Evidence map›Paper›PMID 36100894›Full record

ArticleBMC medical genomics2022

KCNJ14 knockdown significantly inhibited the proliferation and migration of colorectal cells.

Bin Li, Ning Ge, Zhongping Pan, Chaofeng Hou, Kun Xie, Dongfang Wang, Junwei Liu, Jie Wan, Feihong Deng, Mengyi Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

11 authors at 1 institution in 1 country.

Bin LiDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Ning GeDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Zhongping PanDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Chaofeng HouDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Kun XieDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Dongfang WangDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Junwei LiuDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Jie WanDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Feihong DengDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Mengyi LiDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China.
Shuping LuoDepartment of Colorectal Surgery, Zhengzhou Central Hospital Affiliated To Zhengzhou University, 16 Tongbai North Road, Zhengzhou, Henan, China. ShupingLuoLady@outlook.com.
Zhengzhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study attempted to verify the potential of KCNJ14 as a biomarker in colorectal cancer (CRC).

methodsData on transcriptomics and DNA methylation and the clinical information of CRC patients were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases. Biological information analysis methods were conducted to determine the role of KCNJ14 in the prognosis, diagnosis, immune cell infiltration, and regulation mechanism of CRC patients. The effect of KCNJ14 on the proliferation and migration of HCT116 and SW480 CRC cell lines was verified by in vitro experiments (MTT, colony-forming, wound healing, and transwell assays). Western blotting was performed to detect the effect of KCNJ14 on the levels of mTOR signalling pathway-related proteins.

resultsKCNJ14 expression was remarkably increased in CRC tissues and cell lines, which reduced the overall survival time of patients. KCNJ14 mRNA was negatively regulated by its methylation site cg17660703, which can also endanger the prognosis of patients with CRC. Functional enrichment analysis suggested that KCNJ14 is involved in the mTOR, NOD-like receptor, and VEGF signalling pathways. KCNJ14 expression was positively correlated with the number of CD4 + T cells and negatively correlated with that of CD8 + T cells in the immune microenvironment. KCNJ14 knockdown significantly reduced not only the proliferation and migration of CRC cell lines but also the levels of mTOR signalling pathway-related proteins.

conclusionsThis study not only increases the molecular understanding of KCNJ14 but also provides a potentially valuable biological target for the treatment of colorectal cancer.

Indexed as

Colorectal NeoplasmsCell Line, TumorCell MovementCell ProliferationHumansPotassium Channels, Inwardly RectifyingTOR Serine-Threonine KinasesTumor MicroenvironmentKir2.4 channelPotassium Channels, Inwardly RectifyingTOR Serine-Threonine KinasesBiological targetColorectal cancerKCNJ14MethylationPrognosis

Identifiers

PMID36100894
PMCPMC9472386
OpenAlexW4295760574

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.