Evidence map›Paper›PMID 28522860›Full record

ArticleScientific reports2017

Involvement of FAK-ERK2 signaling pathway in CKAP2-induced proliferation and motility in cervical carcinoma cell lines.

Qi-Sang Guo, Yu Song, Ke-Qin Hua, Shu-Jun Gao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. The spindle protein CKAP2 regulates microtubule dynamics and ensures faithful chromosome segregation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Review
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  14. Clinical significance of focal adhesion kinase (FAK) in cervical cancer progression and metastasis.International journal of clinical and experimental pathology · 2020
    Article
  15. Article
  16. 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

4 authors at 2 institutions in 1 country.

Qi-Sang GuoCervical Diseases Diagnosis & Treatment Center, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, 200011, P. R. China.
Yu SongCervical Diseases Diagnosis & Treatment Center, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, 200011, P. R. China.
Ke-Qin HuaDepartment of Gynecology, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, 200011, P. R. China. huakeqinjiaoshou@163.com.
Shu-Jun GaoCervical Diseases Diagnosis & Treatment Center, Obstetrics and Gynecology Hospital, Fudan University, Shanghai, 200011, P. R. China. 031108282@fudan.edu.cn.
Obstetrics and Gynecology Hospital of Fudan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical carcinoma is the fourth most common cause of death in woman, caused by human papillomavirus (HPV) infections and arising from the cervix. Cytoskeleton-associated protein 2 (CKAP2), also known as tumor-associated microtubule-associated protein, has been linked to tumorigenic effects. In the present study, we screened CKAP2 as a new candidate gene which promotes development of cervical carcinoma, in two independent datasets (TCGA and GSE27678). Results showed that CKAP2 expression was significantly up-regulated in cervical cancerous tissues compared with normal counterparts. Gene set enrichment analysis (GSEA) showed that metastasis, cell cycle and FAK pathways were related with elevated CKAP2 expression. Knockdown of CKAP2 expression significantly inhibited cell proliferation, migration and invasion both in HeLa and C-33A cells. And depletion of CKAP2 down-regulated the expression of metastasis and cell cycle related proteins as well as the phosphorylation of ERK2 (p-ERK2), except E-cadherin. In vivo experiment revealed that knockdown of CKAP2 inhibited C-33A cells proliferation. However, FAK inhibitor PF-562271 and ERK2 inhibitor VX-11e treatment significantly inhibited CKAP2 overexpression-induced cell proliferation, migration and invasion in SiHa cells. In conclusion, our study suggests that CKAP2 acts as a functional oncogene in cervical carcinoma development and may exert its function by targeting FAK-ERK2 signaling pathway.

Indexed as

Cell MovementCell ProliferationAdultCarcinomaCytoskeletal ProteinsFemaleFocal Adhesion Protein-Tyrosine KinasesHeLa CellsHumansMitogen-Activated Protein Kinase 1Neoplasm MetastasisSignal TransductionUterine Cervical NeoplasmsCKAP2 protein, humanCytoskeletal ProteinsFocal Adhesion Protein-Tyrosine KinasesMitogen-Activated Protein Kinase 1

Identifiers

PMID28522860
PMCPMC5437009
OpenAlexW2612669734

What OpenQuestion holds

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LicenceCC BY
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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.