Evidence map›Paper›PMID 24726842›Full record

ArticleEuropean journal of pharmacology2014

VN/14-1 induces ER stress and autophagy in HP-LTLC human breast cancer cells and has excellent oral pharmacokinetic profile in female Sprague Dawley rats.

Abhijit M Godbole, Senthilmurugan Ramalingam, Vidya P Ramamurthy, Aakanksha Khandelwal, Robert D Bruno, Vijay V Upreti, Lalji K Gediya, Puranik Purushottamachar, Hannah W Mbatia, Sankar Addya and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

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    Article
  3. Article
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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

12 authors at 4 institutions in 1 country.

Abhijit M GodboleDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Center for Biomolecular Therapeutics, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Senthilmurugan RamalingamDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Center for Biomolecular Therapeutics, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Vidya P RamamurthyDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Center for Biomolecular Therapeutics, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Aakanksha KhandelwalDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Robert D BrunoDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Vijay V UpretiDepartment of Pharmaceutical sciences, School of Pharmacy, University of Maryland, Baltimore, MD 21201, USA.
Lalji K GediyaDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Center for Biomolecular Therapeutics, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Puranik PurushottamacharDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Center for Biomolecular Therapeutics, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Hannah W MbatiaDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Center for Biomolecular Therapeutics, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Sankar AddyaDepartment of Cancer Biology, Kimmel Cancer Center, Jefferson Medical College, Thomas Jefferson University, PA 19107, USA.
Nicholas AmbulosGenomic Core Facility, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA.
Vincent C O NjarDepartment of Pharmacology, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Center for Biomolecular Therapeutics, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA; Marlene Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201-1559, USA. Electronic address: vnjar@som.umaryland.edu.
University of Maryland, Baltimore · USThomas Jefferson University · USU-M Rogel Cancer CenterUniversity of Baltimore · US

Funding

Functional organization of the superior temporal gyrus for speech perceptionR01DC012379 · NIDCD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Edward Chang · 2012 to 2026
$8.3M
Development of VN/14-1 and Related Analogs for Breast Cancer TherapyR01CA129379 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI NJAR, VINCENT COLLINS OFUKA · 2010 to 2014
$2.5M
NCI NIH HHS 1R01 CA 129379NCI NIH HHS R01 CA129379NIDCD NIH HHS R01 DC012379
6 · The paper itself

Abstract

Resistance to aromatase inhibitors is a major concern in the treatment of breast cancer. Long-term letrozole cultured (LTLC) cells represent a model of resistance to aromatase inhibitors. The LTLC cells were earlier generated by culturing MCF-7Ca, the MCF-7 human breast cancer cell line stably transfected with human placental aromatase gene for a prolonged period in the presence of letrozole. In the present study the effect of RAMBA, VN/14-1 on the sensitivity of LTLC cells upon multiple passaging and the mechanisms of action of VN/14-1 in such high passage LTLC (HP-LTLC) cells was investigated. We report that multiple passaging of LTLC cells (HP-LTLC cell clones) led to profound decrease in their sensitivity to VN/14-1. Additionally, microarray studies and protein analysis revealed that VN/14-1 induced marked endoplasmic reticulum (ER) stress and autophagy in HP-LTLC cells. We further report that VN/14-1 in combination with thapsigargin exhibited synergistic anti-cancer effect in HP-LTLC cells. Preliminary pharmacokinetics in rats revealed that VN/14-1 reached a peak plasma concentration (Cmax) within 0.17h after oral dosing. Its absolute oral bioavailability was >100%. Overall these results indicate potential of VN/14-1 for further clinical development as a potential oral agent for the treatment of breast cancer.

Indexed as

Administration, OralAnimalsAntineoplastic AgentsAutophagyBiological AvailabilityBreast NeoplasmsCell CycleCell Line, TumorCell ProliferationDown-RegulationDrug SynergismEndoplasmic Reticulum StressFemaleHumansImidazolesIntracellular Space4-(1H-imidazol-1-yl)retinoic acidAntineoplastic AgentsImidazolesThapsigarginTretinoinAutophagyBreast cancerER stressLTLCPharmacokinetics (PK)RAMBA-VN/14-1

Identifiers

PMID24726842
PMCPMC4047216
OpenAlexW2021752131

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.