PAQR3 suppresses the growth of non-small cell lung cancer cells via modulation of EGFR-mediated autophagy
Macroautophagy/autophagy is an evolutionarily conserved intracellular process that recycles and degrades intracellular components to sustain homeostasis in response to deficiency of nutrients or growth factors. PAQR3 is a newly discovered tumor suppressor that also regulates autophagy induced by nut...
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Veröffentlicht in: | Autophagy 2020-07, Vol.16 (7), p.1236-1247 |
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description | Macroautophagy/autophagy is an evolutionarily conserved intracellular process that recycles and degrades intracellular components to sustain homeostasis in response to deficiency of nutrients or growth factors. PAQR3 is a newly discovered tumor suppressor that also regulates autophagy induced by nutrient starvation via AMPK and MTORC1 signaling pathways. In this study, we investigated whether PAQR3 modulates EGFR-mediated autophagy and whether such regulation is associated with the tumor suppressive activity of PAQR3. PAQR3 is able to inhibit the in vitro and in vivo growth of non-small cell lung cancer (NSCLC) cells. PAQR3 potentiates autophagy induced by EGFR inhibitor erlotinib. Knockdown of PAQR3 abrogates erlotinib-mediated reduction of BECN1 interaction with autophagy inhibitory proteins RUBCN/Rubicon and BCL2. PAQR3 blocks the interaction of BECN1 with the activated form of EGFR and inhibits tyrosine phosphorylation of BECN1. Furthermore, inhibition of autophagy by knocking down ATG7 abrogates the tumor suppressive activity of PAQR3 in NSCLC cells. Collectively, these data indicate that PAQR3 suppresses tumor progression of NSCLC cells through modulating EGFR-regulated autophagy.
AKT: thymoma viral proto-oncogene; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG14: autophagy related 14; BCL2: B cell leukemia/lymphoma 2; BECN1: beclin 1; CCK-8: cell counting kit-8; CQ: chloroquine diphosphate; DMEM: Dulbecco's modified Eagle's medium; EdU: 5-ethynyl-2ʹ-deoxyuridine; EGFR: epidermal growth factor receptor; FBS: fetal bovine serum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IgG: Immunoglobulin G; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; MTORC1: mechanistic target of rapamycin kinase complex 1; MTT: thiazolyl blue tetrazolium bromide; NSCLC: Non-small cell lung cancer; MAP2K/MEK: mitogen-activated protein kinase kinase; MAPK/ERK: mitogen-activated protein kinase; PAQR3: progestin and adipoQ receptor family member 3; PI3K: phosphatidylinositol-4,5-bisphosphate 3-kinase; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4/VPS15: phosphoinositide-3-kinase regulatory subunit 4; PRKAA/AMPK: protein kinase, AMP-activated alpha catalytic; RUBCN: rubicon autophagy regulator; RPS6: ribosomal protein S6; RAS: Ras proto-oncogene; RAF: Raf proto-oncogene; TKI: tyrosine kinase inhibitor; TUBA4A: tubulin alpha 4a; UVRAG: UV radiation resistance associated. |
doi_str_mv | 10.1080/15548627.2019.1659654 |
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AKT: thymoma viral proto-oncogene; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG14: autophagy related 14; BCL2: B cell leukemia/lymphoma 2; BECN1: beclin 1; CCK-8: cell counting kit-8; CQ: chloroquine diphosphate; DMEM: Dulbecco's modified Eagle's medium; EdU: 5-ethynyl-2ʹ-deoxyuridine; EGFR: epidermal growth factor receptor; FBS: fetal bovine serum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IgG: Immunoglobulin G; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; MTORC1: mechanistic target of rapamycin kinase complex 1; MTT: thiazolyl blue tetrazolium bromide; NSCLC: Non-small cell lung cancer; MAP2K/MEK: mitogen-activated protein kinase kinase; MAPK/ERK: mitogen-activated protein kinase; PAQR3: progestin and adipoQ receptor family member 3; PI3K: phosphatidylinositol-4,5-bisphosphate 3-kinase; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4/VPS15: phosphoinositide-3-kinase regulatory subunit 4; PRKAA/AMPK: protein kinase, AMP-activated alpha catalytic; RUBCN: rubicon autophagy regulator; RPS6: ribosomal protein S6; RAS: Ras proto-oncogene; RAF: Raf proto-oncogene; TKI: tyrosine kinase inhibitor; TUBA4A: tubulin alpha 4a; UVRAG: UV radiation resistance associated.