Arisaema heterophyllum Blume Monomer Stigmasterol Targets PPARγ and Inhibits the Viability and Tumorigenicity of Lung Adenocarcinoma Cells NCI-H1975
To clarify the regulatory effect and molecular mechanism of Arisaema heterophyllum Blume (AhBl) monomer stigmasterol on lung adenocarcinoma in human lung adenocarcinoma cells NCI-H1975 cultured in vitro and in nude mice. Oil red O staining, free fatty acid detection, adenosine triphosphate (ATP), an...
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description | To clarify the regulatory effect and molecular mechanism of Arisaema heterophyllum Blume (AhBl) monomer stigmasterol on lung adenocarcinoma in human lung adenocarcinoma cells NCI-H1975 cultured in vitro and in nude mice. Oil red O staining, free fatty acid detection, adenosine triphosphate (ATP), and NADPH were applied to elucidate the regulatory effect of stigmasterol on the energy metabolism of NCI-H1975 cells. Simultaneously, colony formation assay and nude mouse tumorigenesis were performed to clarify the underlying mechanisms of stigmasterol on the proliferation and tumorigenesis of NCI-H1975 cells. Furthermore, peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662 was supplemented to determine the expression changes of cyclins to clarify the regulation mechanism of stigmasterol. The results revealed that stigmasterol administration markedly inhibited the viability but promoted lipid deposition of NCI-H1975 cells. Meanwhile, the reduction of cell energy metabolism affected cell proliferation and colony formation. qPCR and western blot assays indicated that stigmasterol played a role in regulating the expression of cyclins and PPARγ signaling pathway proteins. Nude mouse tumorigenesis suggested that tumor size and weight in the stigmasterol-treated group were apparently lower as compared with the control group. Tumor tissue cells developed varying degrees of degeneration and large areas of ischemic necrosis presented in the central and peripheral cells. Immunohistochemistry results revealed that Ki67 expression in the stigmasterol group was substantially inhibited, while PPARγ expression was greatly elevated as compared with the control. GW9662 could mediate the inhibitory effect of stigmasterol on NCI-H1975 cells. The current study demonstrated that stigmasterol targeted PPARγ and inhibited the viability and tumorigenicity of lung adenocarcinoma cells NCI-H1975. |
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Oil red O staining, free fatty acid detection, adenosine triphosphate (ATP), and NADPH were applied to elucidate the regulatory effect of stigmasterol on the energy metabolism of NCI-H1975 cells. Simultaneously, colony formation assay and nude mouse tumorigenesis were performed to clarify the underlying mechanisms of stigmasterol on the proliferation and tumorigenesis of NCI-H1975 cells. Furthermore, peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662 was supplemented to determine the expression changes of cyclins to clarify the regulation mechanism of stigmasterol. The results revealed that stigmasterol administration markedly inhibited the viability but promoted lipid deposition of NCI-H1975 cells. Meanwhile, the reduction of cell energy metabolism affected cell proliferation and colony formation. qPCR and western blot assays indicated that stigmasterol played a role in regulating the expression of cyclins and PPARγ signaling pathway proteins. Nude mouse tumorigenesis suggested that tumor size and weight in the stigmasterol-treated group were apparently lower as compared with the control group. Tumor tissue cells developed varying degrees of degeneration and large areas of ischemic necrosis presented in the central and peripheral cells. Immunohistochemistry results revealed that Ki67 expression in the stigmasterol group was substantially inhibited, while PPARγ expression was greatly elevated as compared with the control. GW9662 could mediate the inhibitory effect of stigmasterol on NCI-H1975 cells. The current study demonstrated that stigmasterol targeted PPARγ and inhibited the viability and tumorigenicity of lung adenocarcinoma cells NCI-H1975.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2022/5377690</identifier><identifier>PMID: 35911149</identifier><language>eng</language><publisher>New York: Hindawi</publisher><subject>Adenocarcinoma ; Adenosine triphosphate ; Apoptosis ; Arisaema heterophyllum ; Cancer therapies ; Cell culture ; Cell proliferation ; Chinese medicine ; Colonies ; Cyclins ; Degeneration ; Disease ; Drugs ; Energy metabolism ; Herbal medicine ; Herbs ; Immunohistochemistry ; Ischemia ; Lung cancer ; Metabolism ; Metastasis ; Peroxisome proliferator-activated receptors ; Pharmacology ; Signal transduction ; Tumorigenesis ; Tumorigenicity ; Tumors ; Viability</subject><ispartof>Evidence-based complementary and alternative medicine, 2022-07, Vol.2022, p.1-15</ispartof><rights>Copyright © 2022 Na Song et al.