Evidence map›Paper›PMID 35117489›Full record

ArticleTranslational cancer research2020

Effects of knockout of long-chain non-coding RNA LSINCT5 on proliferation, apoptosis, epithelial-mesenchymal transition, and p38MAPK pathway of pancreatic cancer PANC-1 cells.

Yunlong Dai, Liguo Wu, Zhijun Zhang, Yang Ou, Junwei Huang

Open access · diamondAbstract read
In one paragraph

Article in Translational cancer research, 2020. 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
0.1field-weighted citation impact, top 64% 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, 2 citations in OpenAlex.

  1. Review
  2. LSINCT5: a pivotal oncogenic long non-coding RNA in cancers.Functional & integrative genomics · 2025
    Review
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.

Yunlong DaiDepartment of Hepatobiliary Surgery, People's Hospital of Wenjiang District, Chengdu 611130, China.
Liguo WuDepartment of Gastroenterology, People's Hospital of Wenjiang District, Chengdu 611130, China.
Zhijun ZhangDepartment of Hepatobiliary Surgery, People's Hospital of Wenjiang District, Chengdu 611130, China.
Yang OuDepartment of Hepatobiliary Surgery, People's Hospital of Wenjiang District, Chengdu 611130, China.
Junwei HuangDepartment of Hepatobiliary Surgery, People's Hospital of Wenjiang District, Chengdu 611130, China.
Wenzhou City People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOur study aims to investigate the effects of the knockout of long non-coding RNA LSINCT5 (lncRNA LSINCT5) on the proliferation, apoptosis, epithelial-mesenchymal transition (EMT), and p38MAPK pathway of pancreatic cancer PANC-1 cells, to provide a basis for searching for the therapeutic targets of pancreatic cancer.

methodsThe laboratory findings and clinical data of 21 patients with pancreatic cancer were retrospectively collected, and the survival rates of patients with high or low lncRNA LSINCT5 expressions were analyzed. PANC-1 cells were randomly divided into the control group, shRNA-NC group, and sh-LSINCT5 group, and the constructed sh-LSINCT5 and shRNA-NC vectors were transfected into the corresponding cells. The successful interference of lncRNA LSINCT5 was confirmed by reverse transcription polymerase chain reaction (RT-PCR). CCK-8 and spherogenesis assay detected the proliferation and spherogenesis of PANC-1 cells. The apoptosis rate was evaluated by flow cytometry. Western blotting was used to identify the expressions of KI67, PCNA, SOX2, OCT4, E-cadherin, N-cadherin, and Vimentin and the activation of Caspase-3 and Caspase-9.

resultsThe survival rate of patients with low lncRNA LSINCT5 expression was higher than that of patients with high lncRNA LSINCT5 expression. Compared with the control group, lncRNA LSINCT5 knockout significantly down-regulated the expressions of KI67, PCNA, SOX2, OCT4, cleaved Caspase-3, cleaved Caspase-9, N-cadherin and Vimentin (all P<0.05) and significantly decreased the cell proliferation, sphere size, and number of spheres in PANC-1 cells (all P<0.05); meanwhile, it up-regulated the protein expression of E-cadherin (P<0.05), along with the significantly increased number of apoptotic PANC-1 cells (P<0.05). In addition, compared with the control group, the level of p38 phosphorylation significantly dropped after lncRNA LSINCT5 knockout (P<0.05).

conclusionsKnockout of lncRNA LSINCT5 can inhibit the proliferation, EMT, and p38MAPK pathway of PANC-1 cells and meanwhile promote the apoptosis of PANC-1 cells. Therefore, lncRNA LSINCT5 may be a promising therapeutic target for pancreatic cancer.

Indexed as

apoptosisepithelial-mesenchymal transition (EMT)lncRNA LSINCT5pancreatic cancerproliferation

Identifiers

PMID35117489
PMCPMC8797644
OpenAlexW3006703655

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.