Evidence map›Paper›PMID 39851099›Full record

ArticleCombinatorial chemistry & high throughput screening2026

Angelicin Inhibits NSCLC Tumor Growth via the Inhibition of Cancer-Associated Fibroblasts.

Binbin Ding, Hang Yin, Shuo Cao, Kai Cheng, Luna Ge

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Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Cancer-associated fibroblasts as a potential therapeutic target for thyroid cancers.International journal of surgery (London, England) · 2026
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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Binbin DingBiomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Hang YinBiomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Shuo CaoBiomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Kai ChengDepartment of PET/CT Center, Shandong Cancer Hospital and Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Ji'nan 250117, Shandong, China.
Luna GeBiomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study aimed to investigate the effect of angelicin on the NSCLC tumor growth.

backgroundAccumulating evidence shows that cancer-associated fibroblasts (CAFs) play an important role in tumor progression and metastasis, making CAFs an increasingly attractive target for therapeutic intervention. Targeted therapies against CAFs have been considered to have the potential to significantly improve cancer treatment outcomes, overcome resistance, and improve immune evasion. Angelicin (Ang), an active ingredient isolated from the Chinese herbal medicine Psoralea corylifolia Linn., has been reported to inhibit tumor progression. Due to its natural origin, angelicin has good clinical safety and low toxicity. Further clinical studies and exploration of its role as a CAF inhibitor in difficult-to-treat tumors like as NSCLC are expected to offer up a new channel for cancer treatment. Furthermore, angelicin's low cost and good biocompatibility make it have important application potential in cancer combination therapy, especially when used in combination with traditional therapies such as chemotherapy and immunotherapy, which may significantly improve treatment outcomes and reduce side effects. However, the mechanism of its anti-tumor effect remains poorly defined. The aim of this study was to investigate whether ANG modulates CAF activity to inhibit NSCLC progression.

methodsNIH3T3 cells are a mouse fibroblast cell line, and the use of NIH3T3 cells as a model for CAFs is mainly due to their natural fibroblast phenotype, ease of culture, good response to stimuli, and ability to simulate the functions of fibroblasts in the tumor microenvironment. NIH3T3 was treated with TGF-β (4ug/ml) and H

resultsThe result showed that Ang significantly inhibited TGF-β and H

conclusionAng reduced the growth, invasion, and migration of lung cancer by inactive CAFs. This provides a rationale for tumor microenvironment-based treatment of lung cancer and clinical translation of Ang. As a potential anti-cancer drug, Ang has shown significant effects in inhibiting cancer-related fibroblasts (CAFs) and disrupting the tumor microenvironment. However, there are still challenges in translating these findings into clinical treatments, such as heterogeneity of the tumor microenvironment, differences in patient responses, and side effects. Therefore, future research should focus on exploring personalized treatment strategies, evaluating the clinical safety and effectiveness of the drug, and delving deeper into the molecular mechanisms and target sites of Ang.

Indexed as

Antineoplastic AgentsCancer-Associated FibroblastsCarcinoma, Non-Small-Cell LungFurocoumarinsLung NeoplasmsAnimalsCell MovementCell ProliferationDose-Response Relationship, DrugDrug Screening Assays, AntitumorHumansMiceangelicinAntineoplastic AgentsFurocoumarinsangelicinanti-tumorCancer-associated fibroblastslung cancer progressionnetwork pharmacology.RNA sequencing

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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.