Loading…

Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance

Autophagy is the process of recycling and utilization of degraded organelles and macromolecules in the cell compartments formed during the fusion of autophagosomes with lysosomes. During autophagy induction the healthy and tumor cells adapt themselves to harsh conditions such as cellular stress or i...

Full description

Saved in:
Bibliographic Details
Published in:Molecular and cellular biochemistry 2022-02, Vol.477 (2), p.593-604
Main Authors: Belyaeva, Elizaveta, Kharwar, Rajesh Kumar, Ulasov, Ilya V., Karlina, Irina, Timashev, Petr, Mohammadinejad, Reza, Acharya, Arbind
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c442t-70cd52d0f24e8a7e4e56deeab1a4120a809bc4618269a2cf654cae257ef0fbc93
cites cdi_FETCH-LOGICAL-c442t-70cd52d0f24e8a7e4e56deeab1a4120a809bc4618269a2cf654cae257ef0fbc93
container_end_page 604
container_issue 2
container_start_page 593
container_title Molecular and cellular biochemistry
container_volume 477
creator Belyaeva, Elizaveta
Kharwar, Rajesh Kumar
Ulasov, Ilya V.
Karlina, Irina
Timashev, Petr
Mohammadinejad, Reza
Acharya, Arbind
description Autophagy is the process of recycling and utilization of degraded organelles and macromolecules in the cell compartments formed during the fusion of autophagosomes with lysosomes. During autophagy induction the healthy and tumor cells adapt themselves to harsh conditions such as cellular stress or insufficient supply of nutrients in the cell environment to maintain their homeostasis. Autophagy is currently seen as a form of programmed cell death along with apoptosis and necroptosis. In recent years multiple studies have considered the autophagy as a potential mechanism of anticancer therapy in malignant glioma. Although, subsequent steps in autophagy development are known and well-described, on molecular level the mechanism of autophagosome initiation and maturation using autophagy-related proteins is under investigation. This article reviews current state about the mechanism of autophagy, its molecular pathways and the most recent studies on roles of autophagy-related proteins and their isoforms in glioma progression and its treatment.
doi_str_mv 10.1007/s11010-021-04308-w
format article
fullrecord <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2605596640</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A691070886</galeid><sourcerecordid>A691070886</sourcerecordid><originalsourceid>FETCH-LOGICAL-c442t-70cd52d0f24e8a7e4e56deeab1a4120a809bc4618269a2cf654cae257ef0fbc93</originalsourceid><addsrcrecordid>eNp9kUFv1DAQhS0EokvhD3BAkbj04jJ2HCfhVlUUKlXiAgdO1qwzTl0l9mInqvbf42VLEQghHyzNfO_p2Y-x1wLOBUD7LgsBAjhIwUHV0PH7J2wjmrbmqhf9U7aBGoB3om1P2Iuc76DQIMRzdlKrrlEg5YZ9u87RxTTnKroK1yXubnHc80QTLjRUuxQX8iG_r1KcqPKhGicfZzwsxkQ5-xgqDEO13FLC3b4qM58XDJZesmcOp0yvHu5T9vXqw5fLT_zm88fry4sbbpWSC2_BDo0cwElFHbakqNEDEW4FKiEBO-i3VmnRSd2jtE43yiLJpiUHbmv7-pSdHX1LpO8r5cXMPluaJgwU12ykhqbptVZQ0Ld_oXdxTaGkK5Sstexl-chHasSJjA8uLgntwdRc6F5AC12nC3X-D6qcgWZvYyDny_wPgTwKbIo5J3Jml_yMaW8EmEOf5tinKX2an32a-yJ685B43c40PEp-FViA-gjksgojpd9P-o_tDxFGqrE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2623629204</pqid></control><display><type>article</type><title>Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance</title><source>Springer Nature</source><creator>Belyaeva, Elizaveta ; Kharwar, Rajesh Kumar ; Ulasov, Ilya V. ; Karlina, Irina ; Timashev, Petr ; Mohammadinejad, Reza ; Acharya, Arbind</creator><creatorcontrib>Belyaeva, Elizaveta ; Kharwar, Rajesh Kumar ; Ulasov, Ilya V. ; Karlina, Irina ; Timashev, Petr ; Mohammadinejad, Reza ; Acharya, Arbind</creatorcontrib><description>Autophagy is the process of recycling and utilization of degraded organelles and macromolecules in the cell compartments formed during the fusion of autophagosomes with lysosomes. During autophagy induction the healthy and tumor cells adapt themselves to harsh conditions such as cellular stress or insufficient supply of nutrients in the cell environment to maintain their homeostasis. Autophagy is currently seen as a form of programmed cell death along with apoptosis and necroptosis. In recent years multiple studies have considered the autophagy as a potential mechanism of anticancer therapy in malignant glioma. Although, subsequent steps in autophagy development are known and well-described, on molecular level the mechanism of autophagosome initiation and maturation using autophagy-related proteins is under investigation. This article reviews current state about the mechanism of autophagy, its molecular pathways and the most recent studies on roles of autophagy-related proteins and their isoforms in glioma progression and its treatment.