</description><identifier>ISSN: 1554-8627</identifier><identifier>EISSN: 1554-8635</identifier><identifier>DOI: 10.1080/15548627.2019.1659654</identifier><identifier>PMID: 31448672</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Animals ; ATG7 ; autophagy ; Autophagy - drug effects ; Beclin-1 - metabolism ; BECN1 ; Carcinoma, Non-Small-Cell Lung - drug therapy ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Line, Tumor ; Cell Proliferation - drug effects ; EGFR ; ErbB Receptors - metabolism ; Erlotinib Hydrochloride - pharmacology ; Erlotinib Hydrochloride - therapeutic use ; HEK293 Cells ; Humans ; Intracellular Signaling Peptides and Proteins - metabolism ; lung cancer ; Lung Neoplasms - drug therapy ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Membrane Proteins - metabolism ; Mice, Nude ; Phosphorylation - drug effects ; Proto-Oncogene Mas ; Research Paper ; tumor suppressor</subject><ispartof>Autophagy, 2020-07, Vol.16 (7), p.1236-1247</ispartof><rights>2019 Informa UK Limited, trading as Taylor & Francis Group 2019</rights><rights>2019 Informa UK Limited, trading as Taylor & Francis Group 2019 Informa UK Limited, trading as Taylor & Francis Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-2511e8e563094a2fb9a692994aa5fded60a3f843ad8ef17d2c92764549ec204b3</citedby><cites>FETCH-LOGICAL-c468t-2511e8e563094a2fb9a692994aa5fded60a3f843ad8ef17d2c92764549ec204b3</cites><orcidid>0000-0002-6630-0693</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469495/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7469495/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31448672$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cao, Qianqian</creatorcontrib><creatorcontrib>You, Xue</creatorcontrib><creatorcontrib>Xu, Lijiao</creatorcontrib><creatorcontrib>Wang, Lin</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><title>PAQR3 suppresses the growth of non-small cell lung cancer cells via modulation of EGFR-mediated autophagy</title><title>Autophagy</title><addtitle>Autophagy</addtitle><description>Macroautophagy/autophagy is an evolutionarily conserved intracellular process that recycles and degrades intracellular components to sustain homeostasis in response to deficiency of nutrients or growth factors. PAQR3 is a newly discovered tumor suppressor that also regulates autophagy induced by nutrient starvation via AMPK and MTORC1 signaling pathways. In this study, we investigated whether PAQR3 modulates EGFR-mediated autophagy and whether such regulation is associated with the tumor suppressive activity of PAQR3. PAQR3 is able to inhibit the in vitro and in vivo growth of non-small cell lung cancer (NSCLC) cells. PAQR3 potentiates autophagy induced by EGFR inhibitor erlotinib. Knockdown of PAQR3 abrogates erlotinib-mediated reduction of BECN1 interaction with autophagy inhibitory proteins RUBCN/Rubicon and BCL2. PAQR3 blocks the interaction of BECN1 with the activated form of EGFR and inhibits tyrosine phosphorylation of BECN1. Furthermore, inhibition of autophagy by knocking down ATG7 abrogates the tumor suppressive activity of PAQR3 in NSCLC cells. Collectively, these data indicate that PAQR3 suppresses tumor progression of NSCLC cells through modulating EGFR-regulated autophagy.