</rights><rights>Copyright © 2022 Na Song et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Na Song et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-7420ee6c5dca1b436b170b4220c32d1c5b0c9e98099f0b5271aa4f2dc2905caa3</citedby><cites>FETCH-LOGICAL-c425t-7420ee6c5dca1b436b170b4220c32d1c5b0c9e98099f0b5271aa4f2dc2905caa3</cites><orcidid>0000-0002-8101-242X ; 0000-0003-1511-8004</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/PMC9328949/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9328949/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><contributor>Baba, Shoib</contributor><creatorcontrib>Song, Na</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Lai, Zonglang</creatorcontrib><creatorcontrib>Liang, Shuting</creatorcontrib><creatorcontrib>Zou, Wenjuan</creatorcontrib><creatorcontrib>Wang, Juan</creatorcontrib><creatorcontrib>Zheng, Dandan</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>He, Yuxi</creatorcontrib><creatorcontrib>Cheng, Jun</creatorcontrib><creatorcontrib>Wu, Yue</creatorcontrib><title>Arisaema heterophyllum Blume Monomer Stigmasterol Targets PPARγ and Inhibits the Viability and Tumorigenicity of Lung Adenocarcinoma Cells NCI-H1975</title><title>Evidence-based complementary and alternative medicine</title><description>To clarify the regulatory effect and molecular mechanism of Arisaema heterophyllum Blume (AhBl) monomer stigmasterol on lung adenocarcinoma in human lung adenocarcinoma cells NCI-H1975 cultured in vitro and in nude mice. Oil red O staining, free fatty acid detection, adenosine triphosphate (ATP), and NADPH were applied to elucidate the regulatory effect of stigmasterol on the energy metabolism of NCI-H1975 cells. Simultaneously, colony formation assay and nude mouse tumorigenesis were performed to clarify the underlying mechanisms of stigmasterol on the proliferation and tumorigenesis of NCI-H1975 cells. Furthermore, peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662 was supplemented to determine the expression changes of cyclins to clarify the regulation mechanism of stigmasterol. The results revealed that stigmasterol administration markedly inhibited the viability but promoted lipid deposition of NCI-H1975 cells. Meanwhile, the reduction of cell energy metabolism affected cell proliferation and colony formation. qPCR and western blot assays indicated that stigmasterol played a role in regulating the expression of cyclins and PPARγ signaling pathway proteins. Nude mouse tumorigenesis suggested that tumor size and weight in the stigmasterol-treated group were apparently lower as compared with the control group. Tumor tissue cells developed varying degrees of degeneration and large areas of ischemic necrosis presented in the central and peripheral cells. Immunohistochemistry results revealed that Ki67 expression in the stigmasterol group was substantially inhibited, while PPARγ expression was greatly elevated as compared with the control. GW9662 could mediate the inhibitory effect of stigmasterol on NCI-H1975 cells. The current study demonstrated that stigmasterol targeted PPARγ and inhibited the viability and tumorigenicity of lung adenocarcinoma cells NCI-H1975.</description><subject>Adenocarcinoma</subject><subject>Adenosine triphosphate</subject><subject>Apoptosis</subject><subject>Arisaema heterophyllum</subject><subject>Cancer therapies</subject><subject>Cell culture</subject><subject>Cell proliferation</subject><subject>Chinese medicine</subject><subject>Colonies</subject><subject>Cyclins</subject><subject>Degeneration</subject><subject>Disease</subject><subject>Drugs</subject><subject>Energy metabolism</subject><subject>Herbal medicine</subject><subject>Herbs</subject><subject>Immunohistochemistry</subject><subject>Ischemia</subject><subject>Lung cancer</subject><subject>Metabolism</subject><subject>Metastasis</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Pharmacology</subject><subject>Signal 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heterophyllum Blume Monomer Stigmasterol Targets PPARγ and Inhibits the Viability and Tumorigenicity of Lung Adenocarcinoma Cells NCI-H1975</title><author>Song, Na ; Wang, Jing ; Lai, Zonglang ; Liang, Shuting ; Zou, Wenjuan ; Wang, Juan ; Zheng, Dandan ; Li, Ying ; He, Yuxi ; Cheng, Jun ; Wu, Yue</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c425t-7420ee6c5dca1b436b170b4220c32d1c5b0c9e98099f0b5271aa4f2dc2905caa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenocarcinoma</topic><topic>Adenosine triphosphate</topic><topic>Apoptosis</topic><topic>Arisaema heterophyllum</topic><topic>Cancer therapies</topic><topic>Cell culture</topic><topic>Cell proliferation</topic><topic>Chinese medicine</topic><topic>Colonies</topic><topic>Cyclins</topic><topic>Degeneration</topic><topic>Disease</topic><topic>Drugs</topic><topic>Energy metabolism</topic><topic>Herbal medicine</topic><topic>Herbs</topic><topic>Immunohistochemistry</topic><topic>Ischemia</topic><topic>Lung cancer</topic><topic>Metabolism</topic><topic>Metastasis</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Pharmacology</topic><topic>Signal transduction</topic><topic>Tumorigenesis</topic><topic>Tumorigenicity</topic><topic>Tumors</topic><topic>Viability</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Song, Na</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Lai, Zonglang</creatorcontrib><creatorcontrib>Liang, Shuting</creatorcontrib><creatorcontrib>Zou, Wenjuan</creatorcontrib><creatorcontrib>Wang, Juan</creatorcontrib><creatorcontrib>Zheng, Dandan</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>He, Yuxi</creatorcontrib><creatorcontrib>Cheng, Jun</creatorcontrib><creatorcontrib>Wu, Yue</creatorcontrib><collection>Hindawi Publishing 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Shoib</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Arisaema heterophyllum Blume Monomer Stigmasterol Targets PPARγ and Inhibits the Viability and Tumorigenicity of Lung Adenocarcinoma Cells NCI-H1975</atitle><jtitle>Evidence-based complementary and alternative medicine</jtitle><date>2022-07-20</date><risdate>2022</risdate><volume>2022</volume><spage>1</spage><epage>15</epage><pages>1-15</pages><issn>1741-427X</issn><eissn>1741-4288</eissn><abstract>To clarify the regulatory effect and molecular mechanism of Arisaema heterophyllum Blume (AhBl) monomer stigmasterol on lung adenocarcinoma in human lung adenocarcinoma cells NCI-H1975 cultured in vitro and in nude mice. Oil red O staining, free fatty acid detection, adenosine triphosphate (ATP), and NADPH were applied to elucidate the regulatory effect of stigmasterol on the energy metabolism of NCI-H1975 cells. Simultaneously, colony formation assay and nude mouse tumorigenesis were performed to clarify the underlying mechanisms of stigmasterol on the proliferation and tumorigenesis of NCI-H1975 cells. Furthermore, peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662 was supplemented to determine the expression changes of cyclins to clarify the regulation mechanism of stigmasterol. The results revealed that stigmasterol administration markedly inhibited the viability but promoted lipid deposition of NCI-H1975 cells. Meanwhile, the reduction of cell energy metabolism affected cell proliferation and colony formation. qPCR and western blot assays indicated that stigmasterol played a role in regulating the expression of cyclins and PPARγ signaling pathway proteins. Nude mouse tumorigenesis suggested that tumor size and weight in the stigmasterol-treated group were apparently lower as compared with the control group. Tumor tissue cells developed varying degrees of degeneration and large areas of ischemic necrosis presented in the central and peripheral cells. Immunohistochemistry results revealed that Ki67 expression in the stigmasterol group was substantially inhibited, while PPARγ expression was greatly elevated as compared with the control. GW9662 could mediate the inhibitory effect of stigmasterol on NCI-H1975 cells. The current study demonstrated that stigmasterol targeted PPARγ and inhibited the viability and tumorigenicity of lung adenocarcinoma cells NCI-H1975.</abstract><cop>New York</cop><pub>Hindawi</pub><pmid>35911149</pmid><doi>10.1155/2022/5377690</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-8101-242X</orcidid><orcidid>https://orcid.org/0000-0003-1511-8004</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adenocarcinoma Adenosine triphosphate Apoptosis Arisaema heterophyllum Cancer therapies Cell culture Cell proliferation Chinese medicine Colonies Cyclins Degeneration Disease Drugs Energy metabolism Herbal medicine Herbs Immunohistochemistry Ischemia Lung cancer Metabolism Metastasis Peroxisome proliferator-activated receptors Pharmacology Signal transduction Tumorigenesis Tumorigenicity Tumors Viability |
title | Arisaema heterophyllum Blume Monomer Stigmasterol Targets PPARγ and Inhibits the Viability and Tumorigenicity of Lung Adenocarcinoma Cells NCI-H1975 |
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