MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability

Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate of just 13 %. Conventional therapies fail due to acquired chemoresistance. We previously identified MutY-Homolog (MYH), a protein that repairs oxidative DNA damage, as a therapeutic target that induces apoptosis in PDAC cells. H...

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Vydáno v:	Neoplasia (New York, N.Y.) Ročník 61; s. 101138
Hlavní autoři:	Ephraums, James, Youkhana, Janet, Raina, Aparna S., Schulstad, Grace, Croft, Kento, Mawson, Amanda, Kokkinos, John, Gonzales-Aloy, Estrella, Ignacio, Rosa Mistica C., McCarroll, Joshua A., Boyer, Cyrille, Goldstein, David, Pajic, Marina, Haghighi, Koroush S., Johns, Amber, Gill, Anthony J., Erkan, Mert, Initiative (APGI), Australian Pancreatic Cancer Genome, Phillips, Phoebe A., Sharbeen, George
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Elsevier Inc 01.03.2025 Elsevier
Témata:	Animals Antineoplastic Agents - pharmacology Apoptosis - drug effects Apoptosis - genetics Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor Cell Proliferation - drug effects Chemosensitisation Disease Models, Animal DNA Damage DNA Glycosylases - genetics DNA Glycosylases - metabolism DNA repair DNA Repair - genetics Gene Knockdown Techniques Humans Mice Oxaliplatin Oxidative stress Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Phthalazines - pharmacology Piperazines - pharmacology RNA, Small Interfering - genetics Xenograft Model Antitumor Assays Oxidative stress Chemosensitisation DNA repair Pancreatic cancer
ISSN:	1476-5586, 1476-5586
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Abstract	Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate of just 13 %. Conventional therapies fail due to acquired chemoresistance. We previously identified MutY-Homolog (MYH), a protein that repairs oxidative DNA damage, as a therapeutic target that induces apoptosis in PDAC cells. However, we did not understand the mechanism driving these anti-PDAC effects, nor did we have a means to therapeutically inhibit MYH. In this study, we demonstrated that MYH inhibition induces DNA damage and checkpoint activation in PDAC cells. Using a clinically-relevant PDAC mouse model, we showed that therapeutic MYH-siRNA delivery using Star 3 nanoparticles increased intratumoural PDAC cell death, but did not inhibit tumour growth. Finally, we showed that MYH knockdown in PDAC cells sensitised them to the anti-proliferative and anti-clonogenic effects of oxaliplatin and olaparib. Our findings identify a potential novel therapeutic approach for PDAC that induces a therapeutically exploitable DNA repair vulnerability.
AbstractList	Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate of just 13 %. Conventional therapies fail due to acquired chemoresistance. We previously identified MutY-Homolog (MYH), a protein that repairs oxidative DNA damage, as a therapeutic target that induces apoptosis in PDAC cells. However, we did not understand the mechanism driving these anti-PDAC effects, nor did we have a means to therapeutically inhibit MYH. In this study, we demonstrated that MYH inhibition induces DNA damage and checkpoint activation in PDAC cells. Using a clinically-relevant PDAC mouse model, we showed that therapeutic MYH-siRNA delivery using Star 3 nanoparticles increased intratumoural PDAC cell death, but did not inhibit tumour growth. Finally, we showed that MYH knockdown in PDAC cells sensitised them to the anti-proliferative and anti-clonogenic effects of oxaliplatin and olaparib. Our findings identify a potential novel therapeutic approach for PDAC that induces a therapeutically exploitable DNA repair vulnerability. Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate of just 13 %. Conventional therapies fail due to acquired chemoresistance. We previously identified MutY-Homolog (MYH), a protein that repairs oxidative DNA damage, as a therapeutic target that induces apoptosis in PDAC cells. However, we did not understand the mechanism driving these anti-PDAC effects, nor did we have a means to therapeutically inhibit MYH. In this study, we demonstrated that MYH inhibition induces DNA damage and checkpoint activation in PDAC cells. Using a clinically-relevant PDAC mouse model, we showed that therapeutic MYH-siRNA delivery using Star 3 nanoparticles increased intratumoural PDAC cell death, but did not inhibit tumour growth. Finally, we showed that MYH knockdown in PDAC cells sensitised them to the anti-proliferative and anti-clonogenic effects of oxaliplatin and olaparib. Our findings identify a potential novel therapeutic approach for PDAC that induces a therapeutically exploitable DNA repair vulnerability.Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate of just 13 %. Conventional therapies fail due to acquired chemoresistance. We previously identified MutY-Homolog (MYH), a protein that repairs oxidative DNA damage, as a therapeutic target that induces apoptosis in PDAC cells. However, we did not understand the mechanism driving these anti-PDAC effects, nor did we have a means to therapeutically inhibit MYH. In this study, we demonstrated that MYH inhibition induces DNA damage and checkpoint activation in PDAC cells. Using a clinically-relevant PDAC mouse model, we showed that therapeutic MYH-siRNA delivery using Star 3 nanoparticles increased intratumoural PDAC cell death, but did not inhibit tumour growth. Finally, we showed that MYH knockdown in PDAC cells sensitised them to the anti-proliferative and anti-clonogenic effects of oxaliplatin and olaparib. Our findings identify a potential novel therapeutic approach for PDAC that induces a therapeutically exploitable DNA repair vulnerability.