AKT: thymoma viral proto-oncogene; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG14: autophagy related 14; BCL2: B cell leukemia/lymphoma 2; BECN1: beclin 1; CCK-8: cell counting kit-8; CQ: chloroquine diphosphate; DMEM: Dulbecco's modified Eagle's medium; EdU: 5-ethynyl-2ʹ-deoxyuridine; EGFR: epidermal growth factor receptor; FBS: fetal bovine serum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IgG: Immunoglobulin G; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; MTORC1: mechanistic target of rapamycin kinase complex 1; MTT: thiazolyl blue tetrazolium bromide; NSCLC: Non-small cell lung cancer; MAP2K/MEK: mitogen-activated protein kinase kinase; MAPK/ERK: mitogen-activated protein kinase; PAQR3: progestin and adipoQ receptor family member 3; PI3K: phosphatidylinositol-4,5-bisphosphate 3-kinase; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4/VPS15: phosphoinositide-3-kinase regulatory subunit 4; PRKAA/AMPK: protein kinase, AMP-activated alpha catalytic; RUBCN: rubicon autophagy regulator; RPS6: ribosomal protein S6; RAS: Ras proto-oncogene; RAF: Raf proto-oncogene; TKI: tyrosine kinase inhibitor; TUBA4A: tubulin alpha 4a; UVRAG: UV radiation resistance associated.</description><subject>Animals</subject><subject>ATG7</subject><subject>autophagy</subject><subject>Autophagy - drug effects</subject><subject>Beclin-1 - metabolism</subject><subject>BECN1</subject><subject>Carcinoma, Non-Small-Cell Lung - drug therapy</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>EGFR</subject><subject>ErbB Receptors - metabolism</subject><subject>Erlotinib Hydrochloride - pharmacology</subject><subject>Erlotinib Hydrochloride - therapeutic use</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>lung cancer</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice, Nude</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Mas</subject><subject>Research Paper</subject><subject>tumor suppressor</subject><issn>1554-8627</issn><issn>1554-8635</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UU1v1DAQtRCIlsJPAPnIJVt_x74gqqotlSoBFZyt2cTeNUriYCet9t_XYbcruHDxjGbeezPjh9B7SlaUaHJOpRRasXrFCDUrqqRRUrxAp0u90orLl8ec1SfoTc6_COFKG_YanXAqCrlmpyh8u_h-z3GexzG5nF3G09bhTYqP0xZHj4c4VLmHrsONK083DxvcwNC49KeQ8UMA3Md27mAKcVgoVzfX91Xv2gCTazHMUxy3sNm9Ra88dNm9O8Qz9PP66sfll-ru683t5cVd1Qilp4pJSp12UnFiBDC_NqAMMyUH6VvXKgLca8Gh1c7TumWNYbUSUhjXMCLW_Ax92uuO87ps0bhhStDZMYUe0s5GCPbfzhC2dhMfbC2UEUYWgY8HgRR_zy5Ptg95ORYGF-dsGdNEMm44KVC5hzYp5pycP46hxC422Web7GKTPdhUeB_-3vHIevalAD7vAWHwMfXwGFPX2gl2XUw-lf8PuYD_O-MJDwSjQQ</recordid><startdate>20200702</startdate><enddate>20200702</enddate><creator>Cao, Qianqian</creator><creator>You, Xue</creator><creator>Xu, Lijiao</creator><creator>Wang, Lin</creator><creator>Chen, Yan</creator><general>Taylor & Francis</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6630-0693</orcidid></search><sort><creationdate>20200702</creationdate><title>PAQR3 suppresses the growth of non-small cell lung cancer cells via modulation of EGFR-mediated autophagy</title><author>Cao, Qianqian ; You, Xue ; Xu, Lijiao ; Wang, Lin ; Chen, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-2511e8e563094a2fb9a692994aa5fded60a3f843ad8ef17d2c92764549ec204b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>ATG7</topic><topic>autophagy</topic><topic>Autophagy - drug effects</topic><topic>Beclin-1 - metabolism</topic><topic>BECN1</topic><topic>Carcinoma, Non-Small-Cell Lung - drug therapy</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>EGFR</topic><topic>ErbB Receptors - metabolism</topic><topic>Erlotinib Hydrochloride - pharmacology</topic><topic>Erlotinib Hydrochloride - therapeutic use</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>lung cancer</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice, Nude</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Mas</topic><topic>Research Paper</topic><topic>tumor