Evidence map›Paper›PMID 34327135›Full record

ArticleFrontiers in oncology2021

Suppressing ERK Pathway Impairs Glycochenodeoxycholate-Mediated Survival and Drug-Resistance in Hepatocellular Carcinoma Cells.

Bingxin Li, Maojun Zhou, Jue Wang, Hongjuan Xu, Manyi Yang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. 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

5 authors at 2 institutions in 1 country.

Bingxin LiDepartment of Hepatobiliary and Pancreatic Surgery, National Health Commission (NHC) Key Laboratory of Nanobiological Technology, Xiangya Hospital, Central South University, Changsha, China.
Maojun ZhouDepartment of Oncology, NHC Key Laboratory of Cancer Proteomics, National Center for Geriatrics Clinical Research, State Local Joint Engineering Laboratory for Anticancer Drugs, Xiangya Hospital, Central South University, Changsha, China.
Jue WangDepartment of Hepatobiliary and Pancreatic Surgery, National Health Commission (NHC) Key Laboratory of Nanobiological Technology, Xiangya Hospital, Central South University, Changsha, China.
Hongjuan XuDepartment of Hepatobiliary and Pancreatic Surgery, National Health Commission (NHC) Key Laboratory of Nanobiological Technology, Xiangya Hospital, Central South University, Changsha, China.
Manyi YangDepartment of Hepatobiliary and Pancreatic Surgery, National Health Commission (NHC) Key Laboratory of Nanobiological Technology, Xiangya Hospital, Central South University, Changsha, China.
Xiangya Hospital Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycochenodeoxycholate (GCDA), a toxic component in bile salts, is involved in carcinogenesis of gastrointestinal tumors. The objective of this research was to study the function of ERK1/2 in the GCDA-mediated survival and drug-resistance in hepatocellular carcinoma cells (HCCs). Firstly, extracellular signal-regulated kinase 1/2 (ERK1/2) was detected extensively expressed in liver cancer cells, and silencing ERK1/2 by RNA interference could suppress GCDA-stimulated survival and promote apoptosis. Furthermore, phosphorylation of endogenous ERK1/2 could be potently stimulated by GCDA in combination with enhanced chemoresistance in QGY-7703 hepatocellular carcinoma cells. The GCDA-mediated proliferation and chemoresistance could be impaired by PD98059, which acted as an inhibitor to block the phosphorylation of ERK1/2. Mechanistically, PD98059 was able to potently suppress GCDA-stimulated nuclear aggregation of ERK1/2 and p-ERK1/2, upregulate pro-survival protein Mcl-1 and downregulate pro-apoptotic protein Bim. The results of this study indicated that disruption of ERK1/2 by blocking phosphorylation or nuclear translocation may put forward new methods for solving the problem of GCDA-related proliferation and drug-resistance in liver cancer treatment.

Indexed as

anti-apoptosis proteinsextracellular signal-regulated kinase 1/2glycochenodeoxycholatehepatocellular carcinoma cellspro-apoptotic proteins

Identifiers

PMID34327135
PMCPMC8313996
OpenAlexW3126831059

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.