ArticleFrontiers in oncology2026
Inhibitory effect of the multi-target TKI, anlotinib, in 5-FU resistant colorectal cancer HCT-8/15 cells: down regulation of drug resistance-associated protein expression.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Colorectal cancer is the most prevalent gastrointestinal malignancy. Treatment usually includes 5-fluorouracil (5-FU), oxaliplatin, and irinotecan, with 5-FU usually being the first choice. 5-FU treatment failure occurs when cancer cells acquire resistance. Therefore, it is crucial to identify compounds effective against 5-FU-resistant tumors. Herein, we determined the efficacy and mechanism of anlotinib in 5-FU-resistant colon cancer cells. Materials and methods: Human colon cancer cells (HCT-8/5-FU and HCT-15/5-FU) resistant to 5-FU were subjected to treatment with anlotinib, 5-FU, or both. Cell proliferation was assessed via MTS and clone formation assays. Cell cycle progression was studied using flow cytometry. Through immunoblotting, we evaluated changes in the protein levels of p-AKT and multidrug resistance 1. Results: MTS assays indicated that HCT-8/5-FU and HCT-15/5-FU cells were sensitive to anlotinib and resistant to 5-FU. At 48 h, HCT-8/5-FU had an IC50 of 2246.5 ± 204.5 μM, while HCT-15/5-FU had an IC50 of 18.49 ± 3.23 mM for 5-FU. The IC50 of anlotinib for HCT-8/5-FU cells was 53.69 ± 8.10μM at 24 h and 17.39 ± 1.98μM at 48 h. The IC50 values for HCT-15/5-FU at 24 and 48 h were 55.03 ± 3.44μM and 8.83 ± 3.02μM, respectively. Anlotinib enhanced 5-FU sensitivity in resistant cells, with low concentrations (IC10) considerably enhancing the antiproliferative effects of 5-FU. Further, anlotinib significantly increased the number of cells in the G0-G1 phase dose-dependently, while the proportion of cells entering S phase decreased. MDR1 and AKT expression decreased with increasing anlotinib concentration. Conclusion: Anlotinib suppressed the proliferation of 5-FU-resistant colon cancer cells by preventing entry into S phase, thus sensitizing cells to 5-FU. Moreover, anlotinib may reverse the effect of 5-FU on drug-resistant cells by down-regulating the expression of multidrug-resistant proteins, in which the AKT signaling pathway may play an important role.
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.