ArticleNumber	101138
Author	Youkhana, Janet Gonzales-Aloy, Estrella Mawson, Amanda McCarroll, Joshua A. Boyer, Cyrille Haghighi, Koroush S. Sharbeen, George Ephraums, James Pajic, Marina Schulstad, Grace Croft, Kento Ignacio, Rosa Mistica C. Gill, Anthony J. Erkan, Mert Initiative (APGI), Australian Pancreatic Cancer Genome Phillips, Phoebe A. Raina, Aparna S. Johns, Amber Goldstein, David Kokkinos, John
Author_xml	– sequence: 1 givenname: James surname: Ephraums fullname: Ephraums, James organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 2 givenname: Janet surname: Youkhana fullname: Youkhana, Janet organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 3 givenname: Aparna S. surname: Raina fullname: Raina, Aparna S. organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 4 givenname: Grace orcidid: 0000-0001-9854-6375 surname: Schulstad fullname: Schulstad, Grace organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 5 givenname: Kento orcidid: 0009-0002-0926-5219 surname: Croft fullname: Croft, Kento organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 6 givenname: Amanda orcidid: 0000-0002-2534-6492 surname: Mawson fullname: Mawson, Amanda organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 7 givenname: John orcidid: 0000-0002-9819-2404 surname: Kokkinos fullname: Kokkinos, John organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 8 givenname: Estrella orcidid: 0000-0003-4323-2904 surname: Gonzales-Aloy fullname: Gonzales-Aloy, Estrella organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 9 givenname: Rosa Mistica C. orcidid: 0000-0002-5343-4190 surname: Ignacio fullname: Ignacio, Rosa Mistica C. organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 10 givenname: Joshua A. surname: McCarroll fullname: McCarroll, Joshua A. organization: Australian Centre for Nanomedicine (ACN), UNSW Sydney, Australia – sequence: 11 givenname: Cyrille surname: Boyer fullname: Boyer, Cyrille organization: Australian Centre for Nanomedicine (ACN), UNSW Sydney, Australia – sequence: 12 givenname: David surname: Goldstein fullname: Goldstein, David organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 13 givenname: Marina surname: Pajic fullname: Pajic, Marina organization: The Kinghorn Cancer Centre, Garvan Institute of Medical Research; NSW 2010, Australia – sequence: 14 givenname: Koroush S. surname: Haghighi fullname: Haghighi, Koroush S. organization: Prince of Wales Hospital, School of Clinical Medicine, Randwick Clinical Campus, UNSW Sydney; NSW 2052, Australia – sequence: 15 givenname: Amber surname: Johns fullname: Johns, Amber organization: Garvan Institute of Medical Research; NSW 2010, Australia – sequence: 16 givenname: Anthony J. surname: Gill fullname: Gill, Anthony J. organization: The Kinghorn Cancer Centre, Garvan Institute of Medical Research; NSW 2010, Australia – sequence: 17 givenname: Mert orcidid: 0000-0002-2753-0234 surname: Erkan fullname: Erkan, Mert organization: Mehmet Ali Aydinlar Acibadem University, Atakent University Hospital; Istanbul 34303, Turkey – sequence: 18 givenname: Australian Pancreatic Cancer Genome surname: Initiative (APGI) fullname: Initiative (APGI), Australian Pancreatic Cancer Genome organization: Australian Pancreatic Cancer Genome Initiative (APGI), Garvan Institute of Medical Research; NSW 2010, Australia – sequence: 19 givenname: Phoebe A. surname: Phillips fullname: Phillips, Phoebe A. email: p.phillips@unsw.edu.au organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia – sequence: 20 givenname: George orcidid: 0000-0002-6373-1930 surname: Sharbeen fullname: Sharbeen, George email: g.sharbeen@unsw.edu.au organization: Pancreatic Cancer Translational Research Group, School of Biomedical Sciences, Lowy Cancer Research Centre, UNSW Sydney; NSW 2052, Australia
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Keywords	Oxidative stress Chemosensitisation DNA repair Pancreatic cancer
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Snippet	Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year survival rate of just 13 %. Conventional therapies fail due to acquired chemoresistance. We...
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SubjectTerms	Animals Antineoplastic Agents - pharmacology Apoptosis - drug effects Apoptosis - genetics Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor Cell Proliferation - drug effects Chemosensitisation Disease Models, Animal DNA Damage DNA Glycosylases - genetics DNA Glycosylases - metabolism DNA repair DNA Repair - genetics Gene Knockdown Techniques Humans Mice Oxaliplatin Oxidative stress Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Phthalazines - pharmacology Piperazines - pharmacology RNA, Small Interfering - genetics Xenograft Model Antitumor Assays
Title	MYH knockdown in pancreatic cancer cells creates an exploitable DNA repair vulnerability
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