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Morin Hydrate Sensitizes Hepatoma Cells and Xenograft Tumor towards Cisplatin by Downregulating PARP-1-HMGB1 Mediated Autophagy
The cross-talk between apoptosis and autophagy influences anticancer drug sensitivity and cellular death in various cancer cell lines. However, the fundamental mechanisms behind this phenomenon are still unidentified. We demonstrated anti-cancerous role of cisplatin (CP) and morin hydrate (Mh) as an...
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Published in: | International journal of molecular sciences 2020-11, Vol.21 (21), p.8253 |
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description | The cross-talk between apoptosis and autophagy influences anticancer drug sensitivity and cellular death in various cancer cell lines. However, the fundamental mechanisms behind this phenomenon are still unidentified. We demonstrated anti-cancerous role of cisplatin (CP) and morin hydrate (Mh) as an individual and/or in combination (CP-Mh) in hepatoma cells and tumor model. Exposure of CP resulted in the production of intracellular reactive oxygen species (ROS)-mediated cellular vacuolization, expansion of mitochondria membrane and activation of endoplasmic reticulum (ER)-stress. Consequently, Cyt
translocation led to the increase of Bax/Bcl-2 ratio, which simultaneously triggered caspase-mediated cellular apoptosis. In addition, CP-induced PARP-1 activation led to ADP-ribosylation of HMGB1, which consequently developed autophagy as evident by the LC3I/II ratio. Chemically-induced inhibition of autophagy marked by increased cell death signified a protective role of autophagy against CP treatment. CP-Mh abrogates the PARP-1 expression and significantly reduced HMGB1-cytoplasmic translocation with subsequent inhibition of the HMGB1-Beclin1 complex formation. In the absence of PARP-1, a reduced HMGB1 mediated autophagy was observed followed by induced caspase-dependent apoptosis. To confirm the role of PARP-1-HMGB1 signaling in autophagy, we used the PARP-1 inhibitor, 4-amino-1,8-naphthalimide (ANI), HMGB1 inhibitor, ethyl pyruvate (EP), autophagy inhibitors, 3-methyl adenine (3-MA) and bafilomycin (baf) and small interfering RNAs (siRNA) to target Atg5 in combination of CP and Mh. Exposure to these inhibitors enhanced the sensitivity of HepG2 cells to CP. Collectively, our findings indicate that CP-Mh in combination served as a prominent regulator of autophagy and significant inducer of apoptosis that maintains a homeostatic balance towards HepG2 cells and the subcutaneous tumor model. |
doi_str_mv | 10.3390/ijms21218253 |
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translocation led to the increase of Bax/Bcl-2 ratio, which simultaneously triggered caspase-mediated cellular apoptosis. In addition, CP-induced PARP-1 activation led to ADP-ribosylation of HMGB1, which consequently developed autophagy as evident by the LC3I/II ratio. Chemically-induced inhibition of autophagy marked by increased cell death signified a protective role of autophagy against CP treatment. CP-Mh abrogates the PARP-1 expression and significantly reduced HMGB1-cytoplasmic translocation with subsequent inhibition of the HMGB1-Beclin1 complex formation. In the absence of PARP-1, a reduced HMGB1 mediated autophagy was observed followed by induced caspase-dependent apoptosis. To confirm the role of PARP-1-HMGB1 signaling in autophagy, we used the PARP-1 inhibitor, 4-amino-1,8-naphthalimide (ANI), HMGB1 inhibitor, ethyl pyruvate (EP), autophagy inhibitors, 3-methyl adenine (3-MA) and bafilomycin (baf) and small interfering RNAs (siRNA) to target Atg5 in combination of CP and Mh. Exposure to these inhibitors enhanced the sensitivity of HepG2 cells to CP. Collectively, our findings indicate that CP-Mh in combination served as a prominent regulator of autophagy and significant inducer of apoptosis that maintains a homeostatic balance towards HepG2 cells and the subcutaneous tumor model.