Evidence map›Paper›PMID 24696725›Full record

ArticleInternational journal of clinical and experimental pathology2014

RNAi screening with shRNAs against histone methylation-related genes reveals determinants of sorafenib sensitivity in hepatocellular carcinoma cells.

Guang-Ming Li, Yu-Gang Wang, Qin Pan, Jun Wang, Jian-Gao Fan, Chao Sun

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 29% of its field
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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Loss-of-function mutations of microRNA-142-3p promoteWorld journal of gastroenterology · 2025
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  10. Deletion of Mouse Setd4 Promotes the Recovery of Hematopoietic Failure.International journal of radiation oncology, biology, physics · 2020
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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

6 authors at 2 institutions in 1 country.

Guang-Ming LiDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200092, China.
Yu-Gang WangDepartment of Gastroenterology, Shanghai Changning Central Hospital Shanghai 200336, China.
Qin PanDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200092, China.
Jun WangDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200092, China.
Jian-Gao FanDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200092, China.
Chao SunDepartment of Gastroenterology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine Shanghai 200092, China.
XinHua Hospital · CNKaiping Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sorafenib is the first drug currently approved to treat advanced hepatocellular carcinoma (HCC). However, very low response rate and acquired drug resistance makes rare patients benefit from sorafenib therapy, therefore it is urgent to find biomarkers for sorafenib sensitivity. Histone modifications, including histone methylation, have been demonstrated to influence the initiation and progression of HCC. It is of great interest to elicit the possibility whether histone methylation plays a role in regulation of sorafenib sensitivity. In present work, a high throughput RNAi screening with 176 shRNA pools against 88 histone methyltransferases (HMTs) and histone demethyltransferases genes was applied to HepG2 cells. Silencing of 3 genes (ASH1L, C17ORF49 and SETD4) was validated to specifically promote HepG2 cells sensitivity to sorafenib. Western blotting results showed that those 3 HMT genes knockdown alone or sorafenib treatments alone both induce AKT/ERK activation. However, combination treatment with sorafenib and silencing of C17ORF49 or SETD4 downregulated AKT phosphorylation and hence induced HCC cells death. Our work may provide potential biomarkers for sorafenib sensitivity and therapeutic combination for sorafenib treatment in HCC patients.

Indexed as

Antineoplastic AgentsBlotting, WesternCarcinoma, HepatocellularDNA MethylationDrug Resistance, NeoplasmHep G2 CellsHigh-Throughput Screening AssaysHistonesHumansLiver NeoplasmsNiacinamidePhenylurea CompoundsReverse Transcriptase Polymerase Chain ReactionRNA InterferenceRNA, Small InterferingSorafenibAntineoplastic AgentsHistonesNiacinamidePhenylurea CompoundsRNA, Small InterferingSorafenibAKTASH1LC17ORF49Hepatocellular carcinomahistone methylationSETD4sorafenib

Identifiers

PMID24696725
PMCPMC3971312
OpenAlexW327272020

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.