Down-regulation of ACACA suppresses the malignant progression of Prostate Cancer through inhibiting mitochondrial potential
Silencing the expression of ACACA inhibits cell proliferation and induces apoptosis in prostate cancer LNCaP cells. However, the role of ACACA in other prostate cancer cells is not fully understood. Also, the effect of knocking down ACACA gene on mitochondria remains unclear. This study aimed to dis...
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| Veröffentlicht in: | Journal of Cancer 2021, Vol.12 (1), p.232-243 |
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| creator | Zhang, Hui Liu, Shaoyou Cai, Zhouda Dong, Weimin Ye, Jianheng Cai, Zhiduan Han, Zhaodong Liang, Yuxiang Zhuo, Yangjia Luo, Yong Zhu, Xuejin Deng, Yulin Zhang, Yixun Liu, Ren Feng, Yuanfa Lai, Jiarun Zhou, Rui Tan, Huijing Zhong, Weide |
| description | Silencing the expression of ACACA inhibits cell proliferation and induces apoptosis in prostate cancer LNCaP cells. However, the role of ACACA in other prostate cancer cells is not fully understood. Also, the effect of knocking down ACACA gene on mitochondria remains unclear. This study aimed to discover the specific role of ACACA gene in prostate cancer (PCa) DU145 and PC3 cells as well as its effects on mitochondrial potential.
The expression of ACACA gene was detected in human prostate cancer tissue microarrays and assessed in different clinical stages. Then, prostate cancer cell lines with low expression of ACACA were constructed to evaluate the changes in their cell cycle, proliferation, and metabolites. The effect of ACACA on tumor formation
was analyzed. Also, mito-ATP production, mitochondrial staining, and mtDNA, nicotinamide adenine dinucleotide (NAD+/NADH), and reactive oxygen species (ROS) levels were detected.
ACACA was expressed more strongly in prostate cancer tissues. The expression level of ACACA was higher in patients with advanced PCa than in patients with lower grades. The proliferation ability reduced in ACACA-knockdown cells. In
tests, the tumor volume and weight were lower in the experimental group than in the control group. Mito-ATP production decreased significantly after ACACA suppression, mtDNA levels and MitoTracker staining decreased in the experimental group. The ratio of NAD+/NADH and ROS levels were upregulated in the experimental group.
Targeting ACACA gene and mitochondria might serve as a novel therapy for prostate cancer treatment. |
| doi_str_mv | 10.7150/jca.49560 |
| format | Article |
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The expression of ACACA gene was detected in human prostate cancer tissue microarrays and assessed in different clinical stages. Then, prostate cancer cell lines with low expression of ACACA were constructed to evaluate the changes in their cell cycle, proliferation, and metabolites. The effect of ACACA on tumor formation
was analyzed. Also, mito-ATP production, mitochondrial staining, and mtDNA, nicotinamide adenine dinucleotide (NAD+/NADH), and reactive oxygen species (ROS) levels were detected.
ACACA was expressed more strongly in prostate cancer tissues. The expression level of ACACA was higher in patients with advanced PCa than in patients with lower grades. The proliferation ability reduced in ACACA-knockdown cells. In
tests, the tumor volume and weight were lower in the experimental group than in the control group. Mito-ATP production decreased significantly after ACACA suppression, mtDNA levels and MitoTracker staining decreased in the experimental group. The ratio of NAD+/NADH and ROS levels were upregulated in the experimental group.
