Downregulated CCND3 Is a Key Event Driving Lung Adenocarcinoma Metastasis during Acquired Cisplatin Resistance
Cyclin D3 (CCND3), a member of the cyclin D family, is known to promote cell cycle transition. In this study, we found that CCND3 was downregulated in cisplatin-resistant ( -diamminedichloroplatinum, DDP) lung adenocarcinoma (LUAD) cells. The loss of CCND3 indeed impeded cell cycle transition. Unexp...
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| Veröffentlicht in: | International journal of biological sciences 2025, Vol.21 (2), p.708-724 |
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| creator | Su, Yun Ma, Yuting Wang, Yubing Xu, Ping Guo, Miaoling Cao, Haolin Xin, Jianyang Wu, Xi Liu, Xiaoyan Chen, Shan Tao, Xingyu Yang, Huiling Cheng, Chao Huang, Rongquan Pan, Rongshuai Pan, Yuexin Zhou, Beixian Fang, Weiyi Liu, Zhen |
| description | Cyclin D3 (CCND3), a member of the cyclin D family, is known to promote cell cycle transition. In this study, we found that CCND3 was downregulated in cisplatin-resistant (
-diamminedichloroplatinum, DDP) lung adenocarcinoma (LUAD) cells. The loss of CCND3 indeed impeded cell cycle transition. Unexpectedly, its downregulation significantly triggered cytoskeleton remodeling and chemoresistance and accelerated LUAD metastasis
and
. Moreover, the clinical samples showed a significant negative correlation between CCND3 expression and lymphatic metastasis, as well as the unfavorable survival prognosis of patients with LUAD. Mechanistically, CCND3 downregulation in DDP-resistant LUAD cells was attributable to the transcriptional suppression of PI3K/Akt/c-Jun signaling. Reduced CCND3 expression diminished the recruitment of the E3 ubiquitin ligase PARK2 to ubiquitinate and degrade the vimentin protein, thus triggering epithelial-mesenchymal transition (EMT) to result in cytoskeleton remodeling-stimulated metastasis and chemotherapeutic resistance in LUAD. These results demonstrated that activated PI3K/Akt/c-Jun significantly suppressed CCND3 expression, thereby inhibiting vimentin degradation via PARK2-mediated ubiquitination in DDP-resistant LUAD cells. This, in turn, promoted EMT, facilitating cytoskeleton remodeling-stimulated metastasis and chemoresistance to DDP. Overall, these findings provided a new perspective on the role of CCND3 in LUAD progression and acquired cisplatin resistance. |
| doi_str_mv | 10.7150/ijbs.100921 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11705650</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3153913650</sourcerecordid><originalsourceid>FETCH-LOGICAL-c1851-12a7ab654dbc1ccd2f3f2d32582b1a138e6294957814bb58ce4768c50d99eca33</originalsourceid><addsrcrecordid>eNpVkdFr2zAQh0XZaNN2T3svehyUdDrJsqWnEpKuDctWGNuzkOVLpuLIiWSn5L-fTdKSgZAE9_HdHT9CPgO7K0Cyr_6lTHfAmOZwRkaQZXrMuVIfTv4X5DKlF8ZELhU7JxdCFwqyXI9ImDWvIeKqq22LFZ1Of84EnSdq6Xfc04cdhpbOot_5sKKLrr8mFYbG2eh8aNaW_sDWpv74RKsuDtTEbTsfB5dPm97qA_2Ffb21weE1-bi0dcJPx_eK_Pn28Hv6NF48P86nk8XYgZIwBm4LW-Yyq0oHzlV8KZa8ElwqXoIFoTDnOtNy2KIspXKYFblyklVao7NCXJH7g3fTlWusXL9GtLXZRL-2cW8a683_leD_mlWzMwAFk7lkveHL0RCbbYepNWufHNa1Ddh0yQiQQoM4oLcH1MUmpYjL9z7AzBCRGSIyh4h6-uZ0tHf2LRPxD0uGjjg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3153913650</pqid></control><display><type>article</type><title>Downregulated CCND3 Is a Key Event Driving Lung Adenocarcinoma Metastasis during Acquired Cisplatin Resistance</title><source>MEDLINE</source><source>PubMed Central Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Su, Yun ; Ma, Yuting ; Wang, Yubing ; Xu, Ping ; Guo, Miaoling ; Cao, Haolin ; Xin, Jianyang ; Wu, Xi ; Liu, Xiaoyan ; Chen, Shan ; Tao, Xingyu ; Yang, Huiling ; Cheng, Chao ; Huang, Rongquan ; Pan, Rongshuai ; Pan, Yuexin ; Zhou, Beixian ; Fang, Weiyi ; Liu, Zhen</creator><creatorcontrib>Su, Yun ; Ma, Yuting ; Wang, Yubing ; Xu, Ping ; Guo, Miaoling ; Cao, Haolin ; Xin, Jianyang ; Wu, Xi ; Liu, Xiaoyan ; Chen, Shan ; Tao, Xingyu ; Yang, Huiling ; Cheng, Chao ; Huang, Rongquan ; Pan, Rongshuai ; Pan, Yuexin ; Zhou, Beixian ; Fang, Weiyi ; Liu, Zhen</creatorcontrib><description>Cyclin D3 (CCND3), a member of the cyclin D family, is known to promote cell cycle transition. In this study, we found that CCND3 was downregulated in cisplatin-resistant (
