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EGFR-mediated Rad51 expression potentiates intrinsic resistance in prostate cancer via EMT and DNA repair pathways
To study the role of EGFR signaling in regulation of intrinsic resistance in prostate cancer. Radioresistant prostate carcinoma DU145 and PC-3 cells were used to study the effect of shRNA-mediated knockdown of EGFR on intrinsic radioresistance mechanisms. Semi-quantitative PCR, western blotting, gro...
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| Published in: | Life sciences (1973) 2021-12, Vol.286, p.120031-120031, Article 120031 |
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| container_title | Life sciences (1973) |
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| creator | Rajput, Mohit Singh, Ragini Singh, Navneendra Singh, Rana P. |
| description | To study the role of EGFR signaling in regulation of intrinsic resistance in prostate cancer.
Radioresistant prostate carcinoma DU145 and PC-3 cells were used to study the effect of shRNA-mediated knockdown of EGFR on intrinsic radioresistance mechanisms. Semi-quantitative PCR, western blotting, growth kinetics, colony formation, transwell migration, invasion and trypan blue assays along with inhibitors erlotinib, NU7441, B02, PD98059 and LY294002 were used.
EGFR knock-down induced morphological alterations along with reduction in clonogenic potential and cell proliferation in DU145 cells. Migratory potential of prostate cancer cells were reduced concomitant with upregulation of epithelial marker, E-cadherin and decreased expression of mesenchymal markers, vimentin and snail. Further, EGFR knock-down decreased the expression of Rad51 and DNA-PK at mRNA as well as protein levels. Likewise, erlotinib, an EGFR inhibitor, and NU7441, a DNA-PK inhibitor increased the expression of E-cadherin and decreased the level of vimentin. Both these inhibitors also decreased the levels of DNA damage regulatory protein Rad51. Further, Rad51 inhibitor, B02, inhibited the clonogenic potential, cell migration and reduced the expression of vimentin, Ku70 and Ku80, and also, B02 radiosensitized DU145 cells. EGFR-regulated expression of Rad51 was found to be mediated via PI3K/Akt and Erk1/2 pathways.
EGFR was found to regulate DNA damage repair, survival and EMT responses in prostate cancer cells through transcriptional regulation of Rad51. A novel role of EGFR-Erk1/2/Akt-Rad51 axis through modulation of EMT and DNA repair pathways in prostate cancer resistance mechanisms is suggested.
[Display omitted]
•EGFR regulates intrinsic resistance in prostate cancer (PCa) through Rad51.•EGFR-Rad51 regulates DNA damage repair, survival and EMT in PCa.•Kinase regulates mRNA and protein level of Rad51 and DNA-PK.•Rad51 inhibitor, B02, inhibited clonogenic and migration potential of resistant PCa cells. |
| doi_str_mv | 10.1016/j.lfs.2021.120031 |
| format | article |
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Radioresistant prostate carcinoma DU145 and PC-3 cells were used to study the effect of shRNA-mediated knockdown of EGFR on intrinsic radioresistance mechanisms. Semi-quantitative PCR, western blotting, growth kinetics, colony formation, transwell migration, invasion and trypan blue assays along with inhibitors erlotinib, NU7441, B02, PD98059 and LY294002 were used.
EGFR knock-down induced morphological alterations along with reduction in clonogenic potential and cell proliferation in DU145 cells. Migratory potential of prostate cancer cells were reduced concomitant with upregulation of epithelial marker, E-cadherin and decreased expression of mesenchymal markers, vimentin and snail. Further, EGFR knock-down decreased the expression of Rad51 and DNA-PK at mRNA as well as protein levels. Likewise, erlotinib, an EGFR inhibitor, and NU7441, a DNA-PK inhibitor increased the expression of E-cadherin and decreased the level of vimentin. Both these inhibitors also decreased the levels of DNA damage regulatory protein Rad51. Further, Rad51 inhibitor, B02, inhibited the clonogenic potential, cell migration and reduced the expression of vimentin, Ku70 and Ku80, and also, B02 radiosensitized DU145 cells. EGFR-regulated expression of Rad51 was found to be mediated via PI3K/Akt and Erk1/2 pathways.