suppressor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cao, Qianqian</creatorcontrib><creatorcontrib>You, Xue</creatorcontrib><creatorcontrib>Xu, Lijiao</creatorcontrib><creatorcontrib>Wang, Lin</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Autophagy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cao, Qianqian</au><au>You, Xue</au><au>Xu, Lijiao</au><au>Wang, Lin</au><au>Chen, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PAQR3 suppresses the growth of non-small cell lung cancer cells via modulation of EGFR-mediated autophagy</atitle><jtitle>Autophagy</jtitle><addtitle>Autophagy</addtitle><date>2020-07-02</date><risdate>2020</risdate><volume>16</volume><issue>7</issue><spage>1236</spage><epage>1247</epage><pages>1236-1247</pages><issn>1554-8627</issn><eissn>1554-8635</eissn><abstract>Macroautophagy/autophagy is an evolutionarily conserved intracellular process that recycles and degrades intracellular components to sustain homeostasis in response to deficiency of nutrients or growth factors. PAQR3 is a newly discovered tumor suppressor that also regulates autophagy induced by nutrient starvation via AMPK and MTORC1 signaling pathways. In this study, we investigated whether PAQR3 modulates EGFR-mediated autophagy and whether such regulation is associated with the tumor suppressive activity of PAQR3. PAQR3 is able to inhibit the in vitro and in vivo growth of non-small cell lung cancer (NSCLC) cells. PAQR3 potentiates autophagy induced by EGFR inhibitor erlotinib. Knockdown of PAQR3 abrogates erlotinib-mediated reduction of BECN1 interaction with autophagy inhibitory proteins RUBCN/Rubicon and BCL2. PAQR3 blocks the interaction of BECN1 with the activated form of EGFR and inhibits tyrosine phosphorylation of BECN1. Furthermore, inhibition of autophagy by knocking down ATG7 abrogates the tumor suppressive activity of PAQR3 in NSCLC cells. Collectively, these data indicate that PAQR3 suppresses tumor progression of NSCLC cells through modulating EGFR-regulated autophagy.
AKT: thymoma viral proto-oncogene; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG14: autophagy related 14; BCL2: B cell leukemia/lymphoma 2; BECN1: beclin 1; CCK-8: cell counting kit-8; CQ: chloroquine diphosphate; DMEM: Dulbecco's modified Eagle's medium; EdU: 5-ethynyl-2ʹ-deoxyuridine; EGFR: epidermal growth factor receptor; FBS: fetal bovine serum; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IgG: Immunoglobulin G; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; MTORC1: mechanistic target of rapamycin kinase complex 1; MTT: thiazolyl blue tetrazolium bromide; NSCLC: Non-small cell lung cancer; MAP2K/MEK: mitogen-activated protein kinase kinase; MAPK/ERK: mitogen-activated protein kinase; PAQR3: progestin and adipoQ receptor family member 3; PI3K: phosphatidylinositol-4,5-bisphosphate 3-kinase; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4/VPS15: phosphoinositide-3-kinase regulatory subunit 4; PRKAA/AMPK: protein kinase, AMP-activated alpha catalytic; RUBCN: rubicon autophagy regulator; RPS6: ribosomal protein S6; RAS: Ras proto-oncogene; RAF: Raf proto-oncogene; TKI: tyrosine kinase inhibitor; TUBA4A: tubulin alpha 4a; UVRAG: UV radiation resistance associated.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>31448672</pmid><doi>10.1080/15548627.2019.1659654</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6630-0693</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals ATG7 autophagy Autophagy - drug effects Beclin-1 - metabolism BECN1 Carcinoma, Non-Small-Cell Lung - drug therapy Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell Proliferation - drug effects EGFR ErbB Receptors - metabolism Erlotinib Hydrochloride - pharmacology Erlotinib Hydrochloride - therapeutic use HEK293 Cells Humans Intracellular Signaling Peptides and Proteins - metabolism lung cancer Lung Neoplasms - drug therapy Lung Neoplasms - metabolism Lung Neoplasms - pathology Membrane Proteins - metabolism Mice, Nude Phosphorylation - drug effects Proto-Oncogene Mas Research Paper tumor suppressor |
title | PAQR3 suppresses the growth of non-small cell lung cancer cells via modulation of EGFR-mediated autophagy |
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