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-021-04308-w</identifier><identifier>PMID: 34854022</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antimitotic agents ; Antineoplastic agents ; Apoptosis ; Autophagosomes - genetics ; Autophagosomes - metabolism ; Autophagy ; Autophagy-Related Proteins - genetics ; Autophagy-Related Proteins - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Brain tumors ; Cardiology ; Cell death ; Cellular stress response ; Development and progression ; Glioma ; Glioma - genetics ; Glioma - metabolism ; Glioma - therapy ; Gliomas ; Homeostasis ; Humans ; Isoforms ; Life Sciences ; Lysosomes ; Macromolecules ; Medical Biochemistry ; Necroptosis ; Neoplasm Proteins - metabolism ; Nutrients ; Oncology ; Organelles ; Phagosomes ; Proteins ; Tumor cells</subject><ispartof>Molecular and cellular biochemistry, 2022-02, Vol.477 (2), p.593-604</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>COPYRIGHT 2022 Springer</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-70cd52d0f24e8a7e4e56deeab1a4120a809bc4618269a2cf654cae257ef0fbc93</citedby><cites>FETCH-LOGICAL-c442t-70cd52d0f24e8a7e4e56deeab1a4120a809bc4618269a2cf654cae257ef0fbc93</cites><orcidid>0000-0002-7621-9477</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34854022$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Belyaeva, Elizaveta</creatorcontrib><creatorcontrib>Kharwar, Rajesh Kumar</creatorcontrib><creatorcontrib>Ulasov, Ilya V.</creatorcontrib><creatorcontrib>Karlina, Irina</creatorcontrib><creatorcontrib>Timashev, Petr</creatorcontrib><creatorcontrib>Mohammadinejad, Reza</creatorcontrib><creatorcontrib>Acharya, Arbind</creatorcontrib><title>Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>Autophagy is the process of recycling and utilization of degraded organelles and macromolecules in the cell compartments formed during the fusion of autophagosomes with lysosomes. During autophagy induction the healthy and tumor cells adapt themselves to harsh conditions such as cellular stress or insufficient supply of nutrients in the cell environment to maintain their homeostasis. Autophagy is currently seen as a form of programmed cell death along with apoptosis and necroptosis. In recent years multiple studies have considered the autophagy as a potential mechanism of anticancer therapy in malignant glioma. Although, subsequent steps in autophagy development are known and well-described, on molecular level the mechanism of autophagosome initiation and maturation using autophagy-related proteins is under investigation. This article reviews current state about the mechanism of autophagy, its molecular pathways and the most recent studies on roles of autophagy-related proteins and their isoforms in glioma progression and its treatment.</description><subject>Antimitotic agents</subject><subject>Antineoplastic agents</subject><subject>Apoptosis</subject><subject>Autophagosomes - genetics</subject><subject>Autophagosomes - metabolism</subject><subject>Autophagy</subject><subject>Autophagy-Related Proteins - genetics</subject><subject>Autophagy-Related Proteins - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Brain tumors</subject><subject>Cardiology</subject><subject>Cell death</subject><subject>Cellular stress response</subject><subject>Development and progression</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - metabolism</subject><subject>Glioma - therapy</subject><subject>Gliomas</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Isoforms</subject><subject>Life Sciences</subject><subject>Lysosomes</subject><subject>Macromolecules</subject><subject>Medical Biochemistry</subject><subject>Necroptosis</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Nutrients</subject><subject>Oncology</subject><subject>Organelles</subject><subject>Phagosomes</subject><subject>Proteins</subject><subject>Tumor cells</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp9kUFv1DAQhS0EokvhD3BAkbj04jJ2HCfhVlUUKlXiAgdO1qwzTl0l9mInqvbf42VLEQghHyzNfO_p2Y-x1wLOBUD7LgsBAjhIwUHV0PH7J2wjmrbmqhf9U7aBGoB3om1P2Iuc76DQIMRzdlKrrlEg5YZ9u87RxTTnKroK1yXubnHc80QTLjRUuxQX8iG_r1KcqPKhGicfZzwsxkQ5-xgqDEO13FLC3b4qM58XDJZesmcOp0yvHu5T9vXqw5fLT_zm88fry4sbbpWSC2_BDo0cwElFHbakqNEDEW4FKiEBO-i3VmnRSd2jtE43yiLJpiUHbmv7-pSdHX1LpO8r5cXMPluaJgwU12ykhqbptVZQ0Ld_oXdxTaGkK5Sstexl-chHasSJjA8uLgntwdRc6F5AC12nC3X-D6qcgWZvYyDny_wPgTwKbIo5J3Jml_yMaW8EmEOf5tinKX2an32a-yJ685B43c40PEp-FViA-gjksgojpd9P-o_tDxFGqrE</recordid><startdate>20220201</startdate><enddate>20220201</enddate><creator>Belyaeva, Elizaveta</creator><creator>Kharwar, Rajesh Kumar</creator><creator>Ulasov, Ilya V.