Cytosolic chloride ion is a key factor in lysosomal acidification and function of autophagy in human gastric cancer cell
The purpose of the present study was to clarify roles of cytosolic chloride ion (Cl−) in regulation of lysosomal acidification [intra‐lysosomal pH (pHlys)] and autophagy function in human gastric cancer cell line (MKN28). The MKN28 cells cultured under a low Cl− condition elevated pHlys and reduced...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2014-06, Vol.18 (6), p.1124-1133 |
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| creator | Hosogi, Shigekuni Kusuzaki, Katsuyuki Inui, Toshio Wang, Xiangdong Marunaka, Yoshinori |
| description | The purpose of the present study was to clarify roles of cytosolic chloride ion (Cl−) in regulation of lysosomal acidification [intra‐lysosomal pH (pHlys)] and autophagy function in human gastric cancer cell line (MKN28). The MKN28 cells cultured under a low Cl− condition elevated pHlys and reduced the intra‐lysosomal Cl− concentration ([Cl−]lys) via reduction of cytosolic Cl− concentration ([Cl−]c), showing abnormal accumulation of LC3II and p62 participating in autophagy function (dysfunction of autophagy) accompanied by inhibition of cell proliferation via G0/G1 arrest without induction of apoptosis. We also studied effects of direct modification of H+ transport on lysosomal acidification and autophagy. Application of bafilomycin A1 (an inhibitor of V‐type H+‐ATPase) or ethyl isopropyl amiloride [EIPA; an inhibitor of Na+/H+ exchanger (NHE)] elevated pHlys and decreased [Cl−]lys associated with inhibition of cell proliferation via induction of G0/G1 arrest similar to the culture under a low Cl− condition. However, unlike low Cl− condition, application of the compound, bafilomycin A1 or EIPA, induced apoptosis associated with increases in caspase 3 and 9 without large reduction in [Cl−]c compared with low Cl− condition. These observations suggest that the lowered [Cl−]c primarily causes dysfunction of autophagy without apoptosis via dysfunction of lysosome induced by disturbance of intra‐lysosomal acidification. This is the first study showing that cytosolic Cl− is a key factor of lysosome acidification and autophagy. |
| doi_str_mv | 10.1111/jcmm.12257 |
| format | Article |
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The MKN28 cells cultured under a low Cl− condition elevated pHlys and reduced the intra‐lysosomal Cl− concentration ([Cl−]lys) via reduction of cytosolic Cl− concentration ([Cl−]c), showing abnormal accumulation of LC3II and p62 participating in autophagy function (dysfunction of autophagy) accompanied by inhibition of cell proliferation via G0/G1 arrest without induction of apoptosis. We also studied effects of direct modification of H+ transport on lysosomal acidification and autophagy. Application of bafilomycin A1 (an inhibitor of V‐type H+‐ATPase) or ethyl isopropyl amiloride [EIPA; an inhibitor of Na+/H+ exchanger (NHE)] elevated pHlys and decreased [Cl−]lys associated with inhibition of cell proliferation via induction of G0/G1 arrest similar to the culture under a low Cl− condition. However, unlike low Cl− condition, application of the compound, bafilomycin A1 or EIPA, induced apoptosis associated with increases in caspase 3 and 9 without large reduction in [Cl−]c compared with low Cl− condition. These observations suggest that the lowered [Cl−]c primarily causes dysfunction of autophagy without apoptosis via dysfunction of lysosome induced by disturbance of intra‐lysosomal acidification. This is the first study showing that cytosolic Cl− is a key factor of lysosome acidification and autophagy.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12257</identifier><identifier>PMID: 24725767</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Acidification ; Acids - metabolism ; Amiloride ; Amino acids ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - metabolism ; Autophagy ; Autophagy - drug effects ; Blotting, Western ; Cancer ; Caspase ; Caspase-3 ; Cell culture ; Cell Cycle - drug effects ; Cell growth ; Cell proliferation ; Cell Proliferation - drug effects ; chloride ion ; Chlorides ; Chlorides - pharmacology ; Cytosol - metabolism ; Disease ; Gastric cancer ; Homeostasis - drug effects ; Humans ; Hydrogen ; Inhibition ; lysosome ; Lysosomes - metabolism ; Na+/H+-exchanging ATPase ; Original ; Phagocytosis ; Phosphorylation ; Proteins ; Starvation ; Stomach Neoplasms - drug therapy ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Tumor Cells, Cultured</subject><ispartof>Journal of cellular and molecular medicine, 2014-06, Vol.18 (6), p.1124-1133</ispartof><rights>2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2014. This work is published