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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Vydané v:	Neoplasia (New York, N.Y.) Ročník 61; s. 101138
Hlavní autori:	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:	English
Vydavateľské údaje:	United States Elsevier Inc 01.03.2025 Elsevier
Predmet:	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
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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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