Evidence map›Paper›PMID 20717927›Full record

ArticleJournal of cellular biochemistry2010

Lysyl oxidase propeptide sensitizes pancreatic and breast cancer cells to doxorubicin-induced apoptosis.

Chengyin Min, Yingshe Zhao, Mathilde Romagnoli, Philip C Trackman, Gail E Sonenshein, Kathrin H Kirsch

Abstract read
In one paragraph

Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Function of formyl peptide receptor 2 in adriamycin resistance of breast cancer.Experimental biology and medicine (Maywood, N.J.) · 2024
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  17. Lysyl oxidase, extracellular matrix remodeling and cancer metastasis.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012
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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 1 institution in 1 country.

Chengyin MinDepartment of Biochemistry, Boston University School of Medicine, 72 E. Concord St., Boston, Massachusetts 02118, USA.
Yingshe Zhao
Mathilde Romagnoli
Philip C Trackman
Gail E Sonenshein
Kathrin H Kirsch
Boston University · US

Funding

Lysyl Oxidase Propeptide: Breast Cancer InhibitorR01CA143108 · NCI · TUFTS UNIVERSITY BOSTON · PI SONENSHEIN, GAIL E. · 2010 to 2014
$2.5M
NFKB/REL AND THE PATHOGENESIS OF BREAST CANCERR01CA082742 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SONENSHEIN, GAIL E. · 1999 to 2008
$2.2M
Functional role of p130Cas/BCAR1 in breast cancerR01CA106468 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KIRSCH, KATHRIN H · 2005 to 2009
$1.4M
NCI NIH HHS R01 CA082742NCI NIH HHS R01 CA106468NCI NIH HHS R01 CA143108NCI NIH HHS R01 CA82742
6 · The paper itself

Abstract

RAS mutations or its activation by upstream receptor tyrosine kinases are frequently associated with poor response of carcinomas to chemotherapy. The 18 kDa propeptide domain of lysyl oxidase (LOX-PP) released from the secreted precursor protein (Pro-LOX) has been shown to inhibit RAS signaling and the transformed phenotype of breast, pancreatic, lung, and prostate cancer cells in culture, and formation of tumors by Her-2/neu-driven breast cancer cells in a mouse xenograft model. Here, we tested the effects of LOX-PP on MIA PaCa-2 pancreatic cancer cells, driven by mutant RAS. In MIA PaCa-2 cells in culture, LOX-PP attenuated the ERK and AKT activities and decreased the levels of the NF-κB p65 and RelB subunits and cyclin D1, which are activated by RAS signaling. In mouse xenograft growth, LOX-PP reduced growth of tumors by these pancreatic cancer cells, and the nuclear levels of the p65 NF-κB subunit and cyclin D1 proteins. While biological agents attenuate tumor growth when used alone, often they have additive or synergistic effects when used in combination with chemotherapeutic agents. Thus, we next tested the hypotheses that LOX-PP sensitizes pancreatic and breast cancer cells to the chemotherapeutic agent doxorubicin. Purified LOX-PP enhanced the cytotoxic effects of doxorubicin in pancreatic and breast cancer cells, as judged by ATP production, Cell Death ELISA assays, caspase 3 activation, PARP cleavage, and Annexin V staining. Thus, LOX-PP potentiates the cytotoxicity of doxorubicin on breast and pancreatic cancer cells, warranting additional studies with a broader spectrum of current cancer treatment modalities.

Indexed as

AnimalsApoptosisBreast NeoplasmsCell ProliferationDoxorubicinDrug Resistance, NeoplasmEnzyme PrecursorsFemaleHumansMaleMicePancreatic NeoplasmsProtein-Lysine 6-OxidaseSignal TransductionXenograft Model Antitumor AssaysDoxorubicinEnzyme PrecursorsProtein-Lysine 6-Oxidase

Identifiers

PMID20717927
PMCPMC3907072
OpenAlexW1981618937

What OpenQuestion holds

Textmetadata
LicenceTDM
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.