GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin‐mediated mitophagy
Few approaches have been conducted in the treatment of renal cell carcinoma (RCC) after nephrectomy, resulting in a high mortality rate in urological tumours. Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previou...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2023-08, Vol.27 (16), p.2328-2339 |
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| creator | Liu, Ting Zhu, Hengcheng Ge, Minghuan Pan, Zhou Zeng, Yan Leng, Yan Yang, Kang Cheng, Fan |
| description | Few approaches have been conducted in the treatment of renal cell carcinoma (RCC) after nephrectomy, resulting in a high mortality rate in urological tumours. Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previous studies have found that glycerol‐3‐phosphate dehydrogenase 1‐like (GPD1L) is associated with the progression of tumours such as lung cancer, colorectal cancer and oropharyngeal cancer, but the potential mechanism in RCC is still unclear. In this study, microarrays from tumour databases were analysed. The expression of GPD1L was confirmed by RT–qPCR and western blotting. The effect and mechanism of GPD1L were explored using cell counting kit 8, wound healing, invasion, flow cytometry and mitophagy‐related experiments. The role of GPD1L was further confirmed in vivo. The results showed that GPD1L expression was downregulated and positively correlated with prognosis in RCC. Functional experiments revealed that GPD1L prevented proliferation, migration and invasion while promoting apoptosis and mitochondrial injury in vitro. The mechanistic results indicated that GPD1L interacted with PINK1, promoting PINK1/Parkin‐mediated mitophagy. However, inhibition of PINK1 reversed GPD1L‐mediated mitochondrial injury and mitophagy. Moreover, GPD1L prevented tumour growth and promoted mitophagy by activating the PINK1/Parkin pathway in vivo. Our study shows that GPD1L has a positive correlation with the prognosis of RCC. The potential mechanism involves interacting with PINK1 and regulating the PINK1/Parkin pathway. In conclusion, these results reveal that GPD1L can act as a biomarker and target for RCC diagnosis and therapy. |
| doi_str_mv | 10.1111/jcmm.17813 |
| format | Article |
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Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previous studies have found that glycerol‐3‐phosphate dehydrogenase 1‐like (GPD1L) is associated with the progression of tumours such as lung cancer, colorectal cancer and oropharyngeal cancer, but the potential mechanism in RCC is still unclear. In this study, microarrays from tumour databases were analysed. The expression of GPD1L was confirmed by RT–qPCR and western blotting. The effect and mechanism of GPD1L were explored using cell counting kit 8, wound healing, invasion, flow cytometry and mitophagy‐related experiments. The role of GPD1L was further confirmed in vivo. The results showed that GPD1L expression was downregulated and positively correlated with prognosis in RCC. Functional experiments revealed that GPD1L prevented proliferation, migration and invasion while promoting apoptosis and mitochondrial injury in vitro. The mechanistic results indicated that GPD1L interacted with PINK1, promoting PINK1/Parkin‐mediated mitophagy. However, inhibition of PINK1 reversed GPD1L‐mediated mitochondrial injury and mitophagy. Moreover, GPD1L prevented tumour growth and promoted mitophagy by activating the PINK1/Parkin pathway in vivo. Our study shows that GPD1L has a positive correlation with the prognosis of RCC. The potential mechanism involves interacting with PINK1 and regulating the PINK1/Parkin pathway. In conclusion, these results reveal that GPD1L can act as a biomarker and target for RCC diagnosis and therapy.