Evidence map›Paper›PMID 28745317›Full record

ArticleOncogene2017

Reticulocalbin-2 enhances hepatocellular carcinoma proliferation via modulating the EGFR-ERK pathway.

D Ding, H Huang, W Jiang, W Yu, H Zhu, J Liu, H Saiyin, J Wu, H Huang, S Jiang and 1 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Reticulocalbin3: A CaCancer science · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Observational
  16. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

D DingState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.ORCID 0000-0003-2339-7349
H HuangState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
W JiangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University Shanghai Medical College, Shanghai, China.
W YuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
H ZhuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
J LiuCenter for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Key Laboratory for Assisted Reproduction and Reproductive Genetics, Shanghai, China.
H SaiyinState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
J WuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
H HuangDepartment of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA.
S JiangState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
L YuState Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Fudan University · CNMayo Clinic · USShanghai Medical College of Fudan University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a major health threat worldwide. Although the involvement of reticulocalbin-2 (RCN2) in cell differentiation has been reported, its function in oncogenesis is poorly understood. Here, we showed that RCN2 was upregulated in tumors compared with adjacent non-tumorous tissues in HCC patients and RCN2 expression clinically correlated with tumor size, disease recurrence and survival rate. Both knockdown and knockout of RCN2 significantly inhibited HCC cell proliferation by inducing G1/S transition arrest and downregulating cyclin D1 expression, while the proliferative ability was restored in knockout HCC cells with exogenously expressed RCN2. Mechanistically, we demonstrated that RCN2 interacted with the epidermal growth factor receptor (EGFR). Knockout of RCN2 in HCC cells not only inhibited activation of the EGFR-ERK pathway by blocking EGF-mediated EGFR dimerization and internalization but also suppressed cell proliferation and EGFR phosphorylation under long exposure to EGF. We further showed that knockout of RCN2 inhibited EGFR phosphorylation, Ki-67 expression and tumor growth in nude mice. Moreover, we demonstrated that RCN2 knockout sensitized HCC cells to tyrosine kinase inhibitors, including erlotinib, lapatinib and sunitinib. Taken together, our results indicate that RCN2 plays a pivotal role in HCC cell proliferation and tumor growth presumably through regulating activation of the EGFR-ERK pathway. Our work also suggests that RCN2 is a potential therapeutic target of HCC.

Indexed as

MAP Kinase Signaling SystemAnimalsAntineoplastic AgentsCalcium-Binding ProteinsCarcinoma, HepatocellularCell Line, TumorCell ProliferationCell SurvivalErbB ReceptorsFemaleHumansLiver NeoplasmsMaleMice, NudeMiddle AgedNeoplasm TransplantationAntineoplastic AgentsCalcium-Binding ProteinsEGFR protein, humanErbB ReceptorsProtein Kinase InhibitorsRCN2 protein, human

Identifiers

PMID28745317
OpenAlexW2738410190

What OpenQuestion holds

Textmetadata
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.