Evidence map›Paper›PMID 22281836›Full record

ArticleMolecular medicine (Cambridge, Mass.)2012

Characterization of bridging integrator 1 (BIN1) as a potential tumor suppressor and prognostic marker in hepatocellular carcinoma.

Ke Pan, Xiao-ting Liang, Hua-kun Zhang, Jing-jing Zhao, Dan-dan Wang, Jian-jun Li, Qizhou Lian, Alfred E Chang, Qiao Li, Jian-chuan Xia

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2012. 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
1.4field-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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  2. Article
  3. Review
  4. The Prognostic Significance of theIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Review
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  10. Article
  11. Article
  12. Article
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  14. Article
  15. Inverse regulation of bridging integrator 1 and BCR-ABL1 in chronic myeloid leukemia.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Article
  17. Amphiphysin 2 (BIN1) in physiology and diseases.Journal of molecular medicine (Berlin, Germany) · 2014
    Review
  18. Article
  19. Review
  20. 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

10 authors at 4 institutions in 3 countries.

Ke PanState Key Laboratory of Oncology in Southern China, Sun Yat-sen University, Guangzhou, China.
Xiao-ting Liang
Hua-kun Zhang
Jing-jing Zhao
Dan-dan Wang
Jian-jun Li
Qizhou Lian
Alfred E Chang
Qiao Li
Jian-chuan Xia
Sun Yat-sen University · CNSun Yat-sen University Cancer Center · CNUniversity of Hong Kong · HKUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been shown that bridging integrator 1 (BIN1) can interact with c-myelocytomatosis (c-Myc) oncoprotein in cancer. However, the role of BIN1 in hepatocellular carcinoma (HCC) is not clear. In the present study, we investigated the expression and prognostic role of BIN1 in primary HCC and evaluated the function of BIN1 in hepatocarcinogenesis. Using real-time polymerase chain reaction and Western blot analysis, we found significantly decreased expression of BIN1 in primary HCC tumor tissues (n = 42) compared with adjacent normal tissues and in HCC cell lines. Immunohistochemistry analysis also found decreased BIN1 expression in HCC tumor tissues (n = 117). In clinicopathological analysis, loss of BIN1 expression correlated significantly (P < 0.05) with differentiation scores and tumor size. Importantly, decreased expression of BIN1 in tumors was found to be closely associated with a poor prognosis, and we conclude that BIN1 was an independent prognostic factor in a multivariate analysis. In mechanistic studies, restoring BIN1 expression in BIN1-null HCC cells significantly inhibited cell proliferation and colony formation and induced apoptosis of HCC cells. Furthermore, we found that BIN1 overexpression could significantly suppress the motility and invasion of HCC cells in vitro. Our results indicate that BIN1 may function as a potential tumor suppressor and serve as a novel prognostic marker in HCC patients. The BIN1 molecule might play an important role in tumor growth, cell motility and invasion. Modulation of BIN1 expression may lead to clinical applications of this critical molecule in the control of hepatocellular carcinoma as well as in early and effective diagnosis of this aggressive tumor.

Indexed as

Adaptor Proteins, Signal TransducingApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell CycleCell Line, TumorCell MovementFemaleHumansLiver NeoplasmsMaleMiddle AgedNuclear ProteinsPrognosisRNA, MessengerTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingBIN1 protein, humanBiomarkers, TumorNuclear ProteinsRNA, MessengerTumor Suppressor Proteins

Identifiers

PMID22281836
PMCPMC3356425
OpenAlexW201471757

What OpenQuestion holds

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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.