</creator><creator>Karlina, Irina</creator><creator>Timashev, Petr</creator><creator>Mohammadinejad, Reza</creator><creator>Acharya, Arbind</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7621-9477</orcidid></search><sort><creationdate>20220201</creationdate><title>Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance</title><author>Belyaeva, Elizaveta ; Kharwar, Rajesh Kumar ; Ulasov, Ilya V. ; Karlina, Irina ; Timashev, Petr ; Mohammadinejad, Reza ; Acharya, Arbind</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c442t-70cd52d0f24e8a7e4e56deeab1a4120a809bc4618269a2cf654cae257ef0fbc93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Antimitotic agents</topic><topic>Antineoplastic agents</topic><topic>Apoptosis</topic><topic>Autophagosomes - genetics</topic><topic>Autophagosomes - metabolism</topic><topic>Autophagy</topic><topic>Autophagy-Related Proteins - genetics</topic><topic>Autophagy-Related Proteins - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Brain tumors</topic><topic>Cardiology</topic><topic>Cell death</topic><topic>Cellular stress response</topic><topic>Development and progression</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma - metabolism</topic><topic>Glioma - therapy</topic><topic>Gliomas</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Isoforms</topic><topic>Life Sciences</topic><topic>Lysosomes</topic><topic>Macromolecules</topic><topic>Medical Biochemistry</topic><topic>Necroptosis</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Nutrients</topic><topic>Oncology</topic><topic>Organelles</topic><topic>Phagosomes</topic><topic>Proteins</topic><topic>Tumor cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Belyaeva, Elizaveta</creatorcontrib><creatorcontrib>Kharwar, Rajesh Kumar</creatorcontrib><creatorcontrib>Ulasov, Ilya V.</creatorcontrib><creatorcontrib>Karlina, Irina</creatorcontrib><creatorcontrib>Timashev, Petr</creatorcontrib><creatorcontrib>Mohammadinejad, Reza</creatorcontrib><creatorcontrib>Acharya, Arbind</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest_Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Science Journals</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Belyaeva, Elizaveta</au><au>Kharwar, Rajesh Kumar</au><au>Ulasov, Ilya V.</au><au>Karlina, Irina</au><au>Timashev, Petr</au><au>Mohammadinejad, Reza</au><au>Acharya, Arbind</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2022-02-01</date><risdate>2022</risdate><volume>477</volume><issue>2</issue><spage>593</spage><epage>604</epage><pages>593-604</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>Autophagy is the process of recycling and utilization of degraded organelles and macromolecules in the cell compartments formed during the fusion of autophagosomes with lysosomes. During autophagy induction the healthy and tumor cells adapt themselves to harsh conditions such as cellular stress or insufficient supply of nutrients in the cell environment to maintain their homeostasis. Autophagy is currently seen as a form of programmed cell death along with apoptosis and necroptosis. In recent years multiple studies have considered the autophagy as a potential mechanism of anticancer therapy in malignant glioma. Although, subsequent steps in autophagy development are known and well-described, on molecular level the mechanism of autophagosome initiation and maturation using autophagy-related proteins is under investigation. This article reviews current state about the mechanism of autophagy, its molecular pathways and the most recent studies on roles of autophagy-related proteins and their isoforms in glioma progression and its treatment.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34854022</pmid><doi>10.1007/s11010-021-04308-w</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-7621-9477</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0300-8177
ispartof Molecular and cellular biochemistry, 2022-02, Vol.477 (2), p.593-604
issn 0300-8177
1573-4919
language eng
recordid cdi_proquest_miscellaneous_2605596640
source Springer Nature
subjects Antimitotic agents
Antineoplastic agents
Apoptosis
Autophagosomes - genetics
Autophagosomes - metabolism
Autophagy
Autophagy-Related Proteins - genetics
Autophagy-Related Proteins - metabolism
Biochemistry
Biomedical and Life Sciences
Brain tumors
Cardiology
Cell death
Cellular stress response
Development and progression
Glioma
Glioma - genetics
Glioma - metabolism
Glioma - therapy
Gliomas
Homeostasis
Humans
Isoforms
Life Sciences
Lysosomes
Macromolecules
Medical Biochemistry
Necroptosis
Neoplasm Proteins - metabolism
Nutrients
Oncology
Organelles
Phagosomes
Proteins
Tumor cells
title Isoforms of autophagy-related proteins: role in glioma progression and therapy resistance
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T14%3A20%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Isoforms%20of%20autophagy-related%20proteins:%20role%20in%20glioma%20progression%20and%20therapy%20resistance&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Belyaeva,%20Elizaveta&rft.date=2022-02-01&rft.volume=477&rft.issue=2&rft.spage=593&rft.epage=604&rft.pages=593-604&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1007/s11010-021-04308-w&rft_dat=%3Cgale_proqu%3EA691070886%3C/gale_proqu%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c442t-70cd52d0f24e8a7e4e56deeab1a4120a809bc4618269a2cf654cae257ef0fbc93%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2623629204&rft_id=info:pmid/34854022&rft_galeid=A691070886&rfr_iscdi=true