under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5847-5d993822447f5364425cab9afcc01cc263b9f28505082d6d88aee772aa7817b13</citedby><cites>FETCH-LOGICAL-c5847-5d993822447f5364425cab9afcc01cc263b9f28505082d6d88aee772aa7817b13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508152/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4508152/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,1414,11545,27907,27908,45557,45558,46035,46459,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24725767$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hosogi, Shigekuni</creatorcontrib><creatorcontrib>Kusuzaki, Katsuyuki</creatorcontrib><creatorcontrib>Inui, Toshio</creatorcontrib><creatorcontrib>Wang, Xiangdong</creatorcontrib><creatorcontrib>Marunaka, Yoshinori</creatorcontrib><title>Cytosolic chloride ion is a key factor in lysosomal acidification and function of autophagy in human gastric cancer cell</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>The purpose of the present study was to clarify roles of cytosolic chloride ion (Cl−) in regulation of lysosomal acidification [intra‐lysosomal pH (pHlys)] and autophagy function in human gastric cancer cell line (MKN28). The MKN28 cells cultured under a low Cl− condition elevated pHlys and reduced the intra‐lysosomal Cl− concentration ([Cl−]lys) via reduction of cytosolic Cl− concentration ([Cl−]c), showing abnormal accumulation of LC3II and p62 participating in autophagy function (dysfunction of autophagy) accompanied by inhibition of cell proliferation via G0/G1 arrest without induction of apoptosis. We also studied effects of direct modification of H+ transport on lysosomal acidification and autophagy. Application of bafilomycin A1 (an inhibitor of V‐type H+‐ATPase) or ethyl isopropyl amiloride [EIPA; an inhibitor of Na+/H+ exchanger (NHE)] elevated pHlys and decreased [Cl−]lys associated with inhibition of cell proliferation via induction of G0/G1 arrest similar to the culture under a low Cl− condition. However, unlike low Cl− condition, application of the compound, bafilomycin A1 or EIPA, induced apoptosis associated with increases in caspase 3 and 9 without large reduction in [Cl−]c compared with low Cl− condition. These observations suggest that the lowered [Cl−]c primarily causes dysfunction of autophagy without apoptosis via dysfunction of lysosome induced by disturbance of intra‐lysosomal acidification. This is the first study showing that cytosolic Cl− is a key factor of lysosome acidification and autophagy.</description><subject>Acidification</subject><subject>Acids - metabolism</subject><subject>Amiloride</subject><subject>Amino acids</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Blotting, Western</subject><subject>Cancer</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell culture</subject><subject>Cell Cycle - drug effects</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>chloride ion</subject><subject>Chlorides</subject><subject>Chlorides - pharmacology</subject><subject>Cytosol - metabolism</subject><subject>Disease</subject><subject>Gastric cancer</subject><subject>Homeostasis - drug effects</subject><subject>Humans</subject><subject>Hydrogen</subject><subject>Inhibition</subject><subject>lysosome</subject><subject>Lysosomes - metabolism</subject><subject>Na+/H+-exchanging ATPase</subject><subject>Original</subject><subject>Phagocytosis</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Starvation</subject><subject>Stomach Neoplasms - drug therapy</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Tumor Cells, Cultured</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9vFCEYh4nR2Hb14gcwJF5Mk63AwMBcTJpN65-08aJn8i4Du6wMrDBjO9_eme7aqAe5AOHh4X35IfSKkgs6jXc703UXlDEhn6BTKhRb8qbiT49rqip1gs5K2RFS1bRqnqMTxuVE1_IU3a_GPpUUvMFmG1L2rcU-RewLBvzdjtiB6VPGPuIwlonsIGAwvvXOG-hnFGKL3RDNwyY5DEOf9lvYjPOl7dBBxBsofZ6fgGhsxsaG8AI9cxCKfXmcF-jb9dXX1cflzZcPn1aXN0sjFJdL0TZNpRjjXDpR1ZwzYWDdgDOGUGNYXa0bx5QggijW1q1SYK2UDEAqKte0WqD3B-9-WHe2NTb2GYLeZ99BHnUCr_8-iX6rN-mn5pORCjYJ3h4FOf0YbOl158vcAUSbhqKp4KqupJz-eYHe_IPu0pDj1J5mrCFSyobMFZ0fKJNTKdm6x2Io0XOgeg5UPwQ6wa__LP8R_Z3gBNADcOeDHf-j0p9Xt7cH6S94dKze</recordid><startdate>201406</startdate><enddate>201406</enddate><creator>Hosogi, Shigekuni</creator><creator>Kusuzaki, Katsuyuki</creator><creator>Inui, Toshio</creator><creator>Wang, Xiangdong</creator><creator>Marunaka, Yoshinori</creator><general>John Wiley & Sons, Inc</general><general>John Wiley & Sons, Ltd</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</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>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201406</creationdate><title>Cytosolic chloride ion is a key factor in lysosomal acidification and function of autophagy in human gastric cancer cell</title><author>Hosogi, Shigekuni ; Kusuzaki, Katsuyuki ; Inui, Toshio ; Wang, Xiangdong ; Marunaka, Yoshinori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5847-5d993822447f5364425cab9afcc01cc263b9f28505082d6d88aee772aa7817b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acidification</topic><topic>Acids - metabolism</topic><topic>Amiloride</topic><topic>Amino acids</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Autophagy</topic><topic>Autophagy - drug effects</topic><topic>Blotting, Western</topic><topic>Cancer</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cell culture</topic><topic>Cell Cycle - drug effects</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>chloride ion</topic><topic>Chlorides</topic><topic>Chlorides - pharmacology</topic><topic>Cytosol - metabolism</topic><topic>Disease</topic><topic>Gastric cancer</topic><topic>Homeostasis - drug effects</topic><topic>Humans</topic><topic>Hydrogen</topic><topic>Inhibition</topic><topic>lysosome</topic><topic>Lysosomes - metabolism</topic><topic>Na+/H+-exchanging ATPase</topic><topic>Original</topic><topic>Phagocytosis</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Starvation</topic><topic>Stomach Neoplasms - drug therapy</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hosogi, Shigekuni</creatorcontrib><creatorcontrib>Kusuzaki, Katsuyuki</creatorcontrib><creatorcontrib>Inui, Toshio</creatorcontrib><creatorcontrib>Wang, Xiangdong</creatorcontrib><creatorcontrib>Marunaka, Yoshinori</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Wiley Online Library Free Content</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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 China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hosogi, Shigekuni</au><au>Kusuzaki, Katsuyuki</au><au>Inui, Toshio</au><au>Wang, Xiangdong</au><au>Marunaka, Yoshinori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytosolic chloride ion is a key factor in lysosomal acidification and function of autophagy in human gastric cancer cell</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2014-06</date><risdate>2014</risdate><volume>18</volume><issue>6</issue><spage>1124</spage><epage>1133</epage><pages>1124-1133</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>The purpose of the present study was to clarify roles of cytosolic chloride ion (Cl−) in regulation of lysosomal acidification [intra‐lysosomal pH (pHlys)] and autophagy function in human gastric cancer cell line (MKN28). The MKN28 cells cultured under a low Cl− condition elevated pHlys and reduced the intra‐lysosomal Cl− concentration ([Cl−]lys) via reduction of cytosolic Cl− concentration ([Cl−]c), showing abnormal accumulation of LC3II and p62 participating in autophagy function (dysfunction of autophagy) accompanied by inhibition of cell proliferation via G0/G1 arrest without induction of apoptosis. We also studied effects of direct modification of H+ transport on lysosomal acidification and autophagy. Application of bafilomycin A1 (an inhibitor of V‐type H+‐ATPase) or ethyl isopropyl amiloride [EIPA; an inhibitor of Na+/H+ exchanger (NHE)] elevated pHlys and decreased [Cl−]lys associated with inhibition of cell proliferation via induction of G0/G1 arrest similar to the culture under a low Cl− condition. However, unlike low Cl− condition, application of the compound, bafilomycin A1 or EIPA, induced apoptosis associated with increases in caspase 3 and 9 without large reduction in [Cl−]c compared with low Cl− condition. These observations suggest that the lowered [Cl−]c primarily causes dysfunction of autophagy without apoptosis via dysfunction of lysosome induced by disturbance of intra‐lysosomal acidification. This is the first study showing that cytosolic Cl− is a key factor of lysosome acidification and autophagy.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>24725767</pmid><doi>10.1111/jcmm.12257</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Acidification Acids - metabolism Amiloride Amino acids Apoptosis Apoptosis - drug effects Apoptosis Regulatory Proteins - metabolism Autophagy Autophagy - drug effects Blotting, Western Cancer Caspase Caspase-3 Cell culture Cell Cycle - drug effects Cell growth Cell proliferation Cell Proliferation - drug effects chloride ion Chlorides Chlorides - pharmacology Cytosol - metabolism Disease Gastric cancer Homeostasis - drug effects Humans Hydrogen Inhibition lysosome Lysosomes - metabolism Na+/H+-exchanging ATPase Original Phagocytosis Phosphorylation Proteins Starvation Stomach Neoplasms - drug therapy Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Tumor Cells, Cultured |
| title | Cytosolic chloride ion is a key factor in lysosomal acidification and function of autophagy in human gastric cancer cell |
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