Evidence map›Paper›PMID 27521996›Full record

ArticleThe American journal of pathology2016

Knockdown of CSE1L Gene in Colorectal Cancer Reduces Tumorigenesis in Vitro.

Jose M Pimiento, Kevin G Neill, Evita Henderson-Jackson, Steven A Eschrich, Dung-Tsa Chen, Kazim Husain, David Shibata, Domenico Coppola, Mokenge P Malafa

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. 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
1.6field-weighted citation impact, top 16% 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, 32 citations in OpenAlex.

  1. Article
  2. CSE1L Silencing Enhances Cytarabine-mediated Cytotoxicity in Acute Myeloid Leukemia.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Circ_cse1l Inhibits Colorectal Cancer Proliferation by Binding to eIF4A3.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Roles of the CSE1L-mediated nuclear import pathway in epigenetic silencing.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. 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

9 authors at 2 institutions in 1 country.

Jose M PimientoDepartment of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Kevin G NeillDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Evita Henderson-JacksonDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Steven A EschrichDepartment of Bioinformatics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Dung-Tsa ChenDepartment of Biostatistics, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Kazim HusainDepartment of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
David ShibataDepartment of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida; Department of Oncological Sciences, University of South Florida, Tampa, Florida.
Domenico CoppolaDepartment of Anatomic Pathology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida; Department of Oncological Sciences, University of South Florida, Tampa, Florida; Department of Chemical Biology and Molecular Medicine, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida; Department of Tumor Biology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida. Electronic address: domenico.coppola@moffitt.org.
Mokenge P MalafaDepartment of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida.
Moffitt Cancer Center · USUniversity of South Florida · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Intervention of Pancreatic Oncogenic Pathways with Dietary TocotrienolR01CA129227 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MALAFA, MOKENGE P. · 2008 to 2012
$3.2M
NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA129227
6 · The paper itself

Abstract

Human cellular apoptosis susceptibility (chromosomal segregation 1-like, CSE1L) gene plays a role in nuclear-to-cytoplasm transport and chromosome segregation during mitosis, cellular proliferation, and apoptosis. CSE1L is involved in colon carcinogenesis. CSE1L gene expression was assessed with three data sets using Affymetrix U133 + gene chips on normal human colonic mucosa (NR), adenomas (ADs), and colorectal carcinoma (CRC). CSE1L protein expression in CRC, AD, and NR from the same patients was measured by immunohistochemistry using a tissue microarray. We evaluated CSE1L expression in CRC cells (HCT116, SW480, and HT29) and its biological functions. CSE1L mRNA was significantly increased in all AD and CRC compared with NR (P < 0.001 and P = 0.02, respectivly). We observed a change in CSE1L staining intensity and cellular localization by immunohistochemistry. CSE1L was significantly increased during the transition from AD to CRC when compared with NR in a CRC tissue microarray (P = 0.01 and P < 0.001). HCT116, SW480, and HT29 cells also expressed CSE1L protein. CSE1L knockdown by shRNA inhibited protein, resulting in decreased cell proliferation, reduced colony formation in soft agar, and induction of apoptosis. CSE1L protein is expressed early and across all stages of CRC development. shRNA knockdown of CSE1L was associated with inhibition of tumorigenesis in CRC cells. CSE1L may represent a potential target for treatment of CRC.

Indexed as

Gene Expression Regulation, NeoplasticAdenomaAdultAgedAged, 80 and overApoptosisCarcinogenesisCell Line, TumorCell NucleusCell ProliferationCellular Apoptosis Susceptibility ProteinColorectal NeoplasmsCytoplasmEpithelