ArticleOncology research2016
Raltitrexed Inhibits HepG2 Cell Proliferation via G0/G1 Cell Cycle Arrest.
Article in Oncology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 33 citations in OpenAlex.
- MOF enhances the sensitivity and selectivity of sorafenib as an anticancer drug against hepatocellular carcinoma and colorectal cancer in vitro.Scientific reports · 2025Article
- Eugenia brasiliensis: Analysis of the Chemical Profile and Evaluation of Cytotoxic Potential.Chemistry & biodiversity · 2025Article
- Raltitrexed enhanced antitumor effect of anlotinib in human esophageal squamous carcinoma cells on proliferation, invasiveness, and apoptosis.BMC cancer · 2023Article
- Raltitrexed regulates proliferation and apoptosis of HGC-27 cells by upregulating RSK4.BMC pharmacology & toxicology · 2022Article
- Preliminary outcomes of raltitrexed eluting bead-transarterial chemoembolization using Callispheres® beads for gastrointestinal adenocarcinoma liver metastasis.World journal of surgical oncology · 2022Article
- Synthesis, molecular docking, and cytotoxicity of quinazolinone and dihydroquinazolinone derivatives as cytotoxic agents.BMC chemistry · 2022Article
- DTYMK promote hepatocellular carcinoma proliferation by regulating cell cycle.Cell cycle (Georgetown, Tex.) · 2021Article
- LncRNA SNHG6 promotes G1/S-phase transition in hepatocellular carcinoma by impairing miR-204-5p-mediated inhibition of E2F1.Oncogene · 2021Article
- Identification of adhesion-associated DNA methylation patterns in the peripheral nervous system.Experimental and therapeutic medicine · 2021Article
- Genome-wide alterations of uracil distribution patterns in human DNA upon chemotherapeutic treatments.eLife · 2020Article
- Hyperthermic intraperitoneal chemotherapy with recombinant mutant human TNF-α and raltitrexed in mice with colorectal-peritoneal carcinomatosis.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Raltitrexed Enhances the Antitumor Effect of Apatinib in Human Esophageal Squamous Carcinoma Cells via Akt and Erk Pathways.OncoTargets and therapy · 2020Article
- Raltitrexed increases radiation sensitivity of esophageal squamous carcinoma cells.Cancer cell international · 2019Article
- Comparison of two transarterial chemoembolization regimens in patients with unresectable hepatocellular carcinoma: raltitrexed plus oxaliplatinOncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Raltitrexed (RTX) is an antimetabolite drug used as a chemotherapeutic agent for treating colorectal cancer, malignant mesothelioma, and gastric cancer. The antitumor capacity of RTX is attributed to its inhibitory activity on thymidylate synthase (TS), a key enzyme in the synthesis of DNA precursors. The current study is aimed at investigating the potential antitumor effects of RTX in liver cancer. Using the HepG2 cell line as an in vitro model of liver cancer, we evaluated the effects of RTX on cell proliferation employing both a WST-8 assay and a clone formation efficiency assay. In addition, we monitored the ultrastructure changes of HepG2 cells in response to RTX with transmission electric microscopy. To investigate the mechanism underlying the regulation of cell proliferation by RTX, we analyzed cell cycle using cell flow cytometry. Moreover, real-time PCR and Western blot analyses were conducted to examine expression levels of cell cycle regulatory proteins cyclin A and cyclin-dependent kinase 2 (CDK2), as well as their mediators tumor suppressor genes p53 and p16. Our results demonstrate that RTX inhibits HepG2 proliferation by arresting the cell cycle at G0/G1. This cell cycle arrest function was mediated via downregulation of cyclin A and CDK2. The observed elevated expression of p53 and p16 by RTX may contribute to the reduction of cyclin A/CDK2. Our study indicates that RTX could serve as a potential chemotherapeutic agent in the treatment of hepatocellular carcinoma.
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.