Evidence map›Paper›PMID 41318819›Full record

ArticleScientific reports2025

AFP promotes cancer multidrug resistance through activating PI3K/Akt/NF-κB signaling pathway.

Siren Feng, Chao Zhang, Yi Chen, Wei Li, Xu Dong, Yuli Zhou, Xiaowei Li, Fang Wang, Bo Lin, Mengsen Li and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

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

11 authors.

Siren Feng *Key Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Chao Zhang *Key Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Yi Chen *Key Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Wei LiKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Xu DongKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Yuli ZhouKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Xiaowei LiKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Fang WangKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Bo LinKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China.
Mengsen LiKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China. mengsenli@163.com.
Mingyue ZhuKey Laboratory of Tropical Translational Medicine, Ministry of Education, and Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, 3 Xueyuan Road, Haikou, 571199, People's Republic of China. mingyuezhu2002@163.com.

Funding

the Hainan Province Science and Technology Special Foundation ZDYF2021SHFZ222the Hainan Provincial Graduate Innovation Research project Qhys2023-450the National Natural Science Foundation of China 82460602the National Natural Science Foundation of China 82560459the Natural Science Foundation of Hainan Province 824RC517
6 · The paper itself

Abstract

Alpha-fetoprotein (AFP) has the biological function of promoting the malignant behaviors of liver cancer cells, but how it regulates drug resistance in cancer cells is still unclear. This study explore the effect of AFP on multidrug resistance (MDR) in cancers and its potential molecular mechanisms. RNA interference vector for AFP was constructed and transduced into the human liver cancer cell line Bel 7402 (high AFP expression). However, the human cervical cancer cell line HeLa (without AFP expression) was transduced with a overexpressing AFP vector. When these cancer cells were treated with doxorubicin (ADM) and 5-fluorouracil (5-FU), cell survival rate was determined by MTT, apoptosis by TUNEL, and colony formation by colony formation assay. The cancer cells were treated with the PI3K/Akt pathway inhibitor LY294002, and the expression of drug resistance-related proteins MDR1, MRP1, BCRP, Livin, cIAP1, XIAP, Akt, p-Akt, p65, and p-p65 was detected by Western blotting. Bioinformatics analysis of the correlation between AFP regulation and intracellular signaling pathways was performed. The expression and localization of p65 were observed by immunofluorescence staining. Silencing AFP could increase the sensitivity of Bel7402 cells to ADM and 5-FU, whereas AFP overexpression caused resistance to ADM and 5-FU in HeLa cells. AFP was positively correlated with the PI3K/Akt/NF-κB signaling pathway, and there was a significant difference in the correlation between p65 and drug resistance genes. AFP regulates the expression of drug resistance-related genes by activating the PI3K/Akt/NF-κB signaling pathway. AFP plays a pivotal role in MDR of cancer cells, the mechanism may be involved in activating the PI3K/Akt/NF-κB signaling pathway.

Indexed as

alpha-FetoproteinsDrug Resistance, MultipleDrug Resistance, NeoplasmNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionApoptosisCell Line, TumorDoxorubicinFluorouracilGene Expression Regulation, NeoplasticHeLa CellsHumansLiver NeoplasmsAFP protein, humanalpha-FetoproteinsDoxorubicinFluorouracilNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAlpha-fetoproteinCancer cellsMultidrug resistancePI3K/Akt/NF-κB

Identifiers

PMID41318819
PMCPMC12774998

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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.