Drug Resistance in Cancers: A Free Pass for Bullying
The cancer burden continues to grow globally, and drug resistance remains a substantial challenge in cancer therapy. It is well established that cancerous cells with clonal dysplasia generate the same carcinogenic lesions. Tumor cells pass on genetic templates to subsequent generations in evolutiona...
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-10-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/11/21/3383 |
| _version_ | 1797468776153743360 |
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| author | Jing Li Xiao Li Qie Guo |
| author_facet | Jing Li Xiao Li Qie Guo |
| author_sort | Jing Li |
| collection | DOAJ |
| description | The cancer burden continues to grow globally, and drug resistance remains a substantial challenge in cancer therapy. It is well established that cancerous cells with clonal dysplasia generate the same carcinogenic lesions. Tumor cells pass on genetic templates to subsequent generations in evolutionary terms and exhibit drug resistance simply by accumulating genetic alterations. However, recent evidence has implied that tumor cells accumulate genetic alterations by progressively adapting. As a result, intratumor heterogeneity (ITH) is generated due to genetically distinct subclonal populations of cells coexisting. The genetic adaptive mechanisms of action of ITH include activating “cellular plasticity”, through which tumor cells create a tumor-supportive microenvironment in which they can proliferate and cause increased damage. These highly plastic cells are located in the tumor microenvironment (TME) and undergo extreme changes to resist therapeutic drugs. Accordingly, the underlying mechanisms involved in drug resistance have been re-evaluated. Herein, we will reveal new themes emerging from initial studies of drug resistance and outline the findings regarding drug resistance from the perspective of the TME; the themes include exosomes, metabolic reprogramming, protein glycosylation and autophagy, and the relates studies aim to provide new targets and strategies for reversing drug resistance in cancers. |
| first_indexed | 2024-03-09T19:11:16Z |
| format | Article |
| id | doaj.art-54648d7646b344c58c0b7bf5d8cb3795 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-09T19:11:16Z |
| publishDate | 2022-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-54648d7646b344c58c0b7bf5d8cb37952023-11-24T04:07:46ZengMDPI AGCells2073-44092022-10-011121338310.3390/cells11213383Drug Resistance in Cancers: A Free Pass for BullyingJing Li0Xiao Li1Qie Guo2The Department of Clinical Pharmacy, The Affiliated Hospital of Qingdao University, Qingdao 266003, ChinaThe Department of Clinical Pharmacy, The Affiliated Hospital of Qingdao University, Qingdao 266003, ChinaThe Department of Clinical Pharmacy, The Affiliated Hospital of Qingdao University, Qingdao 266003, ChinaThe cancer burden continues to grow globally, and drug resistance remains a substantial challenge in cancer therapy. It is well established that cancerous cells with clonal dysplasia generate the same carcinogenic lesions. Tumor cells pass on genetic templates to subsequent generations in evolutionary terms and exhibit drug resistance simply by accumulating genetic alterations. However, recent evidence has implied that tumor cells accumulate genetic alterations by progressively adapting. As a result, intratumor heterogeneity (ITH) is generated due to genetically distinct subclonal populations of cells coexisting. The genetic adaptive mechanisms of action of ITH include activating “cellular plasticity”, through which tumor cells create a tumor-supportive microenvironment in which they can proliferate and cause increased damage. These highly plastic cells are located in the tumor microenvironment (TME) and undergo extreme changes to resist therapeutic drugs. Accordingly, the underlying mechanisms involved in drug resistance have been re-evaluated. Herein, we will reveal new themes emerging from initial studies of drug resistance and outline the findings regarding drug resistance from the perspective of the TME; the themes include exosomes, metabolic reprogramming, protein glycosylation and autophagy, and the relates studies aim to provide new targets and strategies for reversing drug resistance in cancers.https://www.mdpi.com/2073-4409/11/21/3383drug resistancetumor microenvironmentexosomesmetabolic reprogrammingglycosylationautophagy |
| spellingShingle | Jing Li Xiao Li Qie Guo Drug Resistance in Cancers: A Free Pass for Bullying Cells drug resistance tumor microenvironment exosomes metabolic reprogramming glycosylation autophagy |
| title | Drug Resistance in Cancers: A Free Pass for Bullying |
| title_full | Drug Resistance in Cancers: A Free Pass for Bullying |
| title_fullStr | Drug Resistance in Cancers: A Free Pass for Bullying |
| title_full_unstemmed | Drug Resistance in Cancers: A Free Pass for Bullying |
| title_short | Drug Resistance in Cancers: A Free Pass for Bullying |
| title_sort | drug resistance in cancers a free pass for bullying |
| topic | drug resistance tumor microenvironment exosomes metabolic reprogramming glycosylation autophagy |
| url | https://www.mdpi.com/2073-4409/11/21/3383 |
| work_keys_str_mv | AT jingli drugresistanceincancersafreepassforbullying AT xiaoli drugresistanceincancersafreepassforbullying AT qieguo drugresistanceincancersafreepassforbullying |