Evidence map›Paper›PMID 32203166›Full record

ArticleOncogene2020

Long noncoding RNA CMPK2 promotes colorectal cancer progression by activating the FUBP3-c-Myc axis.

Qingzu Gao, Rui Zhou, Yuan Meng, Rongfei Duan, Ling Wu, Rui Li, Fengliu Deng, Chuang Lin, Liang Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  3. Comprehensive Profiling of NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  6. LncRNA TMEM99 Complexes with IGF2BP2 to Inhibit Autophagy in Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  11. Article
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  15. Article
  16. Article
  17. Article
  18. Article
  19. Significant position of C-myc in colorectal cancer: a promising therapeutic target.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  20. 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

9 authors at 4 institutions in 1 country.

Qingzu Gao *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Rui Zhou *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuan MengDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Rongfei DuanDepartment of Endocrinology, The First Affiliated Hospital of Xinxiang Medical University, Guangzhou, China.
Ling WuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Rui LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Fengliu DengDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Chuang LinDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Liang ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China. liangsmu@foxmail.com.
Southern Medical University · CNNanfang Hospital · CNFirst Affiliated Hospital of Xinxiang Medical University · CNXinxiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) have been shown to play crucial roles in cancer long noncoding RNAs (lncRNAs) have been known to play crucial roles in cancer development and progression by regulating chromatin dynamics and gene expression. However, only a few lncRNAs with annotated functions in the progression of colorectal cancer (CRC) have been identified to date. In the present study, the expression of lncCMPK2 was upregulated in CRC tissues and positively correlated with clinical stages and lymphatic metastasis. The overexpression of lncCMPK2 promoted the proliferation and cell cycle transition of CRC cells. Conversely, the silencing of lncCMPK2 restricted cell proliferation both in vitro and in vivo. lncCMPK2 was localized to the nucleus of CRC cells, bound to far upstream element binding protein 3 (FUBP3), and guided FUBP3 to the far upstream element (FUSE) of the c-Myc gene to activate transcription. lncCMPK2 also stabilized FUBP3. These results provide novel insights into the functional mechanism of lncCMPK2 in CRC progression and highlight its potential as a biomarker of advanced CRC and therapeutic target.

Indexed as

AnimalsCell MovementCell ProliferationColorectal NeoplasmsDisease ProgressionDNA-Binding ProteinsHCT116 CellsHeterograftsHumansMiceProto-Oncogene Proteins c-mycRNA, Long NoncodingSignal TransductionTranscription FactorsDNA-Binding ProteinsFUBP3 protein, humanMYC protein, humanProto-Oncogene Proteins c-mycRNA, Long NoncodingTranscription Factors

Identifiers

PMID32203166
OpenAlexW3011111569

What OpenQuestion holds

Textmetadata
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.