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21218253</identifier><identifier>PMID: 33158052</identifier><language>eng</language><publisher>Switzerland: MDPI</publisher><subject>Animals ; apoptosis ; autophagy ; Autophagy - drug effects ; Autophagy - genetics ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; cisplatin ; Cisplatin - administration & dosage ; Cisplatin - pharmacology ; Down-Regulation - drug effects ; Down-Regulation - genetics ; Drug Synergism ; Drug Therapy, Combination ; Flavonoids - administration & dosage ; Flavonoids - pharmacology ; Hep G2 Cells ; HMGB1 ; HMGB1 Protein - physiology ; Humans ; Liver Neoplasms - drug therapy ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; morin hydrate ; Poly (ADP-Ribose) Polymerase-1 - physiology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays</subject><ispartof>International journal of molecular sciences, 2020-11, Vol.21 (21), p.8253</ispartof><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-2fe18e9c08b97151cb376b72db34a6ee563098f54f2db2f79e6be40f8a56119c3</citedby><cites>FETCH-LOGICAL-c450t-2fe18e9c08b97151cb376b72db34a6ee563098f54f2db2f79e6be40f8a56119c3</cites><orcidid>0000-0003-1612-4473</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/PMC7885522/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7885522/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33158052$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pal Singh, Mahendra</creatorcontrib><creatorcontrib>Pal Khaket, Tejinder</creatorcontrib><creatorcontrib>Bajpai, Vivek K</creatorcontrib><creatorcontrib>Alfarraj, Saleh</creatorcontrib><creatorcontrib>Kim, Se-Gie</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Huh, Yun Suk</creatorcontrib><creatorcontrib>Han, Young-Kyu</creatorcontrib><creatorcontrib>Kang, Sun Chul</creatorcontrib><title>Morin Hydrate Sensitizes Hepatoma Cells and Xenograft Tumor towards Cisplatin by Downregulating PARP-1-HMGB1 Mediated Autophagy</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>The cross-talk between apoptosis and autophagy influences anticancer drug sensitivity and cellular death in various cancer cell lines. However, the fundamental mechanisms behind this phenomenon are still unidentified. We demonstrated anti-cancerous role of cisplatin (CP) and morin hydrate (Mh) as an individual and/or in combination (CP-Mh) in hepatoma cells and tumor model. Exposure of CP resulted in the production of intracellular reactive oxygen species (ROS)-mediated cellular vacuolization, expansion of mitochondria membrane and activation of endoplasmic reticulum (ER)-stress. Consequently, Cyt
translocation led to the increase of Bax/Bcl-2 ratio, which simultaneously triggered caspase-mediated cellular apoptosis. In addition, CP-induced PARP-1 activation led to ADP-ribosylation of HMGB1, which consequently developed autophagy as evident by the LC3I/II ratio. Chemically-induced inhibition of autophagy marked by increased cell death signified a protective role of autophagy against CP treatment. CP-Mh abrogates the PARP-1 expression and significantly reduced HMGB1-cytoplasmic translocation with subsequent inhibition of the HMGB1-Beclin1 complex formation. In the absence of PARP-1, a reduced HMGB1 mediated autophagy was observed followed by induced caspase-dependent apoptosis. To confirm the role of PARP-1-HMGB1 signaling in autophagy, we used the PARP-1 inhibitor, 4-amino-1,8-naphthalimide (ANI), HMGB1 inhibitor, ethyl pyruvate (EP), autophagy inhibitors, 3-methyl adenine (3-MA) and bafilomycin (baf) and small interfering RNAs (siRNA) to target Atg5 in combination of CP and Mh. Exposure to these inhibitors enhanced the sensitivity of HepG2 cells to CP. Collectively, our findings indicate that CP-Mh in combination served as a prominent regulator of autophagy and significant inducer of apoptosis that maintains a homeostatic balance towards HepG2 cells and the subcutaneous tumor model.