Targeting ACACA gene and mitochondria might serve as a novel therapy for prostate cancer treatment.</description><identifier>ISSN: 1837-9664</identifier><identifier>EISSN: 1837-9664</identifier><identifier>DOI: 10.7150/jca.49560</identifier><identifier>PMID: 33391420</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Androgens ; Bioenergetics ; Breast cancer ; Cell cycle ; Enzymes ; Fatty acids ; Gene expression ; Kinases ; Laboratory animals ; Liver cancer ; Mitochondria ; Mitochondrial DNA ; Phosphorylation ; Polymerase chain reaction ; Prostate cancer ; Reactive oxygen species ; Research Paper ; Tumors</subject><ispartof>Journal of Cancer, 2021, Vol.12 (1), p.232-243</ispartof><rights>The author(s).</rights><rights>2021. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c403t-20f40d65b83195dfc887f43fb8adeb90fa98c35be0e1c6adc1c240d06c86a3103</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738814/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7738814/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,4012,27906,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33391420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Hui</creatorcontrib><creatorcontrib>Liu, Shaoyou</creatorcontrib><creatorcontrib>Cai, Zhouda</creatorcontrib><creatorcontrib>Dong, Weimin</creatorcontrib><creatorcontrib>Ye, Jianheng</creatorcontrib><creatorcontrib>Cai, Zhiduan</creatorcontrib><creatorcontrib>Han, Zhaodong</creatorcontrib><creatorcontrib>Liang, Yuxiang</creatorcontrib><creatorcontrib>Zhuo, Yangjia</creatorcontrib><creatorcontrib>Luo, Yong</creatorcontrib><creatorcontrib>Zhu, Xuejin</creatorcontrib><creatorcontrib>Deng, Yulin</creatorcontrib><creatorcontrib>Zhang, Yixun</creatorcontrib><creatorcontrib>Liu, Ren</creatorcontrib><creatorcontrib>Feng, Yuanfa</creatorcontrib><creatorcontrib>Lai, Jiarun</creatorcontrib><creatorcontrib>Zhou, Rui</creatorcontrib><creatorcontrib>Tan, Huijing</creatorcontrib><creatorcontrib>Zhong, Weide</creatorcontrib><title>Down-regulation of ACACA suppresses the malignant progression of Prostate Cancer through inhibiting mitochondrial potential</title><title>Journal of Cancer</title><addtitle>J Cancer</addtitle><description>Silencing the expression of ACACA inhibits cell proliferation and induces apoptosis in prostate cancer LNCaP cells. However, the role of ACACA in other prostate cancer cells is not fully understood. Also, the effect of knocking down ACACA gene on mitochondria remains unclear. This study aimed to discover the specific role of ACACA gene in prostate cancer (PCa) DU145 and PC3 cells as well as its effects on mitochondrial potential.
The expression of ACACA gene was detected in human prostate cancer tissue microarrays and assessed in different clinical stages. Then, prostate cancer cell lines with low expression of ACACA were constructed to evaluate the changes in their cell cycle, proliferation, and metabolites. The effect of ACACA on tumor formation
was analyzed. Also, mito-ATP production, mitochondrial staining, and mtDNA, nicotinamide adenine dinucleotide (NAD+/NADH), and reactive oxygen species (ROS) levels were detected.
ACACA was expressed more strongly in prostate cancer tissues. The expression level of ACACA was higher in patients with advanced PCa than in patients with lower grades. The proliferation ability reduced in ACACA-knockdown cells. In
tests, the tumor volume and weight were lower in the experimental group than in the control group. Mito-ATP production decreased significantly after ACACA suppression, mtDNA levels and MitoTracker staining decreased in the experimental group. The ratio of NAD+/NADH and ROS levels were upregulated in the experimental group.
