Evidence map›Paper›PMID 28388571›Full record

ArticleOncotarget2017

A novel RON splice variant lacking exon 2 activates the PI3K/AKT pathway via PTEN phosphorylation in colorectal carcinoma cells.

Yu Ling, Yeye Kuang, Lin-Lin Chen, Wei-Feng Lao, Yao-Ru Zhu, Le-Qi Wang, Da Wang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 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
1.2field-weighted citation impact, top 22% 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, 21 citations in OpenAlex.

  1. Does human cytomegalovirus provide a novel therapeutic target for patients with glioblastoma?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
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  6. A network map of macrophage-stimulating protein (MSP) signaling.Journal of cell communication and signaling · 2023
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  12. Perspective in Alternative Splicing Coupled to Nonsense-Mediated mRNA Decay.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Review
  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

7 authors at 2 institutions in 1 country.

Yu LingDepartment of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University of Medicine, Hangzhou, Zhejiang 310016, People's Republic of China.
Yeye KuangBiomedical Center, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.
Lin-Lin ChenDepartment of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University of Medicine, Hangzhou, Zhejiang 310016, People's Republic of China.
Wei-Feng LaoDepartment of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University of Medicine, Hangzhou, Zhejiang 310016, People's Republic of China.
Yao-Ru ZhuDepartment of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University of Medicine, Hangzhou, Zhejiang 310016, People's Republic of China.
Le-Qi WangDepartment of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University of Medicine, Hangzhou, Zhejiang 310016, People's Republic of China.
Da WangDepartment of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University of Medicine, Hangzhou, Zhejiang 310016, People's Republic of China.
Sir Run Run Shaw Hospital · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal expression of the Recepteur d'Origine Nantais (RON) receptor tyrosine kinase is accompanied by the generation of multiple splice or truncated variants, which mediate many critical cellular functions that contribute to tumor progression and metastasis. Here, we report a new RON splice variant in the human colorectal cancer (CRC) cell line HT29. This variant is a 165 kda protein generated by alternative pre-mRNA splicing that eliminates exon 2, causing an in-frame deletion of 63 amino acids in the extracellular domain of the RON β chain. The deleted transcript was a single chain expressed in the intracellular compartment. Although it lacked tyrosine phosphorylation activity, the RONΔ165E2 variant could phosphorylate phosphatase and tensin homolog (PTEN), thereby activating the PI3K/AKT pathway. In addition, in vitro and in vivo experiments showed that the RONΔ165E2 promoted cell migration and tumor growth. Finally, in an investigation of 67 clinical CRC samples, the variant was highly expressed in about 58% of the samples, and was positively correlated with the invasive depth of the tumor (P < 0.05). These results demonstrate that the novel RONΔ165E2 variant promoted tumor progression while activating the PI3K/AKT pathway via PTEN phosphorylation.

Indexed as

Alternative SplicingExonsAnimalsApoptosisBiomarkers, TumorCell MovementCell ProliferationColorectal NeoplasmsFemaleFollow-Up StudiesHumansMaleMiceMice, NudeMiddle AgedPhosphatidylinositol 3-KinasesBiomarkers, TumorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanReceptor Protein-Tyrosine KinasesRON proteincolorectal cancer cellPI3K/AKT pathwayPTENRONsplicing variants

Identifiers

PMID28388571
PMCPMC5503598
OpenAlexW2599435730

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.