EGFR was found to regulate DNA damage repair, survival and EMT responses in prostate cancer cells through transcriptional regulation of Rad51. A novel role of EGFR-Erk1/2/Akt-Rad51 axis through modulation of EMT and DNA repair pathways in prostate cancer resistance mechanisms is suggested.
[Display omitted]
•EGFR regulates intrinsic resistance in prostate cancer (PCa) through Rad51.•EGFR-Rad51 regulates DNA damage repair, survival and EMT in PCa.•Kinase regulates mRNA and protein level of Rad51 and DNA-PK.•Rad51 inhibitor, B02, inhibited clonogenic and migration potential of resistant PCa cells.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2021.120031</identifier><identifier>PMID: 34627777</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Biomarkers ; Cell migration ; Cell proliferation ; Chromones - pharmacology ; Damage ; Deoxyribonucleic acid ; DNA ; DNA Damage ; DNA damage repair ; DNA Repair ; DNA-dependent protein kinase ; Drug Resistance, Neoplasm - drug effects ; E-cadherin ; EGFR ; EMT ; Epidermal growth factor receptors ; Epithelial-Mesenchymal Transition - drug effects ; ErbB Receptors - genetics ; ErbB Receptors - metabolism ; Erlotinib Hydrochloride - pharmacology ; Gene expression ; Gene regulation ; Growth kinetics ; Humans ; Inhibitors ; Male ; Mesenchyme ; Morpholines - pharmacology ; Prostate cancer ; Prostate carcinoma ; Prostatic Neoplasms - pathology ; Proteins ; Rad51 ; Rad51 Recombinase - metabolism ; Radioresistance ; Repair ; Transcription ; Vimentin ; Western blotting</subject><ispartof>Life sciences (1973), 2021-12, Vol.286, p.120031-120031, Article 120031</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-c447t-85a4b6dba6acaef2e6ba8c90cd9dac1d5c0aad8c814dc80c4dd8f81a63fa6c963</citedby><cites>FETCH-LOGICAL-c447t-85a4b6dba6acaef2e6ba8c90cd9dac1d5c0aad8c814dc80c4dd8f81a63fa6c963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34627777$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rajput, Mohit</creatorcontrib><creatorcontrib>Singh, Ragini</creatorcontrib><creatorcontrib>Singh, Navneendra</creatorcontrib><creatorcontrib>Singh, Rana P.</creatorcontrib><title>EGFR-mediated Rad51 expression potentiates intrinsic resistance in prostate cancer via EMT and DNA repair pathways</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>To study the role of EGFR signaling in regulation of intrinsic resistance in prostate cancer.
Radioresistant prostate carcinoma DU145 and PC-3 cells were used to study the effect of shRNA-mediated knockdown of EGFR on intrinsic radioresistance mechanisms. Semi-quantitative PCR, western blotting, growth kinetics, colony formation, transwell migration, invasion and trypan blue assays along with inhibitors erlotinib, NU7441, B02, PD98059 and LY294002 were used.
EGFR knock-down induced morphological alterations along with reduction in clonogenic potential and cell proliferation in DU145 cells. Migratory potential of prostate cancer cells were reduced concomitant with upregulation of epithelial marker, E-cadherin and decreased expression of mesenchymal markers, vimentin and snail. Further, EGFR knock-down decreased the expression of Rad51 and DNA-PK at mRNA as well as protein levels. Likewise, erlotinib, an EGFR inhibitor, and NU7441, a DNA-PK inhibitor increased the expression of E-cadherin and decreased the level of vimentin. Both these inhibitors also decreased the levels of DNA damage regulatory protein Rad51. Further, Rad51 inhibitor, B02, inhibited the clonogenic potential, cell migration and reduced the expression of vimentin, Ku70 and Ku80, and also, B02 radiosensitized DU145 cells. EGFR-regulated expression of Rad51 was found to be mediated via PI3K/Akt and Erk1/2 pathways.
