-4231
                Jian Zhang:
                ORCID: https://orcid.org/0000-0002-8243-3031
                Journal
                Journal ID (nlm-ta): J Oncol
                Journal ID (iso-abbrev): J Oncol
                Journal ID (publisher-id): jo
                Title: Journal of Oncology
                Publisher: Hindawi
                ISSN (Print): 1687-8450
                ISSN (Electronic): 1687-8469
                Publication date Collection: 2021
                Publication date (Electronic): 9 July 2021
                Volume: 2021
                Electronic Location Identifier: 9924473
                Affiliations
                1Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
                2Hepatobiliary Center of The First Affiliated Hospital, Nanjing Medical University and Research Unit of Liver Transplantation and Transplant Immunology, Chinese Academy of Medical Sciences, Nanjing, China
                3Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
                Author notes

                Academic Editor: Nihal Ahmad

                Author information
                https://orcid.org/0000-0002-6972-7393
                https://orcid.org/0000-0001-5882-9362
                https://orcid.org/0000-0001-7746-4231
                https://orcid.org/0000-0002-8243-3031
                Article
                DOI: 10.1155/2021/9924473
                PMC ID: 8285166
                PubMed ID: 34306081
                SO-VID: 6704903c-024c-4132-8dbf-12bb0742ce32
                Copyright © Copyright © 2021 Wei Yan et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 19 March 2021
                Date revision received : 30 June 2021
                Date accepted : 1 July 2021
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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