Evidence map›Paper›PMID 31564085›Full record

ArticleClinical and molecular hepatology2020

Vimentin as a potential therapeutic target in sorafenib resistant HepG2, a HCC model cell line.

Ankita Makol, Harpreet Kaur, Sakshi Sharma, Shruthi Kanthaje, Ramanpreet Kaur, Anuradha Chakraborti

Open access · goldAbstract read
In one paragraph

Article in Clinical and molecular hepatology, 2020. 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
1.1field-weighted citation impact, top 22% 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, 28 citations in OpenAlex.

  1. CCDC137 affects sorafenib resistance in hepatocellular carcinoma cells by activating the AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  11. Exacerbation of Liver Tumor Metastasis inPharmaceuticals (Basel, Switzerland) · 2021
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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 1 institution in 1 country.

Ankita MakolDepartment of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Harpreet KaurDepartment of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Sakshi SharmaDepartment of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Shruthi KanthajeDepartment of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Ramanpreet KaurDepartment of Hepatology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Anuradha ChakrabortiDepartment of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Post Graduate Institute of Medical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsHepatocellular carcinoma (HCC) is the most common liver cancer with high mortality rate in patients suffering from liver diseases. The drug of choice used in advanced-stage of HCC is sorafenib. However, adaptive resistance has been observed in HCC patients undergoing long-term sorafenib treatment, lowering its effectiveness. Hence, it is important to overcome drug resistance to improve overall management of HCC. Here, we have identified a candidate biomarker for sorafenib resistance in a HCC model cell line, HepG2.

methodsInitially, comparative proteomic profiling of parental HepG2 [HepG2 (P)] and sorafenib-resistant HepG2 [HepG2 (R)] cells was performed via MALDI (matrix-assisted laser desorption/ionization) which revealed the deregulation of vimentin in HepG2 (R) cells. Gene and protein level expression of vimentin was also observed through quantitative real-time polymerase chain reaction (qRT PCR) and fluorescence-activated cell sorting (FACS), respectively. Furthermore, withaferin A was used to study regulation of vimentin expression and its significance in sorafenib resistance.

resultsBoth gene and protein level of vimentin expression was found to be downregulated in HepG2 (R) in comparison to HepG2 (P). Interestingly, the study demonstrated that withaferin A further lowered the expression of vimentin in HepG2 (R) cells in a dose-dependent manner. Also, inhibition of vimentin lowered ABCG2 expression and decreased cell viability in parental as well as sorafenib resistant HepG2 cells.

conclusionHence, our study for the first time highlighted the probable therapeutic potential of vimentin in sorafenib resistant HepG2, a HCC model cell line.

Indexed as

Antineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2Carcinoma, HepatocellularCell SurvivalChromatography, High Pressure LiquidDown-RegulationDrug Resistance, NeoplasmHep G2 CellsHumansLiver NeoplasmsProteomicsSorafenibSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationVimentinWithanolidesAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily G, Member 2SorafenibVimentinwithaferin AWithanolidesCarcinoma, HepatocellularSorafenib resistanceVimentinWithaferin A

Identifiers

PMID31564085
PMCPMC6940489
OpenAlexW2978186873

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.