Evidence map›Paper›PMID 34057016›Full record

ArticleBioengineered2021

Long non-coding RNA TINCR promotes hepatocellular carcinoma proliferation and invasion via STAT3 signaling by direct interacting with T-cell protein tyrosine phosphatase (TCPTP).

Chengwu Tang, Wenming Feng, Ying Bao, Huimin Du

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Chengwu TangDepartment of General Surgery, The First People's Hospital Affiliated to Huzhou Normal College, Huzhou, Zhejiang, People's Republic of China.
Wenming FengDepartment of General Surgery, The First People's Hospital Affiliated to Huzhou Normal College, Huzhou, Zhejiang, People's Republic of China.
Ying BaoDepartment of General Surgery, The First People's Hospital Affiliated to Huzhou Normal College, Huzhou, Zhejiang, People's Republic of China.
Huimin DuOut-Patient Department, The First People's Hospital Affiliated to Huzhou Normal College, Huzhou, Zhejiang, People's Republic of China.ORCID 0000-0002-9330-0488
Third People's Hospital of Huzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The long non-coding RNAs (lncRNAs) participate in modulating numerous important cancer phenotypes via formation of RNA-protein complex. TINCR (terminal differentiation-induced lncRNA) modulates cancer cell behavior in many human malignancies, such as hepatocellular carcinoma (HCC). Herein, we proposed to investigate the underlying mechanism by which TINCR regulates HCC progression via formation of RNA-protein. RNA pulldown, LC-MS/MS, bioinformatics analysis, and RNA immunoprecipitation (RIP) assays were employed to identify TINCR-interacting protein TCPTP in HCC cells. The siRNAs for TINCR and TCPTP were transfected into HCC cells. The plasmids encoding full length or the 1-360 nt deletion of TINCR were generated and applied to cell transfection. The CCK-8, colony formation, EdU, wound healing along with transwell assays were employed to examine cell proliferation, apoptosis, migration, and infiltration. Real-time PCR, as well as western blot assays were employed to assess the levels of STAT3 phosphorylation and its target genes. We identified 1-360 nt region of TINCR, which directly bound with the phosphatase domain of TCPTP to inhibit its tyrosine phosphatase activity. Then, the results showed that the increasing of cell growth, migration, infiltration, and the reducing of apoptosis in TINCR-knockdown HCC cells was remarkably reversed with TCPTP silence. Additionally, Δ1-360 TINCR overexpression did not affect HCC cell growth, apoptosis, migration, infiltration, and STAT3 target genes expression. Our data revealed that TINCR directly bound TCPTP and suppressed the dephosphorylation of STAT3, thus promoting STAT3 activation and its downstream target genes in HCC progression and tumorigenicity.HighlightsLncRNA TINCR interacted with protein TCPTPLncRNA TINCR maintained STAT3 phosphorylationLncRNA TINCR affected STAT3 signaling in HCCAbbreviations:lncRNAs: long non-coding RNAs; TINCR: terminal differentiation-induced lncRNA; TCPTP: T cell protein tyrosine phosphatase; siRNA: small-interfering RNA; HCC: hepatocellular carcinoma; nt: nucleotide; LC-MS/MS: Liquid Chromatography - Tandem Mass Spectrometry; RIP: RNA immunoprecipitation; ANOVA: analysis of variance; EdU: 5-ethynyl-2'-deoxyuridine; real-time PCR: real-time polymerase chain reaction; CCK-8: cell counting kit-8; aa: amino acids; STAT3: signal transducer and activator of transcription 3.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorGene Knockdown TechniquesHumansProtein Tyrosine Phosphatase, Non-Receptor Type 2RNA, Long NoncodingSignal TransductionSTAT3 Transcription FactorProtein Tyrosine Phosphatase, Non-Receptor Type 2PTPN2 protein, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription FactorTINCR lncRNA, humanHepatocellular carcinomaRNA pull downSTAT3TCPTPTINCR

Identifiers

PMID34057016
PMCPMC8806792
OpenAlexW3164518474

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.