Autophagy modulation in bladder cancer development and treatment (Review)
Bladder cancer (BC) is a potentially life‑threatening malignancy. Due to a high recurrence rate, frequent surveillance strategies and intravesical drug therapies, BC is considered one of the most expensive tumors to treat. As a fundamental evolutionary catabolic process, autophagy plays an important...
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| Veröffentlicht in: | Oncology reports 2019-11, Vol.42 (5), p.1647-1655 |
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| creator | Li, Faping Guo, Hui Yang, Yuxuan Feng, Mingliang Liu, Bin Ren, Xiang Zhou, Honglan |
| description | Bladder cancer (BC) is a potentially life‑threatening malignancy. Due to a high recurrence rate, frequent surveillance strategies and intravesical drug therapies, BC is considered one of the most expensive tumors to treat. As a fundamental evolutionary catabolic process, autophagy plays an important role in the maintenance of cellular environmental homeostasis by degrading and recycling damaged cytoplasmic components, including macromolecules and organelles. Scientific studies in the last two decades have shown that autophagy acts as a double‑edged sword with regard to the treatment of cancer. On one hand, autophagy inhibition is able to increase the sensitivity of cancer cells to treatment, a process known as protective autophagy. On the other hand, autophagy overactivation may lead to cell death, referred to as autophagic cell death, similar to apoptosis. Therefore, it is essential to identify the role of autophagy in cancer cells in order to develop novel therapeutic agents. In addition, autophagy may potentially become a novel therapeutic target in human diseases. In this review, the current knowledge on autophagy modulation in BC development and treatment is summarized. |
| doi_str_mv | 10.3892/or.2019.7286 |
| format | Article |
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Due to a high recurrence rate, frequent surveillance strategies and intravesical drug therapies, BC is considered one of the most expensive tumors to treat. As a fundamental evolutionary catabolic process, autophagy plays an important role in the maintenance of cellular environmental homeostasis by degrading and recycling damaged cytoplasmic components, including macromolecules and organelles. Scientific studies in the last two decades have shown that autophagy acts as a double‑edged sword with regard to the treatment of cancer. On one hand, autophagy inhibition is able to increase the sensitivity of cancer cells to treatment, a process known as protective autophagy. On the other hand, autophagy overactivation may lead to cell death, referred to as autophagic cell death, similar to apoptosis. Therefore, it is essential to identify the role of autophagy in cancer cells in order to develop novel therapeutic agents. In addition, autophagy may potentially become a novel therapeutic target in human diseases. In this review, the current knowledge on autophagy modulation in BC development and treatment is summarized.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2019.7286</identifier><identifier>PMID: 31436298</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Autophagy ; Bladder cancer ; Cancer cells ; Cancer therapies ; Cancer treatment ; Cell death ; Cell Survival ; Chemotherapy ; Clinical outcomes ; Development and progression ; Drug therapy ; Gene Expression Regulation, Neoplastic ; Homeostasis ; Humans ; Intelligence gathering ; Kinases ; Mammals ; Novels ; Protein synthesis ; Proteins ; Radiation therapy ; Review ; Signal Transduction ; Tumors ; Urinary Bladder Neoplasms - metabolism</subject><ispartof>Oncology reports, 2019-11, Vol.42 (5), p.1647-1655</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Li et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-71695275a9be6f770159ddf62295c98ae4b1368efa7e512523141847c894770e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31436298$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Faping</creatorcontrib><creatorcontrib>Guo, Hui</creatorcontrib><creatorcontrib>Yang, Yuxuan</creatorcontrib><creatorcontrib>Feng, Mingliang</creatorcontrib><creatorcontrib>Liu, Bin</creatorcontrib><creatorcontrib>Ren, Xiang</creatorcontrib><creatorcontrib>Zhou, Honglan</creatorcontrib><title>Autophagy modulation in bladder cancer development and treatment (Review)</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Bladder cancer (BC) is a potentially life‑threatening malignancy. Due to a high recurrence rate, frequent