</description><subject>Animals</subject><subject>apoptosis</subject><subject>autophagy</subject><subject>Autophagy - drug effects</subject><subject>Autophagy - genetics</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>cisplatin</subject><subject>Cisplatin - administration & dosage</subject><subject>Cisplatin - pharmacology</subject><subject>Down-Regulation - drug effects</subject><subject>Down-Regulation - genetics</subject><subject>Drug Synergism</subject><subject>Drug Therapy, Combination</subject><subject>Flavonoids - administration & dosage</subject><subject>Flavonoids - pharmacology</subject><subject>Hep G2 Cells</subject><subject>HMGB1</subject><subject>HMGB1 Protein - physiology</subject><subject>Humans</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>morin hydrate</subject><subject>Poly (ADP-Ribose) Polymerase-1 - physiology</subject><subject>Tumor Cells, Cultured</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpVkU9v1DAQxS0EoqXlxhn5AxDqv3FyQVq20K3UFVUpEjfLicepV0kc2V6q5cJXJ-1CtT3N6M2b3zs8hN5R8pHzmpz5zZAYZbRikr9Ax1QwVhBSqpcH-xF6k9KGEMaZrF-jI86prIhkx-jPOkQ_4tXORpMBf4cx-ex_Q8IrmEwOg8FL6PuEzWjxTxhDF43L-HY7hIhzuDfRJrz0aepNnjnNDp-H-zFCt30UOny9uLkuaLFaX3ymeA3WzzEWL7Y5THem252iV870Cd7-myfox9cvt8tVcfXt4nK5uCpaIUkumANaQd2SqqkVlbRtuCobxWzDhSkBZMlJXTkp3Cwxp2ooGxDEVUaWlNYtP0GXe64NZqOn6AcTdzoYrx-FEDttYvZtD9oQS11NFRPCChBtXVrCJJSycVw6pWbWpz1r2jYD2BbGHE3_DPr8Mvo73YVfWlWVlIzNgA97QBtDShHc0y8l-qFUfVjqbH9_mPdk_t8i_wuLG59t</recordid><startdate>20201104</startdate><enddate>20201104</enddate><creator>Pal Singh, Mahendra</creator><creator>Pal Khaket, Tejinder</creator><creator>Bajpai, Vivek K</creator><creator>Alfarraj, Saleh</creator><creator>Kim, Se-Gie</creator><creator>Chen, Lei</creator><creator>Huh, Yun Suk</creator><creator>Han, Young-Kyu</creator><creator>Kang, Sun Chul</creator><general>MDPI</general><general>MDPI AG</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>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-1612-4473</orcidid></search><sort><creationdate>20201104</creationdate><title>Morin Hydrate Sensitizes Hepatoma Cells and Xenograft Tumor towards Cisplatin by Downregulating PARP-1-HMGB1 Mediated Autophagy</title><author>Pal Singh, Mahendra ; Pal Khaket, Tejinder ; Bajpai, Vivek K ; Alfarraj, Saleh ; Kim, Se-Gie ; Chen, Lei ; Huh, Yun Suk ; Han, Young-Kyu ; Kang, Sun Chul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-2fe18e9c08b97151cb376b72db34a6ee563098f54f2db2f79e6be40f8a56119c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>apoptosis</topic><topic>autophagy</topic><topic>Autophagy - drug effects</topic><topic>Autophagy - genetics</topic><topic>Carcinoma, Hepatocellular - drug therapy</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>cisplatin</topic><topic>Cisplatin - administration & dosage</topic><topic>Cisplatin - pharmacology</topic><topic>Down-Regulation - drug effects</topic><topic>Down-Regulation - genetics</topic><topic>Drug Synergism</topic><topic>Drug Therapy, Combination</topic><topic>Flavonoids - administration & dosage</topic><topic>Flavonoids - pharmacology</topic><topic>Hep G2 Cells</topic><topic>HMGB1</topic><topic>HMGB1 Protein - physiology</topic><topic>Humans</topic><topic>Liver Neoplasms - drug therapy</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>morin hydrate</topic><topic>Poly (ADP-Ribose) Polymerase-1 - physiology</topic><topic>Tumor Cells, Cultured</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pal Singh, Mahendra</creatorcontrib><creatorcontrib>Pal Khaket, Tejinder</creatorcontrib><creatorcontrib>Bajpai, Vivek