Evidence map›Paper›PMID 28352193›Full record

ArticleOncoTargets and therapy2017

CDKL1 promotes tumor proliferation and invasion in colorectal cancer.

Chunzhi Qin, Li Ren, Meiling Ji, Shixu Lv, Ye Wei, Dexiang Zhu, Qi Lin, Pingping Xu, Wenju Chang, Jianmin Xu

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 23 citations in OpenAlex.

  1. A Constellation of Fluorescent Biosensors to Illuminate the Galaxy of Protein Kinases.Chembiochem : a European journal of chemical biology · 2026
    Review
  2. Article
  3. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  4. Review
  5. Article
  6. Article
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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 3 institutions in 1 country.

Chunzhi QinDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Li RenDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Meiling JiDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Shixu LvDepartment of Surgical Oncology, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Ye WeiDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Dexiang ZhuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Qi LinDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Pingping XuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Wenju ChangDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Jianmin XuDepartment of General Surgery, Zhongshan Hospital, Fudan University, Shanghai.
Sun Yat-sen University · CNThe First Affiliated Hospital, Sun Yat-sen University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCDKL1 is a member of the cell division cycle 2 (CDC2)-related serine threonine protein kinase family and is overexpressed in malignant tumors such as melanoma, breast cancer, and gastric cancer.

objectiveThis study aimed to evaluate whether CDKL1 can serve as a potential molecular target for colorectal cancer therapy. MATERIALS AND

methodsExpression of CDKL1 in colorectal cancer tissues and cell lines was measured by immunohistochemistry and Western blot, respectively. To investigate the role of CDKL1 in colorectal cancer, CDKL1-small hairpin RNA-expressing lentivirus was constructed and infected into HCT116 and Caco2 cells. The effects of RNA interference (RNAi)-mediated CDKL1 downregulation on cell proliferation and invasion were assessed by CCK-8, colony formation, transwell, and tumorigenicity assays in nude mice. The effects of CDKL1 downregulation on cell cycle and apoptosis were analyzed by flow cytometry. Furthermore, microarray method and data analysis elucidated the molecular mechanisms underlying the phenomenon.

resultsCDKL1 protein was overexpressed in colorectal cancer tissues compared with paired normal tissues. Knockdown of CDKL1 in HCT116 and Caco2 significantly inhibited cell growth, colony formation ability, tumor invasion, and G1-S phase transition of the cell cycle. The knockdown of

conclusionCDKL1 plays a vital role in tumor proliferation and invasion in colorectal cancer in vitro and in vivo and, thus, may be considered as a valuable target for therapeutic intervention.

Indexed as

CDKL1cell cyclecolorectal cancerprotein kinases

Identifiers

PMID28352193
PMCPMC5360398
OpenAlexW2595253147

What OpenQuestion holds

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LicenceCC BY-NC
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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.