surveillance strategies and intravesical drug therapies, BC is considered one of the most expensive tumors to treat. As a fundamental evolutionary catabolic process, autophagy plays an important role in the maintenance of cellular environmental homeostasis by degrading and recycling damaged cytoplasmic components, including macromolecules and organelles. Scientific studies in the last two decades have shown that autophagy acts as a double‑edged sword with regard to the treatment of cancer. On one hand, autophagy inhibition is able to increase the sensitivity of cancer cells to treatment, a process known as protective autophagy. On the other hand, autophagy overactivation may lead to cell death, referred to as autophagic cell death, similar to apoptosis. Therefore, it is essential to identify the role of autophagy in cancer cells in order to develop novel therapeutic agents. In addition, autophagy may potentially become a novel therapeutic target in human diseases. In this review, the current knowledge on autophagy modulation in BC development and treatment is summarized.</description><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Bladder cancer</subject><subject>Cancer cells</subject><subject>Cancer therapies</subject><subject>Cancer treatment</subject><subject>Cell death</subject><subject>Cell Survival</subject><subject>Chemotherapy</subject><subject>Clinical outcomes</subject><subject>Development and progression</subject><subject>Drug therapy</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Intelligence gathering</subject><subject>Kinases</subject><subject>Mammals</subject><subject>Novels</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Radiation therapy</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Tumors</subject><subject>Urinary Bladder Neoplasms - metabolism</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkttrFDEUxgex2Fp981kGBGnBWXOZ3F6EpVgtFARR8C1kM2d2UzLJmsys9L8309baLSUPJ5ff-XJy8lXVG4wWVCryMaYFQVgtBJH8WXWEhcINaSl-XuaI4IZS9uuwepnzFUJEIK5eVIcUt5QTJY-qi-U0xu3GrK_rIXaTN6OLoXahXnnTdZBqa4ItoYMd-LgdIIy1CV09JjDjzerkO-wc_Dl9VR30xmd4fRePq5_nn3-cfW0uv325OFteNpZhNDYCc8WIYEatgPdCIMxU1_WcEMWskgbaFaZcQm8EMEwYKbVi2QorVVtooMfVp1vd7bQaoLOlhmS83iY3mHSto3F6_yS4jV7HneZCMIlRETi5E0jx9wR51IPLFrw3AeKUNaFICKowVQV99wi9ilMK5XkzxQSXUqH_1Np40C70sdxrZ1G95Kil5WOQLNTiCaqMDgZnY4Delf29hPcPEjZg_LjJ0U_zD-V98MMtaFPMOUF_3wyM9OwRHZOePaJnjxT87cMG3sP_TEH_AtyNtAs</recordid><startdate>20191101</startdate><enddate>20191101</enddate><creator>Li, Faping</creator><creator>Guo, Hui</creator><creator>Yang, Yuxuan</creator><creator>Feng, Mingliang</creator><creator>Liu, Bin</creator><creator>Ren, Xiang</creator><creator>Zhou, Honglan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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Due to a high recurrence rate, frequent surveillance strategies and intravesical drug therapies, BC is considered one of the most expensive tumors to treat. As a fundamental evolutionary catabolic process, autophagy plays an important role in the maintenance of cellular environmental homeostasis by degrading and recycling damaged cytoplasmic components, including macromolecules and organelles. Scientific studies in the last two decades have shown that autophagy acts as a double‑edged sword with regard to the treatment of cancer. On one hand, autophagy inhibition is able to increase the sensitivity of cancer cells to treatment, a process known as protective autophagy. On the other hand, autophagy overactivation may lead to cell death, referred to as autophagic cell death, similar to apoptosis. Therefore, it is essential to identify the role of autophagy in cancer cells in order to develop novel therapeutic agents. In addition, autophagy may potentially become a novel therapeutic target in human diseases. In this review, the current knowledge on autophagy modulation in BC development and treatment is summarized.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31436298</pmid><doi>10.3892/or.2019.7286</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Autophagy Bladder cancer Cancer cells Cancer therapies Cancer treatment Cell death Cell Survival Chemotherapy Clinical outcomes Development and progression Drug therapy Gene Expression Regulation, Neoplastic Homeostasis Humans Intelligence gathering Kinases Mammals Novels Protein synthesis Proteins Radiation therapy Review Signal Transduction Tumors Urinary Bladder Neoplasms - metabolism |
| title | Autophagy modulation in bladder cancer development and treatment (Review) |
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