Evidence map›Paper›PMID 34504588›Full record

ArticleExperimental and therapeutic medicine2021

Knockdown of LINC00657 inhibits the viability, migration and invasion of pancreatic cancer cells by regulating the miR-520h/CKS1B axis.

Peng Li, Hongsheng Wang, Ying Tang, Shuo Sun, Yue Ma, Yansong Xu, Guangyu Chen

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.6field-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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. 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

7 authors at 1 institution in 1 country.

Peng LiDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China.
Hongsheng WangDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China.
Ying TangDepartment of Nursing, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China.
Shuo SunDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China.
Yue MaDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China.
Yansong XuDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China.
Guangyu ChenDepartment of Hepatobiliary and Pancreatic Surgery, Affiliated Hospital of Beihua University, Jilin, Jilin 132011, P.R. China.
Beihua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA LINC00657 has a critical role in multiple cancers. The aim of the present study was to investigate the regulatory effect of LINC00657 in pancreatic cancer (PC) and reveal its molecular mechanism of function. The expression levels of LINC00657 and microRNA (miR)-520h were detected by reverse transcription-quantitative PCR in PC tissues and cell lines. MTT, wound healing and Transwell assays were used to detect cell viability, migration and invasion, respectively. Dual-luciferase reporter assay was utilized to examine the relationship between LINC00657 and miR-520h and that between miR-520h and cyclin-dependent kinases regulatory subunit 1 (CKS1B). Western blotting was performed to detect CKS1B expression. The expression levels of LINC00657 and CKS1B were enhanced and miR-520h expression level was reduced in PC tissues and cell lines compared with adjacent normal tissues or HPDE6 cells. LINC00657 knockdown decreased the viability, migration and invasion of PC cells. Additionally, LINC00657 targeted miR-520h and negatively modulated miR-520h expression. Furthermore, miR-520h overexpression inhibited the viability, migration and invasion of PC cells. In addition, miR-520h targeted CKS1B and reversely regulated CKS1B expression. miR-520h inhibition and CKS1B overexpression alleviated the inhibition effect of LINC00657 knockdown on the viability, migration and invasion of PACA-2 PC cells. In conclusion, the results of the present study demonstrated that LINC00657 knockdown repressed the viability, migration and invasion of PC cells via targeting the miR-520h/CKS1B axis, which may offer a future target for PC therapy.

Indexed as

cyclin-dependent kinases regulatory subunit 1LINC00657microRNA-520hpancreatic cancer

Identifiers

PMID34504588
PMCPMC8393733
OpenAlexW3192982571

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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.