EGFR was found to regulate DNA damage repair, survival and EMT responses in prostate cancer cells through transcriptional regulation of Rad51. A novel role of EGFR-Erk1/2/Akt-Rad51 axis through modulation of EMT and DNA repair pathways in prostate cancer resistance mechanisms is suggested.
[Display omitted]
•EGFR regulates intrinsic resistance in prostate cancer (PCa) through Rad51.•EGFR-Rad51 regulates DNA damage repair, survival and EMT in PCa.•Kinase regulates mRNA and protein level of Rad51 and DNA-PK.•Rad51 inhibitor, B02, inhibited clonogenic and migration potential of resistant PCa cells.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Biomarkers</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Chromones - pharmacology</subject><subject>Damage</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>DNA damage repair</subject><subject>DNA Repair</subject><subject>DNA-dependent protein kinase</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>E-cadherin</subject><subject>EGFR</subject><subject>EMT</subject><subject>Epidermal growth factor receptors</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>ErbB Receptors - genetics</subject><subject>ErbB Receptors - metabolism</subject><subject>Erlotinib Hydrochloride - pharmacology</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Growth kinetics</subject><subject>Humans</subject><subject>Inhibitors</subject><subject>Male</subject><subject>Mesenchyme</subject><subject>Morpholines - pharmacology</subject><subject>Prostate cancer</subject><subject>Prostate carcinoma</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proteins</subject><subject>Rad51</subject><subject>Rad51 Recombinase - metabolism</subject><subject>Radioresistance</subject><subject>Repair</subject><subject>Transcription</subject><subject>Vimentin</subject><subject>Western blotting</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kUFvEzEQhS0EakPpD-CCLHHhsunYXjtecaratCAVkKpytib2rHCU7C6209J_j6O0HDjUF8sz3zyN32PsvYC5AGHO1vNNn-cSpJgLCaDEKzYTdtE1YJR4zWYAsm2UBH3M3ua8BgCtF-qIHavWyEU9M5aW11e3zZZCxEKB32LQgtOfKVHOcRz4NBYayr6ZeRxKikOOntduzAUHT7XIpzTWRyHu95XE7yPy5bc7jkPgl9_PKz1hTHzC8usBH_M79qbHTabTp_uE_bxa3l18aW5-XH-9OL9pfNsuSmM1tisTVmjQI_WSzAqt78CHLqAXQXtADNZb0QZvwbch2N4KNKpH4zujTting27d7_eOcnHbmD1tNjjQuMtOagtdq6ojFf34H7oed2mo2zlpQBvdSdVVShwoXz-cE_VuSnGL6dEJcPtA3NrVQNw-EHcIpM58eFLerarL_yaeE6jA5wNA1Yr7SMllH6n6GGIiX1wY4wvyfwH5-Jyg</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Rajput, Mohit</creator><creator>Singh, Ragini</creator><creator>Singh, Navneendra</creator><creator>Singh, Rana P.</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>EGFR-mediated Rad51 expression potentiates intrinsic resistance in prostate cancer via EMT and DNA repair pathways</title><author>Rajput, Mohit ; Singh, Ragini ; Singh, Navneendra ; Singh, Rana P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-85a4b6dba6acaef2e6ba8c90cd9dac1d5c0aad8c814dc80c4dd8f81a63fa6c963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Biomarkers</topic><topic>Cell migration</topic><topic>Cell proliferation</topic><topic>Chromones - pharmacology</topic><topic>Damage</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>DNA damage repair</topic><topic>DNA Repair</topic><topic>DNA-dependent protein kinase</topic><topic>Drug Resistance, Neoplasm - drug effects</topic><topic>E-cadherin</topic><topic>EGFR</topic><topic>EMT</topic><topic>Epidermal growth factor receptors</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>ErbB Receptors - genetics</topic><topic>ErbB Receptors - metabolism</topic><topic>Erlotinib Hydrochloride - pharmacology</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Growth kinetics</topic><topic>Humans</topic><topic>Inhibitors</topic><topic>Male</topic><topic>Mesenchyme</topic><topic>Morpholines - pharmacology</topic><topic>Prostate cancer</topic><topic>Prostate carcinoma</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proteins</topic><topic>Rad51</topic><topic>Rad51 Recombinase - metabolism</topic><topic>Radioresistance</topic><topic>Repair</topic><topic>Transcription</topic><topic>Vimentin</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rajput, Mohit</creatorcontrib><creatorcontrib>Singh, Ragini</creatorcontrib><creatorcontrib>Singh, Navneendra</creatorcontrib><creatorcontrib>Singh, Rana P.</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>Rajput, Mohit</au><au>Singh, Ragini</au><au>Singh, Navneendra</au><au>Singh, Rana P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EGFR-mediated Rad51 expression potentiates intrinsic resistance in prostate cancer via EMT and DNA repair pathways</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>286</volume><spage>120031</spage><epage>120031</epage><pages>120031-120031</pages><artnum>120031</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>To study the role of EGFR signaling in regulation of intrinsic resistance in prostate cancer.
