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Triptolide as a novel agent in pancreatic cancer: the validation using patient derived pancreatic tumor cell line
Seung Tae Kim1, Sun Young Kim1, Jeeyun Lee1
1Division of Hematology-Oncology, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul, 06351, South Korea.
Background:
Triptolide induces apoptosis and DNA damage followed by inhibition of DNA repair associated gene expression. However, there is the limited data for biomarker to predict the benefit to triptolide in various cancers including pancreatic cancer.
Methods:
We investigated the anti tumor efficacy of triptolide in various pancreatic cancer cell lines (Capan-1, Capan-2, SNU-213, SNU-410, HPAFII, and Hs766T) and patient derived cells (PDCs) from metastatic pancreatic cancer patients.
Results:
In vitro cell viability assay for triptolide in 6 PC cell lines, the IC50 was 0.01 uM, 0.02 uM, 0.0096 uM for triptolide in Capan-1, Capan-2 and SNU-213. However, the growth of tumor cells was not significantly reduced by triptolide in Hs766T, SNU-410 and HPAFII. The distinct difference of gene expression was also observed between Capan-1, Capan-2 and SNU-213 and Hs766T, SNU-410 and HPAFII. In analysis of pathway using gene expression profiles, the integrin mediated RAS signaling pathway was associated with the sensitivity of the triptolide in PC cell lines. Immunoblot assay showed that Chk2 phosphorylation after triptolide was distinctively observed in SNU-213 sensitive to triptolide but, not in SNU-410 insensitive to triptolide. This finding in immunoblot assay was also reproduced in PDCs originated from pancreatic cancer patients.
Conclusions:
Our findings might be helpful to completely capture the subset of patients who may benefit to tripolide (minnelide). More robust biomarkers such as KRAS mutation and Chk2 phosphorylation and careful clinical trial design using triptolide (minnelide) are warranted.
Insights
Triptolide shows anti-cancer effects by inducing apoptosis. Biomarkers like KRAS mutation and Chk2 phosphorylation may predict patient response to triptolide (minnelide) in pancreatic cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Triptolide induces apoptosis and DNA damage, inhibiting DNA repair gene expression.
- Limited biomarkers exist to predict triptolide efficacy in cancers, including pancreatic cancer.
Purpose of the Study:
- To investigate the anti-tumor efficacy of triptolide in pancreatic cancer cell lines and patient-derived cells.
- To identify potential biomarkers for predicting triptolide response.
Main Methods:
- Evaluated triptolide's anti-tumor efficacy using in vitro cell viability assays in multiple pancreatic cancer cell lines and patient-derived cells.
- Analyzed gene expression profiles to identify associated pathways.
- Utilized immunoblot assays to assess Chk2 phosphorylation.
Main Results:
- Triptolide demonstrated significant anti-cancer activity in Capan-1, Capan-2, and SNU-213 cell lines (IC50 < 0.02 uM).
- Hs766T, SNU-410, and HPAFII cell lines showed resistance to triptolide.
- Integrin-mediated RAS signaling pathway correlated with triptolide sensitivity; Chk2 phosphorylation was observed in sensitive cells and patient-derived cells.
Conclusions:
- Triptolide exhibits differential efficacy across pancreatic cancer cell lines.
- KRAS mutation and Chk2 phosphorylation are potential biomarkers for identifying patients who may benefit from triptolide (minnelide).
- Further clinical trials with robust biomarkers are warranted for triptolide (minnelide) therapy.
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