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.17813</identifier><identifier>PMID: 37382962</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Antibodies ; Apoptosis ; Bioinformatics ; Carcinoma, Renal Cell - genetics ; Cell growth ; Colorectal carcinoma ; Datasets ; Dehydrogenases ; Flow cytometry ; Glycerol ; Glycerol-3-phosphate ; Glycerol-3-phosphate dehydrogenase ; Humans ; Kidney cancer ; Kidney Neoplasms - genetics ; Lung cancer ; Medical prognosis ; Membranes ; Mitochondria ; Mitophagy ; Mitophagy - genetics ; Nephrectomy ; Original ; Oropharyngeal cancer ; Parkin protein ; Patients ; phosphate dehydrogenase 1‐like ; PINK1/Parkin pathway ; Prognosis ; Protein Kinases - genetics ; Protein Kinases - metabolism ; Proteins ; PTEN-induced putative kinase ; Quality control ; Renal cell carcinoma ; Statistical analysis ; Survival analysis ; Transmission electron microscopy ; Tumors ; Ubiquitin-Protein Ligases - genetics ; Ubiquitin-Protein Ligases - metabolism ; Western blotting ; Wound healing</subject><ispartof>Journal of cellular and molecular medicine, 2023-08, Vol.27 (16), p.2328-2339</ispartof><rights>2023 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2023. This work is published under http://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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4493-8117831c8af44a70139fe3da20132b353568f327601205ae3d29a601ed7b03383</citedby><cites>FETCH-LOGICAL-c4493-8117831c8af44a70139fe3da20132b353568f327601205ae3d29a601ed7b03383</cites><orcidid>0000-0002-3471-6221 ; 0000-0001-7595-1925</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/PMC10424287/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10424287/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37382962$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Ting</creatorcontrib><creatorcontrib>Zhu, Hengcheng</creatorcontrib><creatorcontrib>Ge, Minghuan</creatorcontrib><creatorcontrib>Pan, Zhou</creatorcontrib><creatorcontrib>Zeng, Yan</creatorcontrib><creatorcontrib>Leng, Yan</creatorcontrib><creatorcontrib>Yang, Kang</creatorcontrib><creatorcontrib>Cheng, Fan</creatorcontrib><title>GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin‐mediated mitophagy</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Few approaches have been conducted in the treatment of renal cell carcinoma (RCC) after nephrectomy, resulting in a high mortality rate in urological tumours. Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previous studies have found that glycerol‐3‐phosphate dehydrogenase 1‐like (GPD1L) is associated with the progression of tumours such as lung cancer, colorectal cancer and oropharyngeal cancer, but the potential mechanism in RCC is still unclear. In this study, microarrays from tumour databases were analysed. The expression of GPD1L was confirmed by RT–qPCR and western blotting. The effect and mechanism of GPD1L were explored using cell counting kit 8, wound healing, invasion, flow cytometry and mitophagy‐related experiments. The role of GPD1L was further confirmed in vivo. The results showed that GPD1L expression was downregulated and positively correlated with prognosis in RCC. Functional experiments revealed that GPD1L prevented proliferation, migration and invasion while promoting apoptosis and mitochondrial injury in vitro. The mechanistic results indicated that GPD1L interacted with PINK1, promoting PINK1/Parkin‐mediated mitophagy. However, inhibition of PINK1 reversed GPD1L‐mediated mitochondrial injury and mitophagy. Moreover, GPD1L prevented tumour growth and promoted mitophagy by activating the PINK1/Parkin pathway in vivo. Our study shows that GPD1L has a positive correlation with the prognosis of RCC. The potential mechanism involves interacting with PINK1 and regulating the PINK1/Parkin pathway. In conclusion, these results reveal that GPD1L can act as a biomarker and target for RCC diagnosis and therapy.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Bioinformatics</subject><subject>Carcinoma, Renal Cell - genetics</subject><subject>Cell growth</subject><subject>Colorectal carcinoma</subject><subject>Datasets</subject><subject>Dehydrogenases</subject><subject>Flow cytometry</subject><subject>Glycerol</subject><subject>Glycerol-3-phosphate</subject><subject>Glycerol-3-phosphate dehydrogenase</subject><subject>Humans</subject><subject>Kidney cancer</subject><subject>Kidney Neoplasms - genetics</subject><subject>Lung cancer</subject><subject>Medical prognosis</subject><subject>Membranes</subject><subject>Mitochondria</subject><subject>Mitophagy</subject><subject>Mitophagy - genetics</subject><subject>Nephrectomy</subject><subject>Original</subject><subject>Oropharyngeal cancer</subject><subject>Parkin protein</subject><subject>Patients</subject><subject>phosphate dehydrogenase 1‐like</subject><subject>PINK1/Parkin pathway</subject><subject>Prognosis</subject><subject>Protein Kinases - genetics</subject><subject>Protein Kinases - metabolism</subject><subject>Proteins</subject><subject>PTEN-induced putative kinase</subject><subject>Quality control</subject><subject>Renal cell carcinoma</subject><subject>Statistical analysis</subject><subject>Survival analysis</subject><subject>Transmission electron microscopy</subject><subject>Tumors</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUtu2zAQhomiQZO43fQAgYBsigBO-LJErYLCzbNO60W7JkYyJdORSJeUEniXI-SMOUnGsRu0XZQLcoj58OPDDCEfGT1meE4WZdses0wx8YbssZHiQ5kL-XZbMyXULtmPcUGpSJnI35FdkQnF85TvEX0x_cImiXVzW9guJsE4aJLSNHhBKK3zLSTL4OtgYrTeJcUKmbpvoLOuTqZX376ykymEW-ueHh5bM7PQmVnS2s4v51Cv3pOdCppoPmzfAfl5fvZjfDmcfL-4Gn-eDEuJskPF0F-wUkElJWQUNSsjZsCx4oUYiVGqKsGzlDJOR4AtngN-zCwrqBBKDMjpJnfZF2hRGtcFaPQy2BbCSnuw-u-Os3Nd-zvNqOSSqwwTPm0Tgv_Vm9jp1sb1IMAZ30fN0Y_nuUxzRA__QRe-Dzi4NSVzxSlF7wE52lBl8DEGU73aMKrXi9PrxemXxSF88Kf_K_p7UwiwDXBvG7P6T5S-Ht_cbEKfAWeLo0w</recordid><startdate>202308</startdate><enddate>202308</enddate><creator>Liu, Ting</creator><creator>Zhu, Hengcheng</creator><creator>Ge, Minghuan</creator><creator>Pan, Zhou</creator><creator>Zeng, Yan</creator><creator>Leng, Yan</creator><creator>Yang, Kang</creator><creator>Cheng, Fan</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3471-6221</orcidid><orcidid>https://orcid.org/0000-0001-7595-1925</orcidid></search><sort><creationdate>202308</creationdate><title>GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin‐mediated mitophagy</title><author>Liu, Ting ; Zhu, Hengcheng ; Ge, Minghuan ; Pan, Zhou ; Zeng, Yan ; Leng, Yan ; Yang, Kang ; Cheng, Fan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4493-8117831c8af44a70139fe3da20132b353568f327601205ae3d29a601ed7b03383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Bioinformatics</topic><topic>Carcinoma, Renal Cell - genetics</topic><topic>Cell growth</topic><topic>Colorectal carcinoma</topic><topic>Datasets</topic><topic>Dehydrogenases</topic><topic>Flow cytometry</topic><topic>Glycerol</topic><topic>Glycerol-3-phosphate</topic><topic>Glycerol-3-phosphate dehydrogenase</topic><topic>Humans</topic><topic>Kidney cancer</topic><topic>Kidney Neoplasms - genetics</topic><topic>Lung cancer</topic><topic>Medical prognosis</topic><topic>Membranes</topic><topic>Mitochondria</topic><topic>Mitophagy</topic><topic>Mitophagy - genetics</topic><topic>Nephrectomy</topic><topic>Original</topic><topic>Oropharyngeal cancer</topic><topic>Parkin protein</topic><topic>Patients</topic><topic>phosphate dehydrogenase 1‐like</topic><topic>PINK1/Parkin pathway</topic><topic>Prognosis</topic><topic>Protein Kinases - genetics</topic><topic>Protein Kinases - metabolism</topic><topic>Proteins</topic><topic>PTEN-induced putative kinase</topic><topic>Quality control</topic><topic>Renal cell carcinoma</topic><topic>Statistical analysis</topic><topic>Survival analysis</topic><topic>Transmission electron microscopy</topic><topic>Tumors</topic><topic>Ubiquitin-Protein