Evidence map›Paper›PMID 26847701›Full record

ArticleScientific reports2016

KCTD12 Regulates Colorectal Cancer Cell Stemness through the ERK Pathway.

Liping Li, Tingmei Duan, Xin Wang, Ru-Hua Zhang, Meifang Zhang, Suihai Wang, Fen Wang, Yuanzhong Wu, Haojie Huang, Tiebang Kang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021
    Review
  9. Review
  10. Article
  11. KCells · 2020
    Article
  12. Diacerein treatment prevents colitis-associated cancer in mice.World journal of clinical oncology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. DRUM: Inference of Disease-Associated mFrontiers in genetics · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 4 institutions in 2 countries.

Liping LiState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
Tingmei DuanState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
Xin WangState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
Ru-Hua ZhangState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
Meifang ZhangState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
Suihai WangSchool of Biotechnology, Southern Medical University, Guangzhou 510515, China.
Fen WangDepartment of Pathology, First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Yuanzhong WuState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
Haojie HuangDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Tiebang KangState Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou 510060, China.
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNMayo Clinic · USSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting cancer stem cells (CSCs) in colorectal cancer (CRC) remains a difficult problem, as the regulation of CSCs in CRC is poorly understood. Here we demonstrated that KCTD12, potassium channel tetramerization domain containing 12, is down-regulated in the CSC-like cells of CRC. The silencing of endogenous KCTD12 and the overexpression of ectopic KCTD12 dramatically enhances and represses CRC cell stemness, respectively, as assessed in vitro and in vivo using a colony formation assay, a spheroid formation assay and a xenograft tumor model. Mechanistically, KCTD12 suppresses CRC cell stemness markers, such as CD44, CD133 and CD29, by inhibiting the ERK pathway, as the ERK1/2 inhibitor U0126 abolishes the increase in expression of CRC cell stemness markers induced by the down-regulation of KCTD12. Indeed, a decreased level of KCTD12 is detected in CRC tissues compared with their adjacent normal tissues and is an independent prognostic factor for poor overall and disease free survival in patients with CRC (p = 0.007). Taken together, this report reveals that KCTD12 is a novel regulator of CRC cell stemness and may serve as a novel prognostic marker and therapeutic target for patients with CRC.

Indexed as

Down-RegulationMAP Kinase Signaling SystemAnimalsAntineoplastic AgentsBiomarkers, TumorCell Line, TumorCell ProliferationColorectal NeoplasmsDrug Resistance, NeoplasmFemaleFluorouracilGene Expression Regulation, NeoplasticHT29 CellsHumansImatinib MesylateMaleAntineoplastic AgentsBiomarkers, TumorFluorouracilImatinib MesylateKCTD12 protein, humanProteins

Identifiers

PMID26847701
PMCPMC4742820
OpenAlexW2271345635

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.