Palmitic acid inhibits prostate cancer cell proliferation and metastasis by suppressing the PI3K/Akt pathway
Prostate cancer is one of the most frequent causes of cancer death in men worldwide, and novel drugs for prostate cancer therapies are still being developed. Palmitic acid is a common saturated long-chain fatty acid that is known to exhibit anti-inflammatory and metabolic regulatory effects and anti...
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| Veröffentlicht in: | Life sciences (1973) 2021-12, Vol.286, p.120046-120046, Article 120046 |
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| container_title | Life sciences (1973) |
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| creator | Zhu, Shan Jiao, Wenhui Xu, Yanglu Hou, Lanjiao Li, Hui Shao, Jingrong Zhang, Xiaoliang Wang, Ran Kong, Dexin |
| description | Prostate cancer is one of the most frequent causes of cancer death in men worldwide, and novel drugs for prostate cancer therapies are still being developed. Palmitic acid is a common saturated long-chain fatty acid that is known to exhibit anti-inflammatory and metabolic regulatory effects and antitumor activities in several types of tumors. The present study aims to explore the antiproliferative and antimetastatic activities of palmitic acid on human prostate cancer cells and the underlying mechanism.
MTT and colony formation assays were utilized to determine the antiproliferative effect of palmitic acid. Cell metastasis was evaluated by wound healing, Transwell migration and invasion assay. The in vivo anticancer effect was assessed by a nude mouse xenograft model of prostate cancer. The involved molecular mechanisms were investigated by flow cytometry and Western blot analysis.
Palmitic acid significantly suppressed prostate cancer cell growth in vitro and in vivo. Treatment with palmitic acid induced G1 phase arrest, which was associated with downregulation of cyclin D1 and p-Rb and upregulation of p27. In addition, palmitic acid could inhibit prostate cancer cell metastasis, in which suppression of PKCζ and p-Integrinβ1 and an increase in E-cadherin expression might be involved. Furthermore, a mechanistic study indicated that palmitic acid inhibited the key molecules of the PI3K/Akt pathway to block prostate cancer proliferation and metastasis.
Our findings suggested the antitumor potential of palmitic acid for prostate cancer by targeting the PI3K/Akt pathway. |
| doi_str_mv | 10.1016/j.lfs.2021.120046 |
| format | Article |
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MTT and colony formation assays were utilized to determine the antiproliferative effect of palmitic acid. Cell metastasis was evaluated by wound healing, Transwell migration and invasion assay. The in vivo anticancer effect was assessed by a nude mouse xenograft model of prostate cancer. The involved molecular mechanisms were investigated by flow cytometry and Western blot analysis.
Palmitic acid significantly suppressed prostate cancer cell growth in vitro and in vivo. Treatment with palmitic acid induced G1 phase arrest, which was associated with downregulation of cyclin D1 and p-Rb and upregulation of p27. In addition, palmitic acid could inhibit prostate cancer cell metastasis, in which suppression of PKCζ and p-Integrinβ1 and an increase in E-cadherin expression might be involved. Furthermore, a mechanistic study indicated that palmitic acid inhibited the key molecules of the PI3K/Akt pathway to block prostate cancer proliferation and metastasis.
Our findings suggested the antitumor potential of palmitic acid for prostate cancer by targeting the PI3K/Akt pathway.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2021.120046</identifier><identifier>PMID: 34653428</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animals ; Anticancer properties ; Antiproliferatives ; Antitumor activity ; Apoptosis - drug effects ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell proliferation ; Cell Proliferation - drug effects ; China ; Cyclin D1 ; E-cadherin ; Fatty acids ; Flow cytometry ; G1 phase ; Humans ; Inflammation ; Male ; Metastases ; Metastasis ; Mice ; Mice, Nude ; Molecular modelling ; Neoplasm Invasiveness - prevention & control ; Neoplasm Metastasis - drug therapy ; Palmitic acid ; Palmitic Acid - metabolism ; Palmitic Acid - pharmacology ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K/Akt pathway ; Proliferation ; Prostate cancer ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Protein kinase C ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - drug effects ; Tumors ; Wound healing ; Xenograft Model Antitumor Assays ; Xenografts ; Xenotransplantation</subject><ispartof>Life sciences (1973), 2021-12, Vol.286, p.120046-120046, Article 120046</ispartof><rights>2021 Elsevier Inc.</rights><rights>Copyright © 2021 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Dec 1, 2021</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-66f1a6054e85de192e1dca42ecc5c3068e6fd0c0b1d9b5d1df15c14eaae92ee63</citedby><cites>FETCH-LOGICAL-c381t-66f1a6054e85de192e1dca42ecc5c3068e6fd0c0b1d9b5d1df15c14eaae92ee63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2021.120046$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34653428$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Shan</creatorcontrib><creatorcontrib>Jiao, Wenhui</creatorcontrib><creatorcontrib>Xu, Yanglu</creatorcontrib><creatorcontrib>Hou, Lanjiao</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Shao, Jingrong</creatorcontrib><creatorcontrib>Zhang, Xiaoliang</creatorcontrib><creatorcontrib>Wang, Ran</creatorcontrib><creatorcontrib>Kong, Dexin</creatorcontrib><title>Palmitic acid inhibits prostate cancer cell proliferation and metastasis by suppressing the PI3K/Akt pathway</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Prostate cancer is one of the most frequent causes of cancer death in men worldwide, and novel drugs for prostate cancer therapies are still being developed. Palmitic acid is a common saturated long-chain fatty acid that is known to exhibit anti-inflammatory and metabolic regulatory effects and antitumor activities in several types of tumors. The present study aims to explore the antiproliferative and antimetastatic activities of palmitic acid on human prostate cancer cells and the underlying mechanism.
