Extracellular DNA promotes colorectal tumor cell survival after cytotoxic chemotherapy
Inflammation promotes the growth and survival of malignant cells. Inflammation within the tumor microenvironment is a result of damage-associated molecular patterns released by dead or dying cells that provide survival signals to the surrounding cells. It has been proposed that extracellular DNA can...
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| Published in | The Journal of surgical research Vol. 226; pp. 181 - 191 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.06.2018
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| Abstract | Inflammation promotes the growth and survival of malignant cells. Inflammation within the tumor microenvironment is a result of damage-associated molecular patterns released by dead or dying cells that provide survival signals to the surrounding cells. It has been proposed that extracellular DNA can act as a damage-associated molecular pattern given the association between circulating DNA and autoimmune diseases. Herein, we demonstrate a novel role for genomic extracellular DNA binding to the Toll-like receptor (TLR)-9 on tumor cells in response to cytotoxic insult.
The colorectal tumor cell line HCCT116 was used to study the role of DNA in tumor cell response to chemotherapy. Cell viability was assessed using CCK-8 assay. Cell death mechanisms were assessed by YOYO-1 and lactate dehydrogenase staining for necrosis and TUNEL staining for apoptosis. Autophagy was measured by LC3 punctate formation. TLR9-short hairpin RNA was used to knockdown TLR-9 and determine its role in tumor cell response to DNA.
DNA is released from necrotic tumor cells after chemotherapy. Survival after cytotoxic insult is enhanced by the presence of extracellular DNA as a result of inhibition of apoptosis and enhanced autophagy. Knockdown of TLR-9 enhanced apoptosis, diminished autophagy, and decreased survival after cytotoxic insult in the presence or absence of extracellular DNA.
DNA in the tumor microenvironment promotes survival through induction of autophagy via TLR-9 signaling. This work has important implications for targeting extracellular DNA, TLR-9, and autophagy during treatment with chemotherapy and enhances our understanding of the role of extracellular DNA in the tumor microenvironment. |
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| AbstractList | Inflammation promotes the growth and survival of malignant cells. Inflammation within the tumor microenvironment is a result of damage-associated molecular patterns released by dead or dying cells that provide survival signals to the surrounding cells. It has been proposed that extracellular DNA can act as a damage-associated molecular pattern given the association between circulating DNA and autoimmune diseases. Herein, we demonstrate a novel role for genomic extracellular DNA binding to the Toll-like receptor (TLR)-9 on tumor cells in response to cytotoxic insult.
The colorectal tumor cell line HCCT116 was used to study the role of DNA in tumor cell response to chemotherapy. Cell viability was assessed using CCK-8 assay. Cell death mechanisms were assessed by YOYO-1 and lactate dehydrogenase staining for necrosis and TUNEL staining for apoptosis. Autophagy was measured by LC3 punctate formation. TLR9-short hairpin RNA was used to knockdown TLR-9 and determine its role in tumor cell response to DNA.
DNA is released from necrotic tumor cells after chemotherapy. Survival after cytotoxic insult is enhanced by the presence of extracellular DNA as a result of inhibition of apoptosis and enhanced autophagy. Knockdown of TLR-9 enhanced apoptosis, diminished autophagy, and decreased survival after cytotoxic insult in the presence or absence of extracellular DNA.
DNA in the tumor microenvironment promotes survival through induction of autophagy via TLR-9 signaling. This work has important implications for targeting extracellular DNA, TLR-9, and autophagy during treatment with chemotherapy and enhances our understanding of the role of extracellular DNA in the tumor microenvironment. BACKGROUNDInflammation promotes the growth and survival of malignant cells. Inflammation within the tumor microenvironment is a result of damage-associated molecular patterns released by dead or dying cells that provide survival signals to the surrounding cells. It has been proposed that extracellular DNA can act as a damage-associated molecular pattern given the association between circulating DNA and autoimmune diseases. Herein, we demonstrate a novel role for genomic extracellular DNA binding to the Toll-like receptor (TLR)-9 on tumor cells in response to cytotoxic insult.MATERIALS AND METHODSThe colorectal tumor cell line HCCT116 was used to study the role of DNA in tumor cell response to chemotherapy. Cell viability was assessed using CCK-8 assay. Cell death mechanisms were assessed by YOYO-1 and lactate dehydrogenase staining for necrosis and TUNEL staining for apoptosis. Autophagy was measured by LC3 punctate formation. TLR9-short hairpin RNA was used to knockdown TLR-9 and determine its role in tumor cell response to DNA.RESULTSDNA is released from necrotic tumor cells after chemotherapy. Survival after cytotoxic insult is enhanced by the presence of extracellular DNA as a result of inhibition of apoptosis and enhanced autophagy. Knockdown of TLR-9 enhanced apoptosis, diminished autophagy, and decreased survival after cytotoxic insult in the presence or absence of extracellular DNA.CONCLUSIONSDNA in the tumor microenvironment promotes survival through induction of autophagy via TLR-9 signaling. This work has important implications for targeting extracellular DNA, TLR-9, and autophagy during treatment with chemotherapy and enhances our understanding of the role of extracellular DNA in the tumor microenvironment. |
| Author | Tang, Daolin Lotze, Michael T. Anunobi, Reginald Boone, Brian A. Loux, Tara Kang, Rui Zeh, Herbert J. Cheh, Nick |
| Author_xml | – sequence: 1 givenname: Reginald surname: Anunobi fullname: Anunobi, Reginald – sequence: 2 givenname: Brian A. surname: Boone fullname: Boone, Brian A. – sequence: 3 givenname: Nick surname: Cheh fullname: Cheh, Nick – sequence: 4 givenname: Daolin surname: Tang fullname: Tang, Daolin – sequence: 5 givenname: Rui surname: Kang fullname: Kang, Rui – sequence: 6 givenname: Tara surname: Loux fullname: Loux, Tara – sequence: 7 givenname: Michael T. surname: Lotze fullname: Lotze, Michael T. – sequence: 8 givenname: Herbert J. surname: Zeh fullname: Zeh, Herbert J. email: zehxhx@upmc.edu |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29605400$$D View this record in MEDLINE/PubMed |
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| Keywords | Damage-associated molecular patterns receptors TLR-9 Autophagy Extracellular DNA Apoptosis DAMPs |
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| Snippet | Inflammation promotes the growth and survival of malignant cells. Inflammation within the tumor microenvironment is a result of damage-associated molecular... BACKGROUNDInflammation promotes the growth and survival of malignant cells. Inflammation within the tumor microenvironment is a result of damage-associated... |
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| SubjectTerms | Apoptosis Autophagy Damage-associated molecular patterns receptors DAMPs Extracellular DNA TLR-9 |
| Title | Extracellular DNA promotes colorectal tumor cell survival after cytotoxic chemotherapy |
| URI | https://dx.doi.org/10.1016/j.jss.2018.02.042 https://www.ncbi.nlm.nih.gov/pubmed/29605400 https://search.proquest.com/docview/2020894353 |
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