Evidence map›Paper›PMID 35058597›Full record

ArticleOncogene2022

Oncogenic potential of BEST4 in colorectal cancer via activation of PI3K/Akt signaling.

Xiao-Shun He, Wen-Long Ye, Yu-Juan Zhang, Xiao-Qin Yang, Feng Liu, Jing-Ru Wang, Xiao-Lu Ding, Yun Yang, Ruo-Nan Zhang, Yuan-Yuan Zhao and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  5. Developmental regulation of intestinalbioRxiv : the preprint server for biology · 2025
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  15. Comparison of KRAS gene in circulating tumor DNA levels vs histological grading of colorectal cancer patients through liquid biopsy.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association
    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

14 authors at 2 institutions in 2 countries.

Xiao-Shun He *Department of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0001-9195-3058
Wen-Long Ye *Department of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0003-1501-1135
Yu-Juan Zhang *Department of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0001-9567-1584
Xiao-Qin Yang *Department of Bioinformatics, Medical College of Soochow University, Soochow University, Suzhou, 215123, China.
Feng LiuDepartment of General Surgery, Canglang Hospital of Suzhou, Suzhou, 215009, China.
Jing-Ru WangDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0003-3847-508X
Xiao-Lu DingDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0002-4716-143X
Yun YangDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0001-9048-9265
Ruo-Nan ZhangDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0002-4693-9393
Yuan-Yuan ZhaoDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.ORCID http://orcid.org/0000-0003-2081-0097
Hai-Xia BiDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China.
Ling-Chuan GuoDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China. szglc@hotmail.com.ORCID http://orcid.org/0000-0002-1028-9296
Wen-Juan GanDepartment of Pathology, Dushu Lake Hospital Affiliated to Soochow University, Soochow University, Suzhou, 215124, China. ganwenjuan@suda.edu.cn.ORCID http://orcid.org/0000-0002-0436-1028
Hua WuDepartment of Pathology, Medical College of Soochow University & The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215123, China. wuhua@suda.edu.cn.ORCID http://orcid.org/0000-0002-4210-2377
Soochow University · CNSoochow University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BEST4 is a member of the bestrophin protein family that plays a critical role in human intestinal epithelial cells. However, its role and mechanism in colorectal cancer (CRC) remain largely elusive. Here, we investigated the role and clinical significance of BEST4 in CRC. Our results demonstrate that BEST4 expression is upregulated in clinical CRC samples and its high-level expression correlates with advanced TNM (tumor, lymph nodes, distant metastasis) stage, LNM (lymph node metastasis), and poor survival. Functional studies revealed that ectopic expression of BEST4 promoted CRC cell proliferation and metastasis, whereas the depletion of BEST4 had the opposite effect both in vitro and in vivo. Mechanistically, BEST4 binds to the p85α regulatory subunit of phosphatidylinositol-3-kinase (PI3K) and promotes p110 kinase activity; this leads to activation of Akt signaling and expression of MYC and CCND1, which are critical regulators of cell proliferation and metastasis. In clinical samples, the expression of BEST4 is positively associated with the expression of phosphorylated Akt, MYC and CCND1. Pharmacological inhibition of Akt activity markedly repressed BEST4-mediated Akt signaling and proliferation and metastasis of CRC cells. Importantly, the interaction between BEST4 and p85α was also enhanced by epidermal growth factor (EGF) in CRC cells. Therapeutically, BEST4 suppression effectively sensitized CRC cells to gefitinib treatment in vivo. Taken together, our findings indicate the oncogenic potential of BEST4 in colorectal carcinogenesis and metastasis by modulating BEST4/PI3K/Akt signaling, highlighting a potential strategy for CRC therapy.

Indexed as

Cell ProliferationColorectal NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudePhosphatidylinositol 3-KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID35058597
OpenAlexW4206302123

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.