Evidence map›Paper›PMID 28664914›Full record

ArticleBritish journal of cancer2017

LIM kinase 1 interacts with myosin-9 and alpha-actinin-4 and promotes colorectal cancer progression.

Qing Liao, Rui Li, Rui Zhou, Zhihua Pan, Lijun Xu, Yanqing Ding, Liang Zhao

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
  14. Article
  15. Review
  16. Circular RNAs as biomarkers for lung cancer.Non-coding RNA research · 2023
    Review
  17. Article
  18. Article
  19. Review
  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

7 authors at 2 institutions in 1 country.

Qing LiaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Rui LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Rui ZhouDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Zhihua PanDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Lijun XuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Yanqing DingDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Liang ZhaoDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Southern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLIM kinase 1 (LIMK1) is a key regulator of the cytoskeletal organisation involved in cell proliferation and migration. Even though LIMK1 is frequently dysregulated in epithelial cancers, the role and mechanisms of LIMK1 in colorectal cancer (CRC) remains unclear.

methodsImmunohistochemical analysis was performed to examine the expression and clinical significance of LIMK1 in CRC samples. Loss- and gain-of-function assay was performed to investigate the effects of aberrant expression on cellular biological behaviour of CRC cells in vitro and in vivo. Immunoblotting and immunoprecipitation was used to screen LIMK1-related signalling pathways and downstream factors.

resultsIn this study, our results showed that LIMK1 was upregulated in CRC tissues and localised in both the cytoplasm and the nucleus of CRC cells. Overexpression of LIMK1 in cytoplasmic and nuclear subcellular compartments was closely related to tumour metastasis and poor prognosis of CRC patients. Enhanced expression of cytoplasmic and nuclear LIMK1 significantly increased cell proliferation and migration by driving epithelial-mesenchymal transition and activating the PI3K/Akt signal pathway in vitro as well as promoting growth and metastasis of CRC xenografts, whereas opposite effects were achieved in LIMK1-silenced cells. Furthermore, we identified two tumour metastasis-associated proteins, MYH9 and ACTN4, as direct targets of LIMK1, which were required for a LIMK1-mediated aggressive phenotype.

conclusionsThese findings indicate that LIMK1 plays a critical role in promoting CRC progression at subcellular level. Our findings provide new insights into the metastasis of CRC and advocate for the development of clinical intervention strategies against advanced CRC.

Indexed as

ActininAnimalsCell Line, TumorCell MovementCell NucleusCell ProliferationColorectal NeoplasmsCytoplasmDisease ProgressionEpithelial-Mesenchymal TransitionGene SilencingHumansLim KinasesMiceMice, NudeMolecular Motor ProteinsActininACTN4 protein, humanLIMK1 protein, humanLim KinasesMolecular Motor ProteinsMYH9 protein, humanMyosin Heavy ChainsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID28664914
PMCPMC5558682
OpenAlexW2730651489

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.