ArticleCancer cell international2021
Emodin regulates cell cycle of non-small lung cancer (NSCLC) cells through hyaluronan synthase 2 (HA2)-HA-CD44/receptor for hyaluronic acid-mediated motility (RHAMM) interaction-dependent signaling pathway.
Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- HMMR in human cancers: regulatory mechanism and biological function.Journal of translational medicine · 2025Review
- Combining network pharmacology and RNA sequencing to reveal the mechanism of emodin for the treatment of human neuroblastoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Systematically investigate the mechanism underlying the therapeutic effect of emodin in treatment of prostate cancer.Discover oncology · 2025Article
- Traditional Chinese medicine in lung cancer treatment.Molecular cancer · 2025Review
- Targeting Cancer Hallmarks Using Selected Food Bioactive Compounds: Potentials for Preventive and Therapeutic Strategies.Foods (Basel, Switzerland) · 2024Review
- Smoking-associated gene expression alterations in nasal epithelium reveal immune impairment linked to lung cancer risk.Genome medicine · 2024Article
- Lutein derived from Xenostegia tridentata exhibits anticancer activities against A549 lung cancer cells via hyaluronidase inhibition.PloS one · 2024Article
- Review
- Review
- Plants as a Source of Anticancer Agents: From Bench to Bedside.Molecules (Basel, Switzerland) · 2022Review
- Emodin Ameliorates the Efficacy of Carfilzomib in Multiple Myeloma Cells via Apoptosis and Autophagy.Biomedicines · 2022Article
- Role of Plant-Derived Active Constituents in Cancer Treatment and Their Mechanisms of Action.Cells · 2022Review
- The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers.International journal of biological sciences · 2022Review
- Dasatinib self-assembled nanoparticles decorated with hyaluronic acid for targeted treatment of tumors to overcome multidrug resistance.Drug delivery · 2021Article
- RHAMM Is a Multifunctional Protein That Regulates Cancer Progression.International journal of molecular sciences · 2021Review
- The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb-A Summary Update.International journal of molecular sciences · 2021Review
- Review
- Emodin-induced cell cycle arrest: A promising approach for cancer therapy (Review).Medicine internationalReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNon-small cell lung cancers (NSCLC) account for most cases of lung cancer. More effort is needed to research new drug and combination therapies for this disease. An anthraquinone derivative, emodin shows anticancer potency. We hypothesis that emodin suppresses lung cancer cells through hyaluronan (HA) synthase 2-HA-CD44/receptor for hyaluronic acid-mediated motility (RHAMM) interaction-dependent signaling pathway mediated cell cycle regulation.
methodsWe tested the effect of emodin on viability, apoptosis, and HA secretion of 5 NSCLC cell lines. We used NSCLC cells A549 for two rounds of knockdown study: (1) knocking down either the synthases (HAS2 and HAS3) or the receptors (CD44 and RHAMM); (2) knocking down either HAS2 or HAS3. Then determined the effect of emodin on viability, HA secretion, cell cycle, and expression of cyclin proteins.
resultsEmodin suppressed viability and HA secretion of all 5 NSCLC cell lines except for HA secretion of H460. Emodin had a slight apoptosis induction effect on all cell lines and was not different among cell lines. The knockdown of either the synthases or the receptors blocked emodin effects on viability while the knockdown of HAS2 block emodin effects but not HAS3. Emodin increased cells in the G1/G0 phase, and decreased cells in the S and G2/M phase by down-regulating cyclin A and B and up-regulating cyclin C, D, and E. HAS2 knockdown blocked the effects of emodin on the cell cycle.
conclusionsThis study demonstrated that emodin regulates the cell cycle of NSCLC cells through the HAS2-HA-CD44/RHAMM interaction-dependent signaling pathway.
Indexed as
Identifiers
What 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.