ArticleAmerican journal of translational research2019
Triptolide enhances the sensitivity of pancreatic cancer PANC-1 cells to gemcitabine by inhibiting TLR4/NF-κB signaling.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The trial behind it
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Natural modulators of enhancer of zeste homolog 2 (EZH2): potential epigenetic regulators of aging-associated pathways.Biogerontology · 2026Review
- Review
- Pharmacological, computational, and mechanistic insights into triptolide's role in targeting drug-resistant cancers.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Inflammation, microbiota, and pancreatic cancer.Cancer cell international · 2025Review
- Characteristics of glucose and lipid metabolism and the interaction between gut microbiota and colonic mucosal immunity in pigs during cold exposure.Journal of animal science and biotechnology · 2023Article
- Advances in the treatment of pancreatic cancer with traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- The therapeutic potential of natural products for treating pancreatic cancer.Frontiers in pharmacology · 2022Review
- Natural biomolecules and derivatives as anticancer immunomodulatory agents.Frontiers in immunology · 2022Review
- The Role of Toll-like Receptors (TLRs) Mediated Inflammation in Pancreatic Cancer Pathophysiology.International journal of molecular sciences · 2021Review
- Triptolide: pharmacological spectrum, biosynthesis, chemical synthesis and derivatives.Theranostics · 2021Review
- Development of Potential Antitumor Agents from the Scaffolds of Plant-Derived Terpenoid Lactones.Journal of medicinal chemistry · 2020Article
- Therapeutic applications and delivery systems for triptolide.Drug delivery and translational research · 2020Review
- Pancreatic Cancer (PDAC): Introduction of Evidence-Based Complementary Measures into Integrative Clinical Management.Cancers · 2020Review
- Low‑intensity low‑frequency ultrasound enhances the chemosensitivity of gemcitabine‑resistant ASPC‑1 cells via PI3K/AKT/NF‑κB pathway‑mediated ABC transporters.Oncology reports · 2020Article
- Knockdown of ectodysplasin-A receptor-associated adaptor protein exerts a tumor-suppressive effect in tongue squamous cell carcinoma cells.Experimental and therapeutic medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study aimed to investigate roles of Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signaling in triptolide (TPL)-induced sensitivity of pancreatic cancer cells to gemcitabine (GEM).
methods
resultsThe sensitivity of PANC-1 cells to GEM was reduced by LPS but enhanced by TLR4-siRNA. TPL inhibited expression of TLR4/NF-κB signaling components, which was reversed by LPS. The TPL+GEM group showed more apoptosis than the LPS+TPL+GEM group. Moreover, the activity of NF-κB and the expression of TLR4, p-p65 Survivin, CyclinD1 and Bcl-2 in the TPL+GEM group were lower than in the LPS+TPL+GEM group, whereas Bax expression was higher. The volume of transplanted tumors in the TPL+GEM group was lower than that in the TPL or GEM group. Phospho-p65, Survivin, CyclinD1 and Bcl-2 expression in transplanted tumors was lower in TPL+GEM group than in either single drug group. The Ki-67 staining score of the TPL+GEM group was lower and tumor cells apoptosis rate was increased when compared with TPL or GEM alone.
conclusionsTPL enhances the sensitivity of pancreatic cancer PANC-1 cells to GEM by inhibiting TLR4/NF-κB signaling.
Indexed as
Identifiers
31312385PMC6614654W2994216020What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.