Evidence map›Paper›PMID 30348114›Full record

ArticleBMC cancer2018

ACTL6A expression promotes invasion, metastasis and epithelial mesenchymal transition of colon cancer.

Zhijun Zeng, Hao Yang, Shuai Xiao

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

30 citing papers in PubMed, 69 citations in OpenAlex.

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  6. Actin-Like Protein 6A as an Oncogene and Therapeutic Target in Cancer.International journal of medical sciences · 2025
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  18. ACTL6A promotes repair of cisplatin-induced DNA damage, a new mechanism of platinum resistance in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

3 authors at 1 institution in 1 country.

Zhijun ZengDepartment of Geratic Surgery, Central South University, Xiangya Road 87, Changsha, Hunan, 410008, People's Republic of China.
Hao YangDepartment of Geratic Surgery, Central South University, Xiangya Road 87, Changsha, Hunan, 410008, People's Republic of China.
Shuai XiaoDepartment of Geratic Surgery, Central South University, Xiangya Road 87, Changsha, Hunan, 410008, People's Republic of China. xiaoshuai1982@hotmail.com.
Central South University · CN

Funding

National Natural Sciences Foundation of China 81702949Natural Sciences Foundation of Hunan Province 2018JJ3851Youth research fund of Xiangya Hospital 2016Q07
6 · The paper itself

Abstract

backgroundMetastasis is the main cause of death in patients with advanced stage colon cancer. Epithelial mesenchymal transition (EMT) plays an important role in invasion and metastasis. Actin-like 6A (ACTL6A) is vital for embryogenesis and differentiation and is also critical for metastasis and EMT in hepatocellular carcinoma, as observed in our previous study. In the present study, we further explored the role of ACTL6A in colon cancer metastasis.

methodsACTL6A expression levels were analyzed in normal colon, colon adenoma and colon cancer specimens using public databases and tissue samples. ACTL6A expression and its association with clinicopathologic features of colon cancer patients were also analyzed. ACTL6A-overexpression and ACTL6A-knockdown colon cancer cells were used to perform cytological experiments to explore the potential biological function of ACTL6A in metastasis and EMT in colon cancer.

resultsThe data from both the Gene Expression Omnibus (GEO) and Oncomine databases showed that ACTL6A expression levels in colon adenoma and cancer were higher than those in normal colon samples. The ACTL6A expression level in fresh colon cancer specimens was also higher than that in the corresponding adjacent normal colon specimens. Patients with high ACTL6A expression directly correlated with advanced pT status, distant metastasis, poor differentiation and microvascular/perineural invasion. ACTL6A overexpression promoted migration and invasion of colon cancer cells, whereas ACTL6A knockdown exhibited the opposite effect in vitro. Moreover, we demonstrated that ACTL6A promoted EMT in colon cancer cells in vitro.

conclusionsOur findings indicate that ACTL6A exhibits pro-tumor function and acts as an EMT activator in colon cancer. ACTL6A may serve as a potential therapeutic target for colon cancer.

Indexed as

Gene Expression Regulation, NeoplasticActinsAdultAgedCell Line, TumorCell MovementChromosomal Proteins, Non-HistoneColonic NeoplasmsDatabases, GeneticDNA-Binding ProteinsEpithelial-Mesenchymal TransitionFemaleHumansImmunohistochemistryMaleMiddle AgedActinsACTL6A protein, humanChromosomal Proteins, Non-HistoneDNA-Binding ProteinsACTL6AColon cancerEMTInvasionMetastasis

Identifiers

PMID30348114
PMCPMC6198485
OpenAlexW2897767259

What OpenQuestion holds

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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.