Radioresistant prostate carcinoma DU145 and PC-3 cells were used to study the effect of shRNA-mediated knockdown of EGFR on intrinsic radioresistance mechanisms. Semi-quantitative PCR, western blotting, growth kinetics, colony formation, transwell migration, invasion and trypan blue assays along with inhibitors erlotinib, NU7441, B02, PD98059 and LY294002 were used.
EGFR knock-down induced morphological alterations along with reduction in clonogenic potential and cell proliferation in DU145 cells. Migratory potential of prostate cancer cells were reduced concomitant with upregulation of epithelial marker, E-cadherin and decreased expression of mesenchymal markers, vimentin and snail. Further, EGFR knock-down decreased the expression of Rad51 and DNA-PK at mRNA as well as protein levels. Likewise, erlotinib, an EGFR inhibitor, and NU7441, a DNA-PK inhibitor increased the expression of E-cadherin and decreased the level of vimentin. Both these inhibitors also decreased the levels of DNA damage regulatory protein Rad51. Further, Rad51 inhibitor, B02, inhibited the clonogenic potential, cell migration and reduced the expression of vimentin, Ku70 and Ku80, and also, B02 radiosensitized DU145 cells. EGFR-regulated expression of Rad51 was found to be mediated via PI3K/Akt and Erk1/2 pathways.
EGFR was found to regulate DNA damage repair, survival and EMT responses in prostate cancer cells through transcriptional regulation of Rad51. A novel role of EGFR-Erk1/2/Akt-Rad51 axis through modulation of EMT and DNA repair pathways in prostate cancer resistance mechanisms is suggested.
[Display omitted]
•EGFR regulates intrinsic resistance in prostate cancer (PCa) through Rad51.•EGFR-Rad51 regulates DNA damage repair, survival and EMT in PCa.•Kinase regulates mRNA and protein level of Rad51 and DNA-PK.•Rad51 inhibitor, B02, inhibited clonogenic and migration potential of resistant PCa cells.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>34627777</pmid><doi>10.1016/j.lfs.2021.120031</doi><tpages>1</tpages></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Biomarkers Cell migration Cell proliferation Chromones - pharmacology Damage Deoxyribonucleic acid DNA DNA Damage DNA damage repair DNA Repair DNA-dependent protein kinase Drug Resistance, Neoplasm - drug effects E-cadherin EGFR EMT Epidermal growth factor receptors Epithelial-Mesenchymal Transition - drug effects ErbB Receptors - genetics ErbB Receptors - metabolism Erlotinib Hydrochloride - pharmacology Gene expression Gene regulation Growth kinetics Humans Inhibitors Male Mesenchyme Morpholines - pharmacology Prostate cancer Prostate carcinoma Prostatic Neoplasms - pathology Proteins Rad51 Rad51 Recombinase - metabolism Radioresistance Repair Transcription Vimentin Western blotting |
| title | EGFR-mediated Rad51 expression potentiates intrinsic resistance in prostate cancer via EMT and DNA repair pathways |
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