K</creatorcontrib><creatorcontrib>Alfarraj, Saleh</creatorcontrib><creatorcontrib>Kim, Se-Gie</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Huh, Yun Suk</creatorcontrib><creatorcontrib>Han, Young-Kyu</creatorcontrib><creatorcontrib>Kang, Sun Chul</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pal Singh, Mahendra</au><au>Pal Khaket, Tejinder</au><au>Bajpai, Vivek K</au><au>Alfarraj, Saleh</au><au>Kim, Se-Gie</au><au>Chen, Lei</au><au>Huh, Yun Suk</au><au>Han, Young-Kyu</au><au>Kang, Sun Chul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Morin Hydrate Sensitizes Hepatoma Cells and Xenograft Tumor towards Cisplatin by Downregulating PARP-1-HMGB1 Mediated Autophagy</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2020-11-04</date><risdate>2020</risdate><volume>21</volume><issue>21</issue><spage>8253</spage><pages>8253-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The cross-talk between apoptosis and autophagy influences anticancer drug sensitivity and cellular death in various cancer cell lines. However, the fundamental mechanisms behind this phenomenon are still unidentified. We demonstrated anti-cancerous role of cisplatin (CP) and morin hydrate (Mh) as an individual and/or in combination (CP-Mh) in hepatoma cells and tumor model. Exposure of CP resulted in the production of intracellular reactive oxygen species (ROS)-mediated cellular vacuolization, expansion of mitochondria membrane and activation of endoplasmic reticulum (ER)-stress. Consequently, Cyt
translocation led to the increase of Bax/Bcl-2 ratio, which simultaneously triggered caspase-mediated cellular apoptosis. In addition, CP-induced PARP-1 activation led to ADP-ribosylation of HMGB1, which consequently developed autophagy as evident by the LC3I/II ratio. Chemically-induced inhibition of autophagy marked by increased cell death signified a protective role of autophagy against CP treatment. CP-Mh abrogates the PARP-1 expression and significantly reduced HMGB1-cytoplasmic translocation with subsequent inhibition of the HMGB1-Beclin1 complex formation. In the absence of PARP-1, a reduced HMGB1 mediated autophagy was observed followed by induced caspase-dependent apoptosis. To confirm the role of PARP-1-HMGB1 signaling in autophagy, we used the PARP-1 inhibitor, 4-amino-1,8-naphthalimide (ANI), HMGB1 inhibitor, ethyl pyruvate (EP), autophagy inhibitors, 3-methyl adenine (3-MA) and bafilomycin (baf) and small interfering RNAs (siRNA) to target Atg5 in combination of CP and Mh. Exposure to these inhibitors enhanced the sensitivity of HepG2 cells to CP. Collectively, our findings indicate that CP-Mh in combination served as a prominent regulator of autophagy and significant inducer of apoptosis that maintains a homeostatic balance towards HepG2 cells and the subcutaneous tumor model.</abstract><cop>Switzerland</cop><pub>MDPI</pub><pmid>33158052</pmid><doi>10.3390/ijms21218253</doi><orcidid>https://orcid.org/0000-0003-1612-4473</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals apoptosis autophagy Autophagy - drug effects Autophagy - genetics Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology cisplatin Cisplatin - administration & dosage Cisplatin - pharmacology Down-Regulation - drug effects Down-Regulation - genetics Drug Synergism Drug Therapy, Combination Flavonoids - administration & dosage Flavonoids - pharmacology Hep G2 Cells HMGB1 HMGB1 Protein - physiology Humans Liver Neoplasms - drug therapy Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - pathology Male Mice Mice, Inbred BALB C Mice, Nude morin hydrate Poly (ADP-Ribose) Polymerase-1 - physiology Tumor Cells, Cultured Xenograft Model Antitumor Assays |
title | Morin Hydrate Sensitizes Hepatoma Cells and Xenograft Tumor towards Cisplatin by Downregulating PARP-1-HMGB1 Mediated Autophagy |
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