-diamminedichloroplatinum, DDP) lung adenocarcinoma (LUAD) cells. The loss of CCND3 indeed impeded cell cycle transition. Unexpectedly, its downregulation significantly triggered cytoskeleton remodeling and chemoresistance and accelerated LUAD metastasis
and
. Moreover, the clinical samples showed a significant negative correlation between CCND3 expression and lymphatic metastasis, as well as the unfavorable survival prognosis of patients with LUAD. Mechanistically, CCND3 downregulation in DDP-resistant LUAD cells was attributable to the transcriptional suppression of PI3K/Akt/c-Jun signaling. Reduced CCND3 expression diminished the recruitment of the E3 ubiquitin ligase PARK2 to ubiquitinate and degrade the vimentin protein, thus triggering epithelial-mesenchymal transition (EMT) to result in cytoskeleton remodeling-stimulated metastasis and chemotherapeutic resistance in LUAD. These results demonstrated that activated PI3K/Akt/c-Jun significantly suppressed CCND3 expression, thereby inhibiting vimentin degradation via PARK2-mediated ubiquitination in DDP-resistant LUAD cells. This, in turn, promoted EMT, facilitating cytoskeleton remodeling-stimulated metastasis and chemoresistance to DDP. Overall, these findings provided a new perspective on the role of CCND3 in LUAD progression and acquired cisplatin resistance.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.100921</identifier><identifier>PMID: 39781469</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - genetics ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; Adenocarcinoma of Lung - drug therapy ; Adenocarcinoma of Lung - genetics ; Adenocarcinoma of Lung - metabolism ; Adenocarcinoma of Lung - pathology ; Animals ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Cell Line, Tumor ; Cisplatin - pharmacology ; Cisplatin - therapeutic use ; Cyclin D3 - genetics ; Cyclin D3 - metabolism ; Down-Regulation ; Drug Resistance, Neoplasm - genetics ; Epithelial-Mesenchymal Transition ; Female ; Humans ; Lung Neoplasms - drug therapy ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Mice ; Mice, Nude ; Research Paper</subject><ispartof>International journal of biological sciences, 2025, Vol.21 (2), p.708-724</ispartof><rights>The author(s).</rights><rights>The author(s) 2025</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705650/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11705650/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,883,4012,27910,27911,27912,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39781469$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Su, Yun</creatorcontrib><creatorcontrib>Ma, Yuting</creatorcontrib><creatorcontrib>Wang, Yubing</creatorcontrib><creatorcontrib>Xu, Ping</creatorcontrib><creatorcontrib>Guo, Miaoling</creatorcontrib><creatorcontrib>Cao, Haolin</creatorcontrib><creatorcontrib>Xin, Jianyang</creatorcontrib><creatorcontrib>Wu, Xi</creatorcontrib><creatorcontrib>Liu, Xiaoyan</creatorcontrib><creatorcontrib>Chen, Shan</creatorcontrib><creatorcontrib>Tao, Xingyu</creatorcontrib><creatorcontrib>Yang, Huiling</creatorcontrib><creatorcontrib>Cheng, Chao</creatorcontrib><creatorcontrib>Huang, Rongquan</creatorcontrib><creatorcontrib>Pan, Rongshuai</creatorcontrib><creatorcontrib>Pan, Yuexin</creatorcontrib><creatorcontrib>Zhou, Beixian</creatorcontrib><creatorcontrib>Fang, Weiyi</creatorcontrib><creatorcontrib>Liu, Zhen</creatorcontrib><title>Downregulated CCND3 Is a Key Event Driving Lung Adenocarcinoma Metastasis during Acquired Cisplatin Resistance</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>Cyclin D3 (CCND3), a member of the cyclin D family, is known to promote cell cycle transition. In this study, we found that CCND3 was downregulated in cisplatin-resistant (
-diamminedichloroplatinum, DDP) lung adenocarcinoma (LUAD) cells. The loss of CCND3 indeed impeded cell cycle transition. Unexpectedly, its downregulation significantly triggered cytoskeleton remodeling and chemoresistance and accelerated LUAD metastasis
and
