ArticleThoracic cancer2022
ACT001 inhibits the proliferation of non-small cell lung cancer cells by upregulating NKTR expression.
Article in Thoracic cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- ACT001 suppresses ox-LDL-mediated macrophage ferroptosis via activating the NRF2 pathway: AnExperimental and therapeutic medicine · 2026Article
- RBM5 Acts as a Tumor Suppressor in Breast Cancer Through Binding to G-quadruplexes in the BAP1 Gene Promoter to Activate Its Expression.Molecules (Basel, Switzerland) · 2026Article
- Parthenolide and Its Derivatives in the Treatment of Respiratory Tract Diseases: Therapeutic Effects and Molecular Mechanisms.Drug design, development and therapy · 2026Review
- Advances in Naturally and Synthetically Derived Bioactive Sesquiterpenes and Their Derivatives: Applications in Targeting Cancer and Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2025Review
- ACT001 Inhibits Tumor Progression and Modulates Immune Responses in Non-Small Cell Lung Cancer.Journal of clinical laboratory analysis · 2025Article
- ACT001 inhibits the proliferation of non-small cell lung cancer cells by upregulating NKTR expression.Thoracic cancer · 2022Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung cancer, the primary cause of cancer-related deaths worldwide, is diagnosed at an advanced stage and has a poor prognosis. Non-small cell lung cancer (NSCLC) is a major histological type of lung malignancy. This study investigated the effect of ACT001, a novel sesquiterpene lactone derivative, on the proliferation of NSCLC cells and explored the underlying mechanism.
methodsThe effect of ACT001 on cell proliferation was examined by clone formation and MTT assay. Differentially expressed genes and enrichment pathways were analyzed by RNA-seq. Flow cytometry and cell cycle-related protein expression analysis were performed to study the cell cycle. Phosphorylated AKT was detected to explore the mechanism in natural killer cell triggering receptor (NKTR) KD cells with AKT activator and/or inhibitor. The therapeutic effect of ACT001 in vivo was studied in the xenograft tumor model.
resultsACT001 inhibited the proliferation and G1/S transition in NSCLC cell lines. By RNA-seq analysis, NKTR may be the target of ACT001. Moreover, knockdown NKTR promoted cell proliferation and reversed the effects of ACT001. In addition, ACT001 inhibited AKT phosphorylation, but NKTR knockdown promoted AKT phosphorylation.
conclusionOur results suggested NKTR may be the target of ACT001 in NSCLC. ACT001 holds promise as a novel method for the treatment of NSCLC.
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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 Socratic graph.