Ligases - genetics</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><topic>Western blotting</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Ting</creatorcontrib><creatorcontrib>Zhu, Hengcheng</creatorcontrib><creatorcontrib>Ge, Minghuan</creatorcontrib><creatorcontrib>Pan, Zhou</creatorcontrib><creatorcontrib>Zeng, Yan</creatorcontrib><creatorcontrib>Leng, Yan</creatorcontrib><creatorcontrib>Yang, Kang</creatorcontrib><creatorcontrib>Cheng, Fan</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Ting</au><au>Zhu, Hengcheng</au><au>Ge, Minghuan</au><au>Pan, Zhou</au><au>Zeng, Yan</au><au>Leng, Yan</au><au>Yang, Kang</au><au>Cheng, Fan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin‐mediated mitophagy</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2023-08</date><risdate>2023</risdate><volume>27</volume><issue>16</issue><spage>2328</spage><epage>2339</epage><pages>2328-2339</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Few approaches have been conducted in the treatment of renal cell carcinoma (RCC) after nephrectomy, resulting in a high mortality rate in urological tumours. Mitophagy is a mechanism of mitochondrial quality control that enables selective degradation of damaged and unnecessary mitochondria. Previous studies have found that glycerol‐3‐phosphate dehydrogenase 1‐like (GPD1L) is associated with the progression of tumours such as lung cancer, colorectal cancer and oropharyngeal cancer, but the potential mechanism in RCC is still unclear. In this study, microarrays from tumour databases were analysed. The expression of GPD1L was confirmed by RT–qPCR and western blotting. The effect and mechanism of GPD1L were explored using cell counting kit 8, wound healing, invasion, flow cytometry and mitophagy‐related experiments. The role of GPD1L was further confirmed in vivo. The results showed that GPD1L expression was downregulated and positively correlated with prognosis in RCC. Functional experiments revealed that GPD1L prevented proliferation, migration and invasion while promoting apoptosis and mitochondrial injury in vitro. The mechanistic results indicated that GPD1L interacted with PINK1, promoting PINK1/Parkin‐mediated mitophagy. However, inhibition of PINK1 reversed GPD1L‐mediated mitochondrial injury and mitophagy. Moreover, GPD1L prevented tumour growth and promoted mitophagy by activating the PINK1/Parkin pathway in vivo. Our study shows that GPD1L has a positive correlation with the prognosis of RCC. The potential mechanism involves interacting with PINK1 and regulating the PINK1/Parkin pathway. In conclusion, these results reveal that GPD1L can act as a biomarker and target for RCC diagnosis and therapy.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>37382962</pmid><doi>10.1111/jcmm.17813</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-3471-6221</orcidid><orcidid>https://orcid.org/0000-0001-7595-1925</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies Apoptosis Bioinformatics Carcinoma, Renal Cell - genetics Cell growth Colorectal carcinoma Datasets Dehydrogenases Flow cytometry Glycerol Glycerol-3-phosphate Glycerol-3-phosphate dehydrogenase Humans Kidney cancer Kidney Neoplasms - genetics Lung cancer Medical prognosis Membranes Mitochondria Mitophagy Mitophagy - genetics Nephrectomy Original Oropharyngeal cancer Parkin protein Patients phosphate dehydrogenase 1‐like PINK1/Parkin pathway Prognosis Protein Kinases - genetics Protein Kinases - metabolism Proteins PTEN-induced putative kinase Quality control Renal cell carcinoma Statistical analysis Survival analysis Transmission electron microscopy Tumors Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism Western blotting Wound healing |
| title | GPD1L inhibits renal cell carcinoma progression by regulating PINK1/Parkin‐mediated mitophagy |
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