Evidence map›Paper›PMID 26751936›Full record

ArticleOncogenesis2016

The CaSm (LSm1) oncogene promotes transformation, chemoresistance and metastasis of pancreatic cancer cells.

E C Little, E R Camp, C Wang, P M Watson, D K Watson, D J Cole

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.3field-weighted citation impact, top 33% 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, 38 citations in OpenAlex.

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  15. Processing body (P-body) and its mediators in cancer.Molecular and cellular biochemistry · 2022
    Review
  16. Journal of gastrointestinal oncology · 2022
    Article
  17. Article
  18. 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

6 authors at 2 institutions in 1 country.

E C LittleDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.
E R CampHollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
C WangHollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
P M WatsonHollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
D K WatsonHollings Cancer Center, Medical University of South Carolina, Charleston, SC, USA.
D J ColeDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA.
MUSC Hollings Cancer Center · USMedical University of South Carolina · US

Funding

South Carolina Clinical & Translational Research Institute (SCTR)UL1TR000062 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2012 to 2014
$9.4M
TARGETING THE CASM ONCOGENE AS A NOVEL THERAPY FOR PANCREATIC CANCERR01CA123159 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI COLE, DAVID J · 2007 to 2011
$1.4M
Innovative Delivery Strategy for CaSm Gene Therapy in Pancreatic CancerK08CA142904 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CAMP, ERNEST RAMSAY · 2010 to 2014
$867k
NCATS NIH HHS UL1 TR000062NCI NIH HHS K08 CA142904NCI NIH HHS R01 CA123159
6 · The paper itself

Abstract

The cancer-associated Sm-like (CaSm) oncogene is overexpressed in 87% of human pancreatic tumor samples and CaSm knockdown has demonstrated therapeutic efficacy in murine models of pancreatic cancer. Evidence indicates that CaSm modulates messenger RNA degradation; however, its target genes and the mechanisms by which CaSm promotes pancreatic cancer remain largely unknown. Here, we demonstrate that the CaSm overexpression alters several hallmarks of cancer-including transformation, proliferation, chemoresistance and metastasis. Doxycycline-induced CaSm expression enhanced proliferation and both anchorage-dependent and -independent growth of the human Panc-1 cells in vitro. CaSm induction decreased gemcitabine-induced cytotoxicity and altered the expression of apoptotic regulation genes, including Bad, E2F1 and Bcl-XL. CaSm-overexpressing Panc-1 cells were twofold more migratory and fourfold more invasive than the driver controls and demonstrated characteristics of epithelial-to-mesenchymal transition such as morphological changes and decreased E-cadherin expression. CaSm induction resulted in changes in RNA expression of metastasis-associated genes such as MMP1, SerpinB5, uPAR and Slug. Using a murine model of metastatic pancreatic cancer, injection of CaSm-induced Panc-1 cells resulted in a higher abundance of hepatic metastatic lesions. Overall, CaSm overexpression contributed to a more aggressive cancer phenotype in Panc-1 cells, further supporting the use of CaSm as a therapeutic target against pancreatic cancer.

Identifiers

PMID26751936
PMCPMC4728675
OpenAlexW2223515252

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.