Article ; Online: Cellular Dormancy in Cancer: Mechanisms and Potential Targeting Strategies.
2023 Volume 55, Issue 3, Page(s) 720–736
Abstract: Cancer is a leading cause of disease-related mortality worldwide. Drug resistance is one of the primary reasons for the failure of anticancer therapy. There are a number of underlying mechanisms for anticancer drug resistance including genetic/epigenetic ...
Abstract | Cancer is a leading cause of disease-related mortality worldwide. Drug resistance is one of the primary reasons for the failure of anticancer therapy. There are a number of underlying mechanisms for anticancer drug resistance including genetic/epigenetic modifications, microenvironmental factors, and tumor heterogeneity. In the present scenario, researchers have focused on these novel mechanisms and strategies to tackle them. Recently, researchers have recognized the ability of cancer to become dormant because of anticancer drug resistance, tumor relapse, and progression. Currently, cancer dormancy is classified into "tumor mass dormancy" and "cellular dormancy." Tumor mass dormancy represents the equilibrium between cell proliferation and cell death under the control of blood supply and immune responses. Cellular dormancy denotes the state in which cells undergo quiescence and is characterized by autophagy, stress-tolerance signaling, microenvironmental cues, and epigenetic modifications. Cancer dormancy has been regarded as the stem of primary or distal recurrent tumor formation and poor clinical outcomes in cancer patients. Despite the insufficiency of reliable models of cellular dormancy, the mechanisms underlying the regulation of cellular dormancy have been clarified in numerous studies. A better understanding of the biology of cancer dormancy is critical for the development of effective anticancer therapeutic strategies. In this review, we summarize the characteristics and regulatory mechanisms of cellular dormancy, introduce several potential strategies for targeting cellular dormancy, and discuss future perspectives. |
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MeSH term(s) | Humans ; Neoplasm Recurrence, Local/pathology ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Cell Death ; Signal Transduction ; Autophagy ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use |
Chemical Substances | Antineoplastic Agents |
Language | English |
Publishing date | 2023-03-22 |
Publishing country | Korea (South) |
Document type | Review ; Journal Article |
ZDB-ID | 2133613-1 |
ISSN | 2005-9256 ; 1598-2998 |
ISSN (online) | 2005-9256 |
ISSN | 1598-2998 |
DOI | 10.4143/crt.2023.468 |
Database | MEDical Literature Analysis and Retrieval System OnLINE |
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