ArticleResearch square2026
YBX1 Promotes Drug Resistance in Hepatocellular Carcinoma and Serves as a Potential Therapeutic Target.
Article in Research square, 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
11 authors.
Funding
Abstract
Drug resistance has emerged as a significant factor contributing to the dismal prognosis of patients with hepatocellular carcinoma (HCC). Since tyrosine kinase Inhibitors (TKIs) are the standard first-line therapy for advanced HCC, however, its effectiveness is significantly hindered by the development of drug resistance, the mechanisms of which are still not fully understood. This study aims to investigate the potential role of the transcription factor YBX1 in mediating drug resistance and to validate it as a potential therapeutic target in HCC. We identified increased YBX1 levels in human HCC patient cohorts and found that it is associated with tumor aggressiveness, metastasis, and poor survival, and is a key transcription factor contributing to drug resistance. Our results show that YBX1 overexpression confers sorafenib resistance in HCC. Elevating YBX1 levels in HCC cell lines increased cell survival, viability, and sorafenib IC50 values, as well as tumorigenic features and drug resistance markers. Conversely, siRNA-mediated knockdown of YBX1 reduced these effects. Sorafenib-resistant cells exhibited increased YBX1 and resistance markers. Inhibiting YBX1 significantly decreased the viability of resistant cells. In vivo studies demonstrated that inhibiting YBX1 with the small-molecule SU056 reduces tumor size. Thus, YBX1 is a promising target for extending drug resistance in HCC.
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.