Evidence map›Paper›PMID 30275562›Full record

ArticleOncogene2019

XIAP facilitates breast and colon carcinoma growth via promotion of p62 depletion through ubiquitination-dependent proteasomal degradation.

Xing Huang, Xiao-Nan Wang, Xiao-Dong Yuan, Wen-Yong Wu, Peter E Lobie, Zhengsheng Wu

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

6 authors at 3 institutions in 1 country.

Xing HuangKey Laboratory of Precision Diagnosis and Treatment for Hepatobiliary and Pancreatic Tumor of Zhejiang Province, First Affiliated Hospital, School of Medicine, Zhejiang University, 310003, Hangzhou, Zhejiang, China. dr.huangxing@foxmail.com.
Xiao-Nan WangDepartment of Pathology, Anhui Medical University, 230032, Hefei, Anhui, China.
Xiao-Dong YuanDepartment of Pathology, Anhui Medical University, 230032, Hefei, Anhui, China.
Wen-Yong WuDepartment of General Surgery, The First Affiliated Hospital of Anhui Medical University, 230032, Hefei, Anhui, China.
Peter E LobieTsinghua Berkeley Shenzhen Institute, Tsinghua University, Shenzhen, Guangdong, China.
Zhengsheng WuDepartment of Pathology, Anhui Medical University, 230032, Hefei, Anhui, China. woozson@yahoo.com.
Anhui Medical University · CNTsinghua University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

X-linked inhibitor of apoptosis protein (XIAP) possesses a critical role in promotion of cell survival and maintenance of cellular homeostasis. In cancer, elevated XIAP expression has been associated with malignancy, poor prognosis, and treatment resistance. However, the underlying mechanisms of these effects remain unclear. XIAP has previously been proposed to promote tumor growth through suppression of autophagy. In this study, we examined the expression of XIAP and p62, two critical mediators of autophagy, in breast and colon cancer. We observed a negative correlation between XIAP and p62 expression in normal and cancer tissues of breast and colon, and that the ratio of XIAP and p62 expression determines the cancer phenotype. In vitro, we observed that XIAP interacted with p62 and also that XIAP depletion resulted in increased expression of p62. XIAP functioned as an ubiquitination E3 ligase towards p62 and suppressed p62 expression through ubiquitin-proteasomal degradation. Furthermore, XIAP enhanced cancer cell proliferation, viability, and colony formation in vitro via suppression of p62. In addition, we demonstrated that XIAP-enhanced tumor growth is dependent on depletion of p62 in vivo. Herein, we have therefore delineated a novel mechanism by which XIAP contributes to development and progression of breast and colon carcinoma.

Indexed as

AnimalsApoptosisAutophagyBreast NeoplasmsCell Line, TumorCell ProliferationColonic NeoplasmsFemaleGene Expression Regulation, NeoplasticHumansMiceProteolysisRNA-Binding ProteinsUbiquitinationUbiquitin-Protein LigasesXenograft Model Antitumor AssaysP62 protein, humanRNA-Binding ProteinsUbiquitin-Protein LigasesXIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID30275562
OpenAlexW2892456322

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.