. Moreover, the clinical samples showed a significant negative correlation between CCND3 expression and lymphatic metastasis, as well as the unfavorable survival prognosis of patients with LUAD. Mechanistically, CCND3 downregulation in DDP-resistant LUAD cells was attributable to the transcriptional suppression of PI3K/Akt/c-Jun signaling. Reduced CCND3 expression diminished the recruitment of the E3 ubiquitin ligase PARK2 to ubiquitinate and degrade the vimentin protein, thus triggering epithelial-mesenchymal transition (EMT) to result in cytoskeleton remodeling-stimulated metastasis and chemotherapeutic resistance in LUAD. These results demonstrated that activated PI3K/Akt/c-Jun significantly suppressed CCND3 expression, thereby inhibiting vimentin degradation via PARK2-mediated ubiquitination in DDP-resistant LUAD cells. This, in turn, promoted EMT, facilitating cytoskeleton remodeling-stimulated metastasis and chemoresistance to DDP. Overall, these findings provided a new perspective on the role of CCND3 in LUAD progression and acquired cisplatin resistance.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>Adenocarcinoma of Lung - drug therapy</subject><subject>Adenocarcinoma of Lung - genetics</subject><subject>Adenocarcinoma of Lung - metabolism</subject><subject>Adenocarcinoma of Lung - pathology</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Cell Line, Tumor</subject><subject>Cisplatin - pharmacology</subject><subject>Cisplatin - therapeutic use</subject><subject>Cyclin D3 - genetics</subject><subject>Cyclin D3 - metabolism</subject><subject>Down-Regulation</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>Humans</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Research Paper</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkdFr2zAQh0XZaNN2T3svehyUdDrJsqWnEpKuDctWGNuzkOVLpuLIiWSn5L-fTdKSgZAE9_HdHT9CPgO7K0Cyr_6lTHfAmOZwRkaQZXrMuVIfTv4X5DKlF8ZELhU7JxdCFwqyXI9ImDWvIeKqq22LFZ1Of84EnSdq6Xfc04cdhpbOot_5sKKLrr8mFYbG2eh8aNaW_sDWpv74RKsuDtTEbTsfB5dPm97qA_2Ffb21weE1-bi0dcJPx_eK_Pn28Hv6NF48P86nk8XYgZIwBm4LW-Yyq0oHzlV8KZa8ElwqXoIFoTDnOtNy2KIspXKYFblyklVao7NCXJH7g3fTlWusXL9GtLXZRL-2cW8a683_leD_mlWzMwAFk7lkveHL0RCbbYepNWufHNa1Ddh0yQiQQoM4oLcH1MUmpYjL9z7AzBCRGSIyh4h6-uZ0tHf2LRPxD0uGjjg</recordid><startdate>2025</startdate><enddate>2025</enddate><creator>Su, Yun</creator><creator>Ma, Yuting</creator><creator>Wang, Yubing</creator><creator>Xu, Ping</creator><creator>Guo, Miaoling</creator><creator>Cao, Haolin</creator><creator>Xin, Jianyang</creator><creator>Wu, Xi</creator><creator>Liu, Xiaoyan</creator><creator>Chen, Shan</creator><creator>Tao, Xingyu</creator><creator>Yang, Huiling</creator><creator>Cheng, Chao</creator><creator>Huang, Rongquan</creator><creator>Pan, Rongshuai</creator><creator>Pan, Yuexin</creator><creator>Zhou, Beixian</creator><creator>Fang, Weiyi</creator><creator>Liu, Zhen</creator><general>Ivyspring International Publisher</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>2025</creationdate><title>Downregulated CCND3 Is a Key Event Driving Lung Adenocarcinoma Metastasis during Acquired Cisplatin Resistance</title><author>Su, Yun ; Ma, Yuting ; Wang, Yubing ; Xu, Ping ; Guo, Miaoling ; Cao, Haolin ; Xin, Jianyang ; Wu, Xi ; Liu, Xiaoyan ; Chen, Shan ; Tao, Xingyu ; Yang, Huiling ; Cheng, Chao ; Huang, Rongquan ; Pan, Rongshuai ; Pan, Yuexin ; Zhou, Beixian ; Fang, Weiyi ; Liu, Zhen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1851-12a7ab654dbc1ccd2f3f2d32582b1a138e6294957814bb58ce4768c50d99eca33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2025</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>Adenocarcinoma of Lung - drug therapy</topic><topic>Adenocarcinoma of Lung - genetics</topic><topic>Adenocarcinoma of Lung - metabolism</topic><topic>Adenocarcinoma of Lung - pathology</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Cell Line, Tumor</topic><topic>Cisplatin - pharmacology</topic><topic>Cisplatin - therapeutic use</topic><topic>Cyclin D3 - genetics</topic><topic>Cyclin D3 - metabolism</topic><topic>Down-Regulation</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Female</topic><topic>Humans</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Research