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      The tumor suppressor role and ceRNA network of miR-1294 in cancer

      review-article
      Author(s): 1 , 1 , 2 , 1 , , 1 ,
      Publication date (Electronic, collection):
      Publication date (Electronic, pub):
      Journal: Oncology Research
      Publisher: Tech Science Press
      Keywords: miR-1294, Expression, Cancer, ceRNA, Signaling pathway, Prognosis

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          Abstract

          miRNAs are endogenous small RNAs that are important regulators of gene expression. miR-1294 was found to be significantly down-regulated in 15 cancers and regulated by 21 upstream regulators. miR-1294 affects the proliferation, migration, invasion, and apoptosis of cancer cells. The target genes of miR-1294 are involved in the PI3K/AKT/mTOR, RAS, and JAK/STAT signaling pathways. Six target genes of miR-1294 are the targets of a variety of drugs. Low expression of miR-1294 is associated with resistance to cisplatin and TMZ and a poorer prognosis in patients with ESCC, GC, EOC, PDAC, or NSCLC. Therefore, this work outlines the molecular mechanisms and provides a basis for the clinical significance of the tumor suppressor miR-1294 in cancer.

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          Cisplatin in cancer therapy: molecular mechanisms of action.

          Shaloam R Dasari, Paul Bernard Tchounwou (2014)
          Cisplatin, cisplatinum, or cis-diamminedichloroplatinum (II), is a well-known chemotherapeutic drug. It has been used for treatment of numerous human cancers including bladder, head and neck, lung, ovarian, and testicular cancers. It is effective against various types of cancers, including carcinomas, germ cell tumors, lymphomas, and sarcomas. Its mode of action has been linked to its ability to crosslink with the purine bases on the DNA; interfering with DNA repair mechanisms, causing DNA damage, and subsequently inducing apoptosis in cancer cells. However, because of drug resistance and numerous undesirable side effects such as severe kidney problems, allergic reactions, decrease immunity to infections, gastrointestinal disorders, hemorrhage, and hearing loss especially in younger patients, other platinum-containing anti-cancer drugs such as carboplatin, oxaliplatin and others, have also been used. Furthermore, combination therapies of cisplatin with other drugs have been highly considered to overcome drug-resistance and reduce toxicity. This comprehensive review highlights the physicochemical properties of cisplatin and related platinum-based drugs, and discusses its uses (either alone or in combination with other drugs) for the treatment of various human cancers. A special attention is paid to its molecular mechanisms of action, and its undesirable side effects. Copyright © 2014 Elsevier B.V. All rights reserved.
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            Molecular mechanisms of cisplatin resistance.

            L Galluzzi, L Senovilla, I Vitale … (2012)
            Platinum-based drugs, and in particular cis-diamminedichloroplatinum(II) (best known as cisplatin), are employed for the treatment of a wide array of solid malignancies, including testicular, ovarian, head and neck, colorectal, bladder and lung cancers. Cisplatin exerts anticancer effects via multiple mechanisms, yet its most prominent (and best understood) mode of action involves the generation of DNA lesions followed by the activation of the DNA damage response and the induction of mitochondrial apoptosis. Despite a consistent rate of initial responses, cisplatin treatment often results in the development of chemoresistance, leading to therapeutic failure. An intense research has been conducted during the past 30 years and several mechanisms that account for the cisplatin-resistant phenotype of tumor cells have been described. Here, we provide a systematic discussion of these mechanism by classifying them in alterations (1) that involve steps preceding the binding of cisplatin to DNA (pre-target resistance), (2) that directly relate to DNA-cisplatin adducts (on-target resistance), (3) concerning the lethal signaling pathway(s) elicited by cisplatin-mediated DNA damage (post-target resistance) and (4) affecting molecular circuitries that do not present obvious links with cisplatin-elicited signals (off-target resistance). As in some clinical settings cisplatin constitutes the major therapeutic option, the development of chemosensitization strategies constitute a goal with important clinical implications.
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              Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies

              Giuseppa Pistritto, Daniela Trisciuoglio, Claudia Ceci … (2016)
              Apoptosis is a form of programmed cell death that results in the orderly and efficient removal of damaged cells, such as those resulting from DNA damage or during development. Apoptosis can be triggered by signals from within the cell, such as genotoxic stress, or by extrinsic signals, such as the binding of ligands to cell surface death receptors. Deregulation in apoptotic cell death machinery is an hallmark of cancer. Apoptosis alteration is responsible not only for tumor development and progression but also for tumor resistance to therapies. Most anticancer drugs currently used in clinical oncology exploit the intact apoptotic signaling pathways to trigger cancer cell death. Thus, defects in the death pathways may result in drug resistance so limiting the efficacy of therapies. Therefore, a better understanding of the apoptotic cell death signaling pathways may improve the efficacy of cancer therapy and bypass resistance. This review will highlight the role of the fundamental regulators of apoptosis and how their deregulation, including activation of anti-apoptotic factors (i.e., Bcl-2, Bcl-xL, etc) or inactivation of pro-apoptotic factors (i.e., p53 pathway) ends up in cancer cell resistance to therapies. In addition, therapeutic strategies aimed at modulating apoptotic activity are briefly discussed.
              Article 0 comments Cited 489 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                FENG ZHU
                SHIWEI DUAN
                Journal
                Journal ID (nlm-ta): Oncol Res
                Journal ID (iso-abbrev): Oncol Res
                Journal ID (publisher-id): OR
                Title: Oncology Research
                Publisher: Tech Science Press (USA )
                ISSN (Print): 0965-0407
                ISSN (Electronic): 1555-3906
                Publication date (Electronic, collection): 2023
                Publication date (Electronic, pub): 1 March 2023
                Volume: 31
                Issue: 1
                Pages: 1-12
                Affiliations
                [1 ]Department of Clinical Medicine, School of Medicine, Zhejiang University City College , Hangzhou, 310000, China
                [2 ]Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University , Hangzhou, 310016, China
                Author notes
                [* ]Address correspondence to: Feng Zhu, zhuf@ 123456zucc.edu.cn ; Shiwei Duan, duansw@ 123456zucc.edu.cn

                #These authors contributed equally to this work

                Article
                Publisher ID: 27359
                DOI: 10.32604/or.2022.027359
                PMC ID: 10207999
                PubMed ID: 37303740
                SO-VID: 2c289a08-7ac0-4e04-8c0e-29328a0fdaff
                Copyright © © 2023 Mao et al.
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 22 October 2022
                Date accepted : 31 January 2023
                Funding
                Funded by: Qiantang Scholarship in Zhejiang University City College
                Award ID: 2020ZDSJ0637
                Categories
                Subject: Review

                Keywords: mir-1294,expression,cancer,cerna,signaling pathway,prognosis
                Data availability:
                Keywords: mir-1294, expression, cancer, cerna, signaling pathway, prognosis

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