Data from Synergistic Effect of Olaparib with Combination of Cisplatin on <i>PTEN</i>-Deficient Lung Cancer Cells Article Swipe
Daisuke Minami
,
Nagio Takigawa
,
Hiromasa Takeda
,
Minoru Takata
,
Nobuaki Ochi
,
Eiki Ichihara
,
Akiko Hisamoto
,
Katsuyuki Hotta
,
Mitsune Tanimoto
,
Katsuyuki Kiura
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6541657
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1541-7786.c.6541657
PARP enzyme plays a key role in the cellular machinery responsible for DNA damage repair. PTEN is a tumor-suppressor gene deactivating PI3K downstream of EGFR signaling. We hypothesize that PTEN-deficient lung cancer cells suppressed DNA damage signaling and that the absence of PTEN can sensitize these cells to a concurrent treatment of a DNA-damaging agent (cisplatin) and a PARP inhibitor (olaparib). To investigate the effect of olaparib and cisplatin on PTEN-deficient lung tumors, two EGFR-mutant (deletion in exon19) non–small cell lung cancer (NSCLC) cell lines, PC-9 (PTEN wild-type) and H1650 (PTEN loss), were used. We transfected intact PTEN gene into H1650 cells (H1650PTEN+) and knocked down PTEN expression in the PC-9 cells (PC-9PTEN−) using short hairpin RNA (shRNA). Combination of cisplatin with olaparib showed a synergistic effect in vitro according to the combination index in H1650 cells. Restoration of PTEN in the H1650 cells decreased sensitivity to the combination. Ablation of PTEN in PC-9 cells increased sensitivity to olaparib and cisplatin. We also examined the effectiveness of cisplatin and olaparib in a xenograft model using H1650 and PC-9PTEN− cells. The combination of cisplatin with olaparib was more effective than each agent individually. This effect was not observed in a xenograft model using H1650PTEN+ and PC-9 cells. Mechanistic investigations revealed that PTEN deficiency caused reductions in nuclear RAD51 and RPA focus formation and phosphorylated Chk1 and Mre11. Thus, genetic inactivation of PTEN led to the suppression of DNA repair. Mol Cancer Res; 11(2); 140–8. ©2012 AACR.
Related Topics
Concepts
Olaparib
PTEN
Cancer research
Cisplatin
Lung cancer
Cancer
Chemistry
Apoptosis
Medicine
Oncology
Internal medicine
PI3K/AKT/mTOR pathway
Poly ADP ribose polymerase
Biochemistry
Chemotherapy
Gene
Polymerase
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/1541-7786.c.6541657
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4391149931
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4391149931Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/1541-7786.c.6541657Digital Object Identifier
- Title
-
Data from Synergistic Effect of Olaparib with Combination of Cisplatin on <i>PTEN</i>-Deficient Lung Cancer CellsWork title
- Type
-
preprintOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-04-03Full publication date if available
- Authors
-
Daisuke Minami, Nagio Takigawa, Hiromasa Takeda, Minoru Takata, Nobuaki Ochi, Eiki Ichihara, Akiko Hisamoto, Katsuyuki Hotta, Mitsune Tanimoto, Katsuyuki KiuraList of authors in order
- Landing page
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https://doi.org/10.1158/1541-7786.c.6541657Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
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https://doi.org/10.1158/1541-7786.c.6541657Direct OA link when available
- Concepts
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Olaparib, PTEN, Cancer research, Cisplatin, Lung cancer, Cancer, Chemistry, Apoptosis, Medicine, Oncology, Internal medicine, PI3K/AKT/mTOR pathway, Poly ADP ribose polymerase, Biochemistry, Chemotherapy, Gene, PolymeraseTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.Ablation | 149 |
| abstract_inverted_index.cellular | 8 |
| abstract_inverted_index.examined | 163 |
| abstract_inverted_index.observed | 196 |
| abstract_inverted_index.olaparib | 66, 122, 158, 169, 184 |
| abstract_inverted_index.revealed | 208 |
| abstract_inverted_index.(deletion | 75 |
| abstract_inverted_index.according | 129 |
| abstract_inverted_index.cisplatin | 68, 120, 167, 182 |
| abstract_inverted_index.decreased | 144 |
| abstract_inverted_index.effective | 187 |
| abstract_inverted_index.formation | 220 |
| abstract_inverted_index.increased | 155 |
| abstract_inverted_index.inhibitor | 59 |
| abstract_inverted_index.machinery | 9 |
| abstract_inverted_index.sensitize | 44 |
| abstract_inverted_index.signaling | 36 |
| abstract_inverted_index.treatment | 50 |
| abstract_inverted_index.xenograft | 172, 199 |
| abstract_inverted_index.cisplatin. | 160 |
| abstract_inverted_index.concurrent | 49 |
| abstract_inverted_index.deficiency | 211 |
| abstract_inverted_index.downstream | 22 |
| abstract_inverted_index.expression | 107 |
| abstract_inverted_index.reductions | 213 |
| abstract_inverted_index.signaling. | 25 |
| abstract_inverted_index.suppressed | 33 |
| abstract_inverted_index.wild-type) | 87 |
| abstract_inverted_index.<i>in | 127 |
| abstract_inverted_index.(cisplatin) | 55 |
| abstract_inverted_index.(olaparib). | 60 |
| abstract_inverted_index.Combination | 118 |
| abstract_inverted_index.Mechanistic | 206 |
| abstract_inverted_index.Restoration | 137 |
| abstract_inverted_index.combination | 132, 180 |
| abstract_inverted_index.hypothesize | 27 |
| abstract_inverted_index.investigate | 62 |
| abstract_inverted_index.non–small | 78 |
| abstract_inverted_index.responsible | 10 |
| abstract_inverted_index.sensitivity | 145, 156 |
| abstract_inverted_index.suppression | 234 |
| abstract_inverted_index.synergistic | 125 |
| abstract_inverted_index.transfected | 95 |
| abstract_inverted_index.<i>Mol | 238 |
| abstract_inverted_index.DNA-damaging | 53 |
| abstract_inverted_index.combination. | 148 |
| abstract_inverted_index.deactivating | 20 |
| abstract_inverted_index.inactivation | 228 |
| abstract_inverted_index.effectiveness | 165 |
| abstract_inverted_index.individually. | 191 |
| abstract_inverted_index.investigations | 207 |
| abstract_inverted_index.phosphorylated | 222 |
| abstract_inverted_index.vitro</i> | 128 |
| abstract_inverted_index.tumor-suppressor | 18 |
| abstract_inverted_index.<i>EGFR</i> | 24 |
| abstract_inverted_index.<i>PTEN</i> | 15, 42, 97, 106, 139, 151, 210, 230 |
| abstract_inverted_index.(<i>PTEN</i> | 86, 90 |
| abstract_inverted_index.<i>EGFR-</i>mutant | 74 |
| abstract_inverted_index.<div>Abstract<p>PARP | 0 |
| abstract_inverted_index.<i>PTEN</i>-deficient | 29, 70 |
| abstract_inverted_index.H1650<sup>PTEN+</sup> | 202 |
| abstract_inverted_index.PC-9<sup>PTEN−</sup> | 177 |
| abstract_inverted_index.(H1650<sup>PTEN+</sup>) | 102 |
| abstract_inverted_index.(PC-9<sup>PTEN−</sup>) | 112 |
| abstract_inverted_index.AACR</i>.</p></div> | 244 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 10 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.7699999809265137 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.55241281 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |