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      Peptidomimetics in cancer targeting

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          Abstract

          The low efficiency of treatment strategies is one of the main obstacles to developing cancer inhibitors. Up to now, various classes of therapeutics have been developed to inhibit cancer progression. Peptides due to their small size and easy production compared to proteins are highly regarded in designing cancer vaccines and oncogenic pathway inhibitors. Although peptides seem to be a suitable therapeutic option, their short lifespan, instability, and low binding affinity for their target have not been widely applicable against malignant tumors. Given the peptides’ disadvantages, a new class of agents called peptidomimetic has been introduced. With advances in physical chemistry and biochemistry, as well as increased knowledge about biomolecule structures, it is now possible to chemically modify peptides to develop efficient peptidomimetics. In recent years, numerous studies have been performed to the evaluation of the effectiveness of peptidomimetics in inhibiting metastasis, angiogenesis, and cancerous cell growth. Here, we offer a comprehensive review of designed peptidomimetics to diagnose and treat cancer.

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          Most cited references137

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          Hallmarks of Cancer: The Next Generation

          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            The Hallmarks of Cancer

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              Apoptosis: a review of programmed cell death.

              The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its immense therapeutic potential. Therefore, research continues to focus on the elucidation and analysis of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis. To that end, the field of apoptosis research has been moving forward at an alarmingly rapid rate. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptosis in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptosis.
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                Author and article information

                Contributors
                dokh@psu.edu
                Journal
                Mol Med
                Mol Med
                Molecular Medicine
                BioMed Central (London )
                1076-1551
                1528-3658
                7 December 2022
                7 December 2022
                2022
                : 28
                : 146
                Affiliations
                [1 ]GRID grid.411746.1, ISNI 0000 0004 4911 7066, Department of Medical Biotechnology, Faculty of Allied Medicine, , Iran University of Medical Sciences, ; Tehran, Iran
                [2 ]GRID grid.411746.1, ISNI 0000 0004 4911 7066, Department of Anatomy, School of Medicine, , Iran University of Medical Sciences, ; Tehran, Iran
                [3 ]GRID grid.411425.7, ISNI 0000 0004 0417 7516, Department of Chemical Engineering, Faculty of Engineering, , Arak University, ; Arak, Iran
                [4 ]GRID grid.411705.6, ISNI 0000 0001 0166 0922, Department of Virology, School of Public Health, , Tehran University of Medical Sciences, ; Tehran, Iran
                [5 ]GRID grid.412831.d, ISNI 0000 0001 1172 3536, Department of Biology, Faculty of Natural Sciences, , University of Tabriz, ; Tabriz, Iran
                [6 ]GRID grid.411705.6, ISNI 0000 0001 0166 0922, Medical Biotechnology Department, School of Advanced Technologies in Medicine, , Tehran University of Medical Sciences, ; Tehran, Iran
                [7 ]GRID grid.240473.6, ISNI 0000 0004 0543 9901, Department of Pharmacology, , Penn State College of Medicine, ; Hershey, PA USA
                [8 ]GRID grid.240473.6, ISNI 0000 0004 0543 9901, Department of Biochemistry & Molecular Biology, , Penn State College of Medicine, ; Hershey, PA USA
                Author information
                http://orcid.org/0000-0002-8225-4025
                Article
                577
                10.1186/s10020-022-00577-3
                9730693
                36476230
                14278e6a-e831-4e19-a122-1c467c592df3
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 4 August 2022
                : 16 November 2022
                Categories
                Review
                Custom metadata
                © The Author(s) 2022

                peptidomimetic,angiogenesis,nanoparticles,drug resistance,metastasis,apoptosis

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