MTT and colony formation assays were utilized to determine the antiproliferative effect of palmitic acid. Cell metastasis was evaluated by wound healing, Transwell migration and invasion assay. The in vivo anticancer effect was assessed by a nude mouse xenograft model of prostate cancer. The involved molecular mechanisms were investigated by flow cytometry and Western blot analysis.
Palmitic acid significantly suppressed prostate cancer cell growth in vitro and in vivo. Treatment with palmitic acid induced G1 phase arrest, which was associated with downregulation of cyclin D1 and p-Rb and upregulation of p27. In addition, palmitic acid could inhibit prostate cancer cell metastasis, in which suppression of PKCζ and p-Integrinβ1 and an increase in E-cadherin expression might be involved. Furthermore, a mechanistic study indicated that palmitic acid inhibited the key molecules of the PI3K/Akt pathway to block prostate cancer proliferation and metastasis.
Our findings suggested the antitumor potential of palmitic acid for prostate cancer by targeting the PI3K/Akt pathway.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animals</subject><subject>Anticancer properties</subject><subject>Antiproliferatives</subject><subject>Antitumor activity</subject><subject>Apoptosis - drug effects</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>China</subject><subject>Cyclin D1</subject><subject>E-cadherin</subject><subject>Fatty acids</subject><subject>Flow cytometry</subject><subject>G1 phase</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Male</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Molecular modelling</subject><subject>Neoplasm Invasiveness - prevention & control</subject><subject>Neoplasm Metastasis - drug therapy</subject><subject>Palmitic acid</subject><subject>Palmitic Acid - metabolism</subject><subject>Palmitic Acid - pharmacology</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K/Akt pathway</subject><subject>Proliferation</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Protein kinase C</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Tumors</subject><subject>Wound healing</subject><subject>Xenograft Model Antitumor Assays</subject><subject>Xenografts</subject><subject>Xenotransplantation</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtrHDEQhIVJsNePH-BLEOSSy6xb0kieISdj4gcxxAf7LDRSj1ebeUXSJOy_j4Z1cvDBp4bm66K6ipBzBmsGTF1s110b1xw4WzMOUKoDsmLVZV2AEuwDWQHwshAc5BE5jnELAFJeikNyJEolRcmrFekeTdf75C011jvqh41vfIp0CmNMJiG1ZrAYqMWuW5adbzGY5MeBmsHRHpPJXPSRNjsa52kKGKMfXmjaIH28F98vrn4mOpm0-WN2p-Rja7qIZ6_zhDzffHu6viseftzeX189FFZULBVKtcwokCVW0iGrOTJnTcnRWmkFqApV68BCw1zdSMdcy6RlJRqDmUUlTsiXvW42_GvGmHTv4_KBGXCco-ay4hXUNS8z-vkNuh3nMGR3mmcLStaKL4JsT9kcSwzY6in43oSdZqCXKvRW5yr0UoXeV5FvPr0qz02P7v_Fv-wz8HUPYI7it8ego_WY03Y-oE3ajf4d-b9A9Jpv</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Zhu, Shan</creator><creator>Jiao, Wenhui</creator><creator>Xu, Yanglu</creator><creator>Hou, Lanjiao</creator><creator>Li, Hui</creator><creator>Shao, Jingrong</creator><creator>Zhang, Xiaoliang</creator><creator>Wang, Ran</creator><creator>Kong, Dexin</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20211201</creationdate><title>Palmitic acid inhibits prostate cancer cell proliferation and metastasis by suppressing the PI3K/Akt pathway</title><author>Zhu, Shan ; Jiao, Wenhui ; Xu, Yanglu ; Hou, Lanjiao ; Li, Hui ; Shao, Jingrong ; Zhang, Xiaoliang ; Wang, Ran ; Kong, Dexin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-66f1a6054e85de192e1dca42ecc5c3068e6fd0c0b1d9b5d1df15c14eaae92ee63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animals</topic><topic>Anticancer properties</topic><topic>Antiproliferatives</topic><topic>Antitumor activity</topic><topic>Apoptosis - drug effects</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>China</topic><topic>Cyclin D1</topic><topic>E-cadherin</topic><topic>Fatty acids</topic><topic>Flow cytometry</topic><topic>G1 phase</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Male</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Molecular modelling</topic><topic>Neoplasm Invasiveness - prevention & control</topic><topic>Neoplasm Metastasis - drug therapy</topic><topic>Palmitic acid</topic><topic>Palmitic Acid - metabolism</topic><topic>Palmitic Acid - pharmacology</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K/Akt pathway</topic><topic>Proliferation</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Protein kinase C</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Tumors</topic><topic>Wound healing</topic><topic>Xenograft Model Antitumor Assays</topic><topic>Xenografts</topic><topic>Xenotransplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Shan</creatorcontrib><creatorcontrib>Jiao, Wenhui</creatorcontrib><creatorcontrib>Xu, Yanglu</creatorcontrib><creatorcontrib>Hou, Lanjiao</creatorcontrib><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Shao, Jingrong</creatorcontrib><creatorcontrib>Zhang, Xiaoliang</creatorcontrib><creatorcontrib>Wang, Ran</creatorcontrib><creatorcontrib>Kong, Dexin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Shan</au><au>Jiao, Wenhui</au><au>Xu, Yanglu</au><au>Hou, Lanjiao</au><au>Li, Hui</au><au>Shao, Jingrong</au><au>Zhang, Xiaoliang</au><au>Wang, Ran</au><au>Kong, Dexin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Palmitic acid inhibits prostate cancer cell proliferation and metastasis by suppressing the PI3K/Akt pathway</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>286</volume><spage>120046</spage><epage>120046</epage><pages>120046-120046</pages><artnum>120046</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Prostate cancer is one of the most frequent causes of cancer death in men worldwide, and novel drugs for prostate cancer therapies are still being developed. Palmitic acid is a common saturated long-chain fatty acid that is known to exhibit anti-inflammatory and metabolic regulatory effects and antitumor activities in several types of tumors. The present study aims to explore the antiproliferative and antimetastatic activities of palmitic acid on human prostate cancer cells and the underlying mechanism.
MTT and colony formation assays were utilized to determine the antiproliferative effect of palmitic acid. Cell metastasis was evaluated by wound healing, Transwell migration and invasion assay. The in vivo anticancer effect was assessed by a nude mouse xenograft model of prostate cancer. The involved molecular mechanisms were investigated by flow cytometry and Western blot analysis.
Palmitic acid significantly suppressed prostate cancer cell growth in vitro and in vivo. Treatment with palmitic acid induced G1 phase arrest, which was associated with downregulation of cyclin D1 and p-Rb and upregulation of p27. In addition, palmitic acid could inhibit prostate cancer cell metastasis, in which suppression of PKCζ and p-Integrinβ1 and an increase in E-cadherin expression might be involved. Furthermore, a mechanistic study indicated that palmitic acid inhibited the key molecules of the PI3K/Akt pathway to block prostate cancer proliferation and metastasis.
Our findings suggested the antitumor potential of palmitic acid for prostate cancer by targeting the PI3K/Akt pathway.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>34653428</pmid><doi>10.1016/j.lfs.2021.120046</doi><tpages>1</tpages></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animals Anticancer properties Antiproliferatives Antitumor activity Apoptosis - drug effects Cell growth Cell Line, Tumor Cell Movement - genetics Cell proliferation Cell Proliferation - drug effects China Cyclin D1 E-cadherin Fatty acids Flow cytometry G1 phase Humans Inflammation Male Metastases Metastasis Mice Mice, Nude Molecular modelling Neoplasm Invasiveness - prevention & control Neoplasm Metastasis - drug therapy Palmitic acid Palmitic Acid - metabolism Palmitic Acid - pharmacology Phosphatidylinositol 3-Kinases - metabolism PI3K/Akt pathway Proliferation Prostate cancer Prostatic Neoplasms - drug therapy Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Protein kinase C Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects Tumors Wound healing Xenograft Model Antitumor Assays Xenografts Xenotransplantation |
| title | Palmitic acid inhibits prostate cancer cell proliferation and metastasis by suppressing the PI3K/Akt pathway |
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