Paper</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Su, Yun</creatorcontrib><creatorcontrib>Ma, Yuting</creatorcontrib><creatorcontrib>Wang, Yubing</creatorcontrib><creatorcontrib>Xu, Ping</creatorcontrib><creatorcontrib>Guo, Miaoling</creatorcontrib><creatorcontrib>Cao, Haolin</creatorcontrib><creatorcontrib>Xin, Jianyang</creatorcontrib><creatorcontrib>Wu, Xi</creatorcontrib><creatorcontrib>Liu, Xiaoyan</creatorcontrib><creatorcontrib>Chen, Shan</creatorcontrib><creatorcontrib>Tao, Xingyu</creatorcontrib><creatorcontrib>Yang, Huiling</creatorcontrib><creatorcontrib>Cheng, Chao</creatorcontrib><creatorcontrib>Huang, Rongquan</creatorcontrib><creatorcontrib>Pan, Rongshuai</creatorcontrib><creatorcontrib>Pan, Yuexin</creatorcontrib><creatorcontrib>Zhou, Beixian</creatorcontrib><creatorcontrib>Fang, Weiyi</creatorcontrib><creatorcontrib>Liu, Zhen</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Su, Yun</au><au>Ma, Yuting</au><au>Wang, Yubing</au><au>Xu, Ping</au><au>Guo, Miaoling</au><au>Cao, Haolin</au><au>Xin, Jianyang</au><au>Wu, Xi</au><au>Liu, Xiaoyan</au><au>Chen, Shan</au><au>Tao, Xingyu</au><au>Yang, Huiling</au><au>Cheng, Chao</au><au>Huang, Rongquan</au><au>Pan, Rongshuai</au><au>Pan, Yuexin</au><au>Zhou, Beixian</au><au>Fang, Weiyi</au><au>Liu, Zhen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Downregulated CCND3 Is a Key Event Driving Lung Adenocarcinoma Metastasis during Acquired Cisplatin Resistance</atitle><jtitle>International journal of biological sciences</jtitle><addtitle>Int J Biol Sci</addtitle><date>2025</date><risdate>2025</risdate><volume>21</volume><issue>2</issue><spage>708</spage><epage>724</epage><pages>708-724</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>Cyclin D3 (CCND3), a member of the cyclin D family, is known to promote cell cycle transition. In this study, we found that CCND3 was downregulated in cisplatin-resistant (
-diamminedichloroplatinum, DDP) lung adenocarcinoma (LUAD) cells. The loss of CCND3 indeed impeded cell cycle transition. Unexpectedly, its downregulation significantly triggered cytoskeleton remodeling and chemoresistance and accelerated LUAD metastasis
and
. Moreover, the clinical samples showed a significant negative correlation between CCND3 expression and lymphatic metastasis, as well as the unfavorable survival prognosis of patients with LUAD. Mechanistically, CCND3 downregulation in DDP-resistant LUAD cells was attributable to the transcriptional suppression of PI3K/Akt/c-Jun signaling. Reduced CCND3 expression diminished the recruitment of the E3 ubiquitin ligase PARK2 to ubiquitinate and degrade the vimentin protein, thus triggering epithelial-mesenchymal transition (EMT) to result in cytoskeleton remodeling-stimulated metastasis and chemotherapeutic resistance in LUAD. These results demonstrated that activated PI3K/Akt/c-Jun significantly suppressed CCND3 expression, thereby inhibiting vimentin degradation via PARK2-mediated ubiquitination in DDP-resistant LUAD cells. This, in turn, promoted EMT, facilitating cytoskeleton remodeling-stimulated metastasis and chemoresistance to DDP. Overall, these findings provided a new perspective on the role of CCND3 in LUAD progression and acquired cisplatin resistance.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher</pub><pmid>39781469</pmid><doi>10.7150/ijbs.100921</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - genetics Adenocarcinoma - metabolism Adenocarcinoma - pathology Adenocarcinoma of Lung - drug therapy Adenocarcinoma of Lung - genetics Adenocarcinoma of Lung - metabolism Adenocarcinoma of Lung - pathology Animals Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Cell Line, Tumor Cisplatin - pharmacology Cisplatin - therapeutic use Cyclin D3 - genetics Cyclin D3 - metabolism Down-Regulation Drug Resistance, Neoplasm - genetics Epithelial-Mesenchymal Transition Female Humans Lung Neoplasms - drug therapy Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology Mice Mice, Nude Research Paper |
| title | Downregulated CCND3 Is a Key Event Driving Lung Adenocarcinoma Metastasis during Acquired Cisplatin Resistance |
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