ArticleTranslational oncology2024
CREB3 facilitates Donafenib resistance in hepatocellular carcinoma cells via the LSD1/CoREST/p65 axis by transcriptionally activating long noncoding RNA ZFAS1.
Article in Translational oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- LncRNA ZFAS1 in hepatocellular carcinoma: A systematic review of molecular mechanisms and clinical translation.Non-coding RNA research · 2026Review
- Pilot study: predicting the interplay between FOXO1 and its downstream long non-coding RNAs in HCC.Frontiers in oncology · 2026Article
- Adrenomedullin orchestrates treatment resistance in hepatocellular carcinoma via immune microenvironment remodeling.Frontiers in genetics · 2025Article
- Research Progress of Long Non-coding RNA-ZFAS1 in Malignant Tumors.Cell biochemistry and biophysics · 2024Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDrug resistance greatly limits the therapeutic effect of a drug. This study aimed to explore the role of long noncoding RNA ZFAS1 in Donafenib resistance of hepatocellular carcinoma (HCC) cells.
methodsThe expression of CREB3, ZFAS1, and p65 in HCC cell lines was measured by RT-qPCR and western blotting. After transfection with sh-ZFAS1, sh-CREB3, or sh-CREB3 + oe-p65 in Donafenib-resistent (DR) HCC cell lines, the transfection efficiency was evaluated by RT-qPCR and western blotting. The proliferation and IC
resultsZFAS1, CREB3, and p65 were upregulated in HepG2-DR and Huh7-DR cells. Silencing of ZFAS1 or CREB3 enhanced the sensitivity of HCC cells to Donafenib, inhibited cell proliferation and IC
conclusionCREB3 overexpression contributed to Donafenib resistance in HCC cells by activating the ZFAS1/p65 axis.
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Registered trials
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