Evidence map›Paper›PMID 27699664›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

RIP1 upregulation promoted tumor progression by activating AKT/Bcl-2/BAX signaling and predicted poor postsurgical prognosis in HCC.

Cong Wang, Bowen Yao, Meng Xu, Xin Zheng

Abstract read
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Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Targeting RIPK1 to modulate cell death and tumour microenvironment in cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Fungal Immunomodulatory Protein fromInternational journal of molecular sciences · 2018
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. CXCL10 accelerates EMT and metastasis by MMP-2 in hepatocellular carcinoma.American journal of translational research · 2017
    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

4 authors.

Cong WangDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, China.
Bowen YaoDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, China.
Meng XuDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, China.
Xin ZhengDepartment of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Xi'an, Shaanxi, 710061, China. raymondzhengxin@foxmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although growing body of evidences have identified a critical role for receptor-interacting protein kinase 1 (RIP1) in mediating cell death signaling, its possible contribution to hepatocellular carcinoma (HCC) progression remains unclear. Here, we displayed that expression of RIP1 was significantly upregulated in HCC tissues than in adjacent liver tissues from 81.9 % HCC patients (P < 0.001) by immunohistochemistry (IHC) staining. Overexpression of RIP1 was found positively associated with HBV infection, advanced TNM staging, portal vein invasion, and intrahepatic metastases. Kaplan-Meier curve analysis indicated that patients with higher RIP1 expression in HCC tissues suffered from unfavorable postsurgical survival. Higher RIP1 expression in HCC tissues was also confirmed to be an independent poor prognostic predictor. Knockdown of RIP1 resulted in suppression of cell viability and proliferation and induced cell apoptosis in MHCC97h cells. Nevertheless, enforced expression of RIP1 promoted cell viability and proliferation of Huh7 cells and inhibited cell apoptosis. Mechanistic studies revealed that RIP1 exerted its function on HCC progression via activating AKT/Bcl-2/BAX signaling. In conclusion, our results provided the evidence of RIP1 overexpression in HCC, and RIP1 could be a novel predictive factor of unfavorable prognosis in HCC patients. Activation of AKT/Bcl-2/BAX signaling contributed to RIP1 promoting HCC progression.

Indexed as

AdultAgedApoptosisbcl-2-Associated X ProteinBiomarkers, TumorBlotting, WesternCarcinoma, HepatocellularCell ProliferationFemaleHumansImmunoenzyme TechniquesLiver NeoplasmsMaleMiddle AgedNeoplasm GradingNuclear Pore Complex ProteinsAGFG1 protein, humanAKT1 protein, humanBAX protein, humanbcl-2-Associated X ProteinBiomarkers, TumorNuclear Pore Complex ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2RNA-Binding ProteinsRNA, MessengerAKTBcl-2/BAXHCCPrognosisRIP1

Identifiers

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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.