Targeting ACACA gene and mitochondria might serve as a novel therapy for prostate cancer treatment.</description><subject>Androgens</subject><subject>Bioenergetics</subject><subject>Breast cancer</subject><subject>Cell cycle</subject><subject>Enzymes</subject><subject>Fatty acids</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Liver cancer</subject><subject>Mitochondria</subject><subject>Mitochondrial DNA</subject><subject>Phosphorylation</subject><subject>Polymerase chain reaction</subject><subject>Prostate cancer</subject><subject>Reactive oxygen species</subject><subject>Research Paper</subject><subject>Tumors</subject><issn>1837-9664</issn><issn>1837-9664</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpdkU1PxCAQhonRqNE9-AcMiRc9dIVCW3oxMetnYqIHPRNKacumhQpUY_zzsroaFQ5MMs-8zMwLwAFG8wJn6HQpxZyWWY42wC5mpEjKPKebv-IdMPN-ieIhZVpQsg12CCElpinaBe8X9tUkTrVTL4K2BtoGni_ihX4aR6e8Vx6GTsFB9Lo1wgQ4OtuuEmv6wVkfRFBwIYxULsLOTm0Htel0pYM2LRx0sLKzpnZa9HC0QZkQo32w1Yjeq9n63QNPV5ePi5vk7v76dnF-l0iKSEhS1FBU51nFCC6zupGMFQ0lTcVEraoSNaJkkmSVQgrLXNQSyzQWoFyyXBCMyB44-9Idp2pQtYy_O9Hz0elBuDduheZ_M0Z3vLUvvCgIY5hGgeO1gLPPk_KBD9pL1ffCKDt5ntIiQywr0hV69A9d2smZOB5PszJOwKIJkTr5omRcnneq-WkGI75ylUdX-aerkT383f0P-e0h-QAZHqBu</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Zhang, Hui</creator><creator>Liu, Shaoyou</creator><creator>Cai, Zhouda</creator><creator>Dong, Weimin</creator><creator>Ye, Jianheng</creator><creator>Cai, Zhiduan</creator><creator>Han, Zhaodong</creator><creator>Liang, Yuxiang</creator><creator>Zhuo, Yangjia</creator><creator>Luo, Yong</creator><creator>Zhu, Xuejin</creator><creator>Deng, Yulin</creator><creator>Zhang, Yixun</creator><creator>Liu, Ren</creator><creator>Feng, Yuanfa</creator><creator>Lai, Jiarun</creator><creator>Zhou, Rui</creator><creator>Tan, Huijing</creator><creator>Zhong, Weide</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2021</creationdate><title>Down-regulation of ACACA suppresses the malignant progression of Prostate Cancer through inhibiting mitochondrial potential</title><author>Zhang, Hui ; 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However, the role of ACACA in other prostate cancer cells is not fully understood. Also, the effect of knocking down ACACA gene on mitochondria remains unclear. This study aimed to discover the specific role of ACACA gene in prostate cancer (PCa) DU145 and PC3 cells as well as its effects on mitochondrial potential.
The expression of ACACA gene was detected in human prostate cancer tissue microarrays and assessed in different clinical stages. Then, prostate cancer cell lines with low expression of ACACA were constructed to evaluate the changes in their cell cycle, proliferation, and metabolites. The effect of ACACA on tumor formation
was analyzed. Also, mito-ATP production, mitochondrial staining, and mtDNA, nicotinamide adenine dinucleotide (NAD+/NADH), and reactive oxygen species (ROS) levels were detected.
ACACA was expressed more strongly in prostate cancer tissues. The expression level of ACACA was higher in patients with advanced PCa than in patients with lower grades. The proliferation ability reduced in ACACA-knockdown cells. In
tests, the tumor volume and weight were lower in the experimental group than in the control group. Mito-ATP production decreased significantly after ACACA suppression, mtDNA levels and MitoTracker staining decreased in the experimental group. The ratio of NAD+/NADH and ROS levels were upregulated in the experimental group.
Targeting ACACA gene and mitochondria might serve as a novel therapy for prostate cancer treatment.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>33391420</pmid><doi>10.7150/jca.49560</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Androgens Bioenergetics Breast cancer Cell cycle Enzymes Fatty acids Gene expression Kinases Laboratory animals Liver cancer Mitochondria Mitochondrial DNA Phosphorylation Polymerase chain reaction Prostate cancer Reactive oxygen species Research Paper Tumors |
| title | Down-regulation of ACACA suppresses the malignant progression of Prostate Cancer through inhibiting mitochondrial potential |
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