Evidence map›Paper›PMID 33000204›Full record

ArticleInternational journal of molecular medicine2020

KCNQ1OT1 contributes to sorafenib resistance and programmed death‑ligand‑1‑mediated immune escape via sponging miR‑506 in hepatocellular carcinoma cells.

Junli Zhang, Xiaohui Zhao, Xiaojuan Ma, Zengyan Yuan, Miao Hu

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

Article in International journal of molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Long Noncoding RNA KCNQ1OT1 is a Prognostic Biomarker and mediates CD8International journal of biological sciences · 2021
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  19. The role of LncRNAs in tumor immunotherapy.Cancer cell international · 2023
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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

5 authors at 1 institution in 1 country.

Junli ZhangSchool of Medical Laboratory, Sanquan College of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Xiaohui ZhaoSchool of Basic Medical Sciences, Sanquan College of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Xiaojuan MaSchool of Medical Laboratory, Sanquan College of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Zengyan YuanSchool of Medical Laboratory, Sanquan College of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Miao HuSchool of Medical Laboratory, Sanquan College of Xinxiang Medical University, Xinxiang, Henan 453003, P.R. China.
Xinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance and immune escape of tumor cells severely compromise the treatment efficiency of hepatocellular carcinoma (HCC). Long non‑coding RNA KCNQ1 overlapping transcript 1 (lncRNA KCNQ1OT1) has been shown to be involved in drug resistance in several cancers. The aim of the present study was to investigate the role of KCNQ1OT1 in sorafenib resistance and immune escape of HCC cells. Reverse transcription‑quantitative PCR analysis, western blotting and immunohistochemistry were performed to detect the expression of KCNQ1OT1, miR‑506 and programmed death‑ligand‑1 (PD‑L1). Cell Counting Kit‑8 assay, flow cytometry and Transwell assays were used to evaluate IC50 value, cell apoptosis and metastasis. ELISA was performed to detect the secretion of cytokines. Dual‑luciferase reporter assay was conducted to verify the targeting relationships between miR‑506 and KCNQ1OT1 or PD‑L1. KCNQ1OT1 and PD‑L1 were found to be upregulated and miR‑506 was downregulated in sorafenib‑resistant HCC tissues and cells. Furthermore, KCNQ1OT1 knockdown reduced the IC50 value of sorafenib, suppressed cell metastasis and promoted apoptosis in sorafenib‑resistant HCC cells. Moreover, KCNQ1OT1 knockdown changed the tumor microenvironment and T‑cell apoptosis in a sorafenib‑resistant HCC/T‑cell co‑culture model. In addition, it was demonstrated that KCNQ1OT1 functioned as a competing endogenous RNA of miR‑506 and increased PD‑L1 expression in sorafenib‑resistant HCC cells. miR‑506 inhibition abolished the effects of KCNQ1OT1 knockdown on sorafenib sensitivity, tumor growth, the tumor microenvironment and T‑cell apoptosis. In conclusion, KCNQ1OT1 knockdown inhibited sorafenib resistance and PD‑L1‑mediated immune escape by sponging miR‑506 in sorafenib‑resistant HCC cells.

Indexed as

Drug Resistance, NeoplasmImmune EvasionApoptosisB7-H1 AntigenBase SequenceCarcinoma, HepatocellularCell Line, TumorCell MovementCytokinesDown-RegulationGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMicroRNAsModels, BiologicalNeoplasm InvasivenessB7-H1 AntigenCytokinesKCNQ1OT1 long non-coding RNA, humanMicroRNAsMIRN506 microRNA, humanPotassium Channels, Voltage-GatedSorafenib

Identifiers

PMID33000204
PMCPMC7521583
OpenAlexW3081038443

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.