Evidence map›Paper›PMID 22101277›Full record

ArticleCell cycle (Georgetown, Tex.)2011

The mitochondrial protein C1qbp promotes cell proliferation, migration and resistance to cell death.

Allison M McGee, Diana L Douglas, Yayun Liang, Salman M Hyder, Christopher P Baines

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

53 citing papers in PubMed, 76 citations in OpenAlex.

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  18. Leaked Mitochondrial C1QBP Inhibits Activation of the DNA Sensor cGAS.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  19. Complement's favourite organelle-Mitochondria?British journal of pharmacology · 2021
    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

5 authors at 2 institutions in 2 countries.

Allison M McGeeDalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA.
Diana L Douglas
Yayun Liang
Salman M Hyder
Christopher P Baines
Schlumberger (Ireland) · IEUniversity of Missouri · US

Funding

Molecular Identity of the Cardiac Mitochondrial PoreR01HL094404 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI BAINES, CHRISTOPHER P · 2009 to 2018
$3.6M
Identifying novel components of the cardiac necrotic programR21HL092327 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI BAINES, CHRISTOPHER P · 2008 to 2009
$412k
NHLBI NIH HHS HL092327NHLBI NIH HHS HL094404NHLBI NIH HHS R01 HL094404NHLBI NIH HHS R21 HL092327
6 · The paper itself

Abstract

Complement 1q-Binding Protein (C1qbp) is a mitochondrial protein reported to be upregulated in cancer. However, whether C1qbp plays a tumor suppressive or tumorigenic role in the progression of cancer is controversial. Moreover, the exact effects of C1qbp on cell proliferation, migration, and death/survival have not been definitely proven. To this end, we comprehensively examined the effects of C1qbp on mitochondrial-dependent cell death, proliferation, and migration in both normal and breast cancer cells using genetic gain- and loss-of-function approaches. In normal fibroblasts, overexpression of C1qbp protected the cells against staurosporine-induce apoptosis, increased proliferation, decreased cellular ATP, and increased cell migration in a wound-healing assay. In contrast, the opposite effects were observed in fibroblasts depleted of C1qbp by RNA interference. C1qbp expression was found to be markedly elevated in 4 different human breast cancer cell lines as well as in ductal and adenocarcinoma tumors from breast cancer patients. Stable knockdown of C1qbp by shRNA in the aggressive MDA-MB-231 breast cancer cell line greatly reduced cell proliferation, increased ATP levels, and decreased cell migration compared to control shRNA-transfected cells. Moreover, C1qbp knockdown elicited a significant increase in doxorubicin-induced apoptosis in the MDA-MB-231 cells. Finally, C1qbp upregulation was not restricted to breast cancer cells and tumors, as levels of C1qbp were also found to be significantly elevated in both human lung and colon cancer cell lines and carcinomas. Together, these results establish a pro-tumor, rather than anti-tumor, role for C1qbp, and indicate that C1qbp could serve as a molecular target for cancer therapeutics.

Indexed as

Cell DeathCell MovementCell ProliferationAdenoviridaeAnimalsCarrier ProteinsDoxorubicinFemaleFibroblastsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHCT116 CellsHT29 CellsHumansHyaluronan ReceptorsMiceC1QBP protein, humanC1qbp protein, mouseCarrier ProteinsDoxorubicinHyaluronan ReceptorsMitochondrial ProteinsStaurosporine

Identifiers

PMID22101277
PMCPMC3272292
OpenAlexW2006902688

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.