Evidence map›Paper›PMID 33995648›Full record

ArticleJournal of Cancer2021

KIF11 is upregulated in colorectal cancer and silencing of it impairs tumor growth and sensitizes colorectal cancer cells to oxaliplatin via p53/GSK3β signaling.

Yan Zhou, Leping Yang, Li Xiong, Kunpeng Wang, Xuyang Hou, Qinglong Li, Fanhua Kong, Xi Liu, Jun He

Open access · goldAbstract read
In one paragraph

Article in Journal of Cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 20 citations in OpenAlex.

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  8. Novel mScientific reports · 2025
    Article
  9. Kinesin Spindle Protein (KIF11) in Mitosis and Cancer.International journal of molecular sciences · 2025
    Review
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  12. Review
  13. Review
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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

9 authors at 3 institutions in 1 country.

Yan ZhouDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Leping YangDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Li XiongDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Kunpeng WangDepartment of General Surgery, Taizhou Central Hospital, Taizhou University Hospital, Taizhou, Zhejiang 318000, China.
Xuyang HouDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Qinglong LiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Fanhua KongDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Xi LiuDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Jun HeDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Second Xiangya Hospital of Central South University · CNCentral South University · CNTaizhou Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the most frequently diagnosed cancer of the digestive tract. Chemotherapy drugs such as oxaliplatin are frequently administered to CRC patients diagnosed with advanced or metastatic disease. A deep understanding of the molecular mechanism underlying CRC tumorigenesis and identification of optimal biomarkers for estimating chemotherapy sensitivity are essential for the treatment of CRC. Numerous members of the kinesin family are dysregulated in cancers, contributing to tumorigenesis, metastasis and drug resistance. KIF11 is a key component of the bipolar spindle and is highly expressed in several cancer types. We analyzed KIF11 expression in clinical samples by Western blotting and qRT-PCR and explored its role and mechanism in CRC growth and sensitivity to oxaliplatin via detection of the phosphorylation profile of kinases and gain-and-loss-of-function assays. We found that KIF11 was upregulated in CRC tissues and was associated with advanced clinical stage and vessel invasion and that knockdown of KIF11 led to tumor growth arrest and increased sensitivity to oxaliplatin via enhanced DNA damage and apoptosis. Mechanistically, aberrantly activated p53 signaling or possibly deactivated GSK3β signaling was responsible for KIF11 knockdown-mediated effects in CRC cells. Thus, our data firmly demonstrated that KIF11 could serve as a potential oncogene and proper biomarker for assessing oxaliplatin sensitivity in CRC.

Indexed as

autophagycolorectal cancerGSK3βKIF11oxaliplatin

Identifiers

PMID33995648
PMCPMC8120193
OpenAlexW3159658612

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.