Pristimerin enhances the effect of cisplatin by inhibiting the miR‑23a/Akt/GSK3β signaling pathway and suppressing autophagy in lung cancer cells
Lung cancer is a common type of cancer with a high mortality rate in China. Cisplatin (Cis) is one of the most effective broad‑spectrum chemotherapeutic drugs for the treatment of advanced lung cancer. However, Cis resistance remains an obstacle in the treatment of advanced lung cancer. Pristimerin...
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| Veröffentlicht in: | International journal of molecular medicine 2019-03, Vol.43 (3), p.1382-1394 |
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| container_title | International journal of molecular medicine |
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| creator | Zhang, Yingbing Wang, Jiquan Hui, Beina Sun, Wenze Li, Bin Shi, Fan Che, Shaomin Chai, Linyan Song, Liping |
| description | Lung cancer is a common type of cancer with a high mortality rate in China. Cisplatin (Cis) is one of the most effective broad‑spectrum chemotherapeutic drugs for the treatment of advanced lung cancer. However, Cis resistance remains an obstacle in the treatment of advanced lung cancer. Pristimerin (Pris), a naturally occurring triterpenoid quinone compound, not only possesses anticancer properties, but also enhances chemosensitivity. Therefore, the present study aimed to investigate whether Pris can enhance the chemosensitivity of lung cancer cells to Cis and identify the underlying mechanism. A Cell Counting kit‑8 and flow cytometry were used to determine cell viability, cell cycle progression and apoptosis in A549 and NCI‑H446 cells. Western blotting was used to determine cell apoptosis‑related, cell cycle‑related and autophagy‑related proteins. The results showed that Pris inhibited cell proliferation, and induced G0/G1 arrest and cell apoptosis in A549 and NCI‑H446 cells. The western blotting revealed that Pris effectively synergized with Cis to induce cell apoptosis by inhibiting the microRNA‑23a/Akt/glycogen synthase kinase 3β signaling pathway and suppressing autophagy. In vivo xenograft experiments confirmed that Pris effectively synergized with Cis to suppress tumor growth. Collectively, these results indicate that Pris synergized with Cis and that this may be a potential therapeutic strategy to overcome lung cancer. |
| doi_str_mv | 10.3892/ijmm.2019.4057 |
| format | Article |
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Cisplatin (Cis) is one of the most effective broad‑spectrum chemotherapeutic drugs for the treatment of advanced lung cancer. However, Cis resistance remains an obstacle in the treatment of advanced lung cancer. Pristimerin (Pris), a naturally occurring triterpenoid quinone compound, not only possesses anticancer properties, but also enhances chemosensitivity. Therefore, the present study aimed to investigate whether Pris can enhance the chemosensitivity of lung cancer cells to Cis and identify the underlying mechanism. A Cell Counting kit‑8 and flow cytometry were used to determine cell viability, cell cycle progression and apoptosis in A549 and NCI‑H446 cells. Western blotting was used to determine cell apoptosis‑related, cell cycle‑related and autophagy‑related proteins. The results showed that Pris inhibited cell proliferation, and induced G0/G1 arrest and cell apoptosis in A549 and NCI‑H446 cells. The western blotting revealed that Pris effectively synergized with Cis to induce cell apoptosis by inhibiting the microRNA‑23a/Akt/glycogen synthase kinase 3β signaling pathway and suppressing autophagy. In vivo xenograft experiments confirmed that Pris effectively synergized with Cis to suppress tumor growth. Collectively, these results indicate that Pris synergized with Cis and that this may be a potential therapeutic strategy to overcome lung cancer.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2019.4057</identifier><identifier>PMID: 30664149</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Autophagy ; Autophagy - drug effects ; Breast cancer ; Cancer therapies ; Cell cycle ; Cell Cycle Checkpoints - drug effects ; Cell Line, Tumor ; Cell Survival - drug effects ; Chemotherapy ; Cisplatin - pharmacology ; Drug Synergism ; Glycogen Synthase Kinase 3 beta - metabolism ; Humans ; Kinases ; Lung cancer ; Lung Neoplasms ; Male ; Mice ; MicroRNAs - genetics ; Pancreatic cancer ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Software ; Triterpenes - pharmacology</subject><ispartof>International journal of molecular medicine, 2019-03, Vol.43 (3), p.1382-1394</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Zhang et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3337-301fd2c302240c74061feb076ac28e16812ddbb24db93de43f91ae44c16a1cf63</citedby><cites>FETCH-LOGICAL-c3337-301fd2c302240c74061feb076ac28e16812ddbb24db93de43f91ae44c16a1cf63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27926,27927</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30664149$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yingbing</creatorcontrib><creatorcontrib>Wang, Jiquan</creatorcontrib><creatorcontrib>Hui, Beina</creatorcontrib><creatorcontrib>Sun, Wenze</creatorcontrib><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Shi, Fan</creatorcontrib><creatorcontrib>Che, Shaomin</creatorcontrib><creatorcontrib>Chai, Linyan</creatorcontrib><creatorcontrib>Song, Liping</creatorcontrib><title>Pristimerin enhances the effect of cisplatin by inhibiting the miR‑23a/Akt/GSK3β signaling pathway and suppressing autophagy in lung cancer cells</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Lung cancer is a common type of cancer with a high mortality rate in China. Cisplatin (Cis) is one of the most effective broad‑spectrum chemotherapeutic drugs for the treatment of advanced lung cancer. However, Cis resistance remains an obstacle in the treatment of advanced lung cancer. Pristimerin (Pris), a naturally occurring triterpenoid quinone compound, not only possesses anticancer properties, but also enhances chemosensitivity. Therefore, the present study aimed to investigate whether Pris can enhance the chemosensitivity of lung cancer cells to Cis and identify the underlying mechanism. A Cell Counting kit‑8 and flow cytometry were used to determine cell viability, cell cycle progression and apoptosis in A549 and NCI‑H446 cells. Western blotting was used to determine cell apoptosis‑related, cell cycle‑related and autophagy‑related proteins. The results showed that Pris inhibited cell proliferation, and induced G0/G1 arrest and cell apoptosis in A549 and NCI‑H446 cells. The western blotting revealed that Pris effectively synergized with Cis to induce cell apoptosis by inhibiting the microRNA‑23a/Akt/glycogen synthase kinase 3β signaling pathway and suppressing autophagy. In vivo xenograft experiments confirmed that Pris effectively synergized with Cis to suppress tumor growth. Collectively, these results indicate that Pris synergized with Cis and that this may be a potential therapeutic strategy to overcome lung cancer.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Breast cancer</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Chemotherapy</subject><subject>Cisplatin - pharmacology</subject><subject>Drug Synergism</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lung Neoplasms</subject><subject>Male</subject><subject>Mice</subject><subject>MicroRNAs - genetics</subject><subject>Pancreatic cancer</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Software</subject><subject>Triterpenes - pharmacology</subject><issn>1107-3756</issn><issn>1791-244X</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>eNpVkUtqHDEQhoVx8CvZemkEXs-MXiNNbwzGJLaJISEPyE6o1aVpjfsVSZ0wO1_B4JPkIDlETpJW7JhkJan06S8VH0LHlMz5qmALv2nbOSO0mAuyVDvogKqCzpgQX3anPSVqxtVS7qPDGDeEsKUoVntonxMpBRXFAXp4H3xMvoXgOwxdbToLEacaMDgHNuHeYevj0Jg0AeUW-672pZ8O6z9U6z_8urtn3CzOb9Pi8uNb_vMHjn7dmSYjg0n1d7PFpqtwHIchQIy5bsbUD7VZ5zzcjFPF5s4BW2ia-BK9cKaJ8OppPUKf37z-dHE1u3l3eX1xfjOznPNpMkJdxSwnjAlilSCSOiiJksayFVC5oqyqypKJqix4BYK7ghoQwlJpqHWSH6Gzx9xhLFuoLHQpmEYPwbcmbHVvvP7_pvO1XvfftORySRSfAk6fAkL_dYSY9KYfwzR71IwqRQrGRabmj5QNfYwB3HMHSnS2qLNFnS3qbHF6cPLvv57xv9r4bzWAnds</recordid><startdate>20190301</startdate><enddate>20190301</enddate><creator>Zhang, Yingbing</creator><creator>Wang, Jiquan</creator><creator>Hui, Beina</creator><creator>Sun, Wenze</creator><creator>Li, Bin</creator><creator>Shi, Fan</creator><creator>Che, Shaomin</creator><creator>Chai, Linyan</creator><creator>Song, Liping</creator><general>Spandidos Publications UK Ltd</general><general>D.A. 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Cisplatin (Cis) is one of the most effective broad‑spectrum chemotherapeutic drugs for the treatment of advanced lung cancer. However, Cis resistance remains an obstacle in the treatment of advanced lung cancer. Pristimerin (Pris), a naturally occurring triterpenoid quinone compound, not only possesses anticancer properties, but also enhances chemosensitivity. Therefore, the present study aimed to investigate whether Pris can enhance the chemosensitivity of lung cancer cells to Cis and identify the underlying mechanism. A Cell Counting kit‑8 and flow cytometry were used to determine cell viability, cell cycle progression and apoptosis in A549 and NCI‑H446 cells. Western blotting was used to determine cell apoptosis‑related, cell cycle‑related and autophagy‑related proteins. The results showed that Pris inhibited cell proliferation, and induced G0/G1 arrest and cell apoptosis in A549 and NCI‑H446 cells. The western blotting revealed that Pris effectively synergized with Cis to induce cell apoptosis by inhibiting the microRNA‑23a/Akt/glycogen synthase kinase 3β signaling pathway and suppressing autophagy. In vivo xenograft experiments confirmed that Pris effectively synergized with Cis to suppress tumor growth. Collectively, these results indicate that Pris synergized with Cis and that this may be a potential therapeutic strategy to overcome lung cancer.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>30664149</pmid><doi>10.3892/ijmm.2019.4057</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Autophagy Autophagy - drug effects Breast cancer Cancer therapies Cell cycle Cell Cycle Checkpoints - drug effects Cell Line, Tumor Cell Survival - drug effects Chemotherapy Cisplatin - pharmacology Drug Synergism Glycogen Synthase Kinase 3 beta - metabolism Humans Kinases Lung cancer Lung Neoplasms Male Mice MicroRNAs - genetics Pancreatic cancer Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Software Triterpenes - pharmacology |
| title | Pristimerin enhances the effect of cisplatin by inhibiting the miR‑23a/Akt/GSK3β signaling pathway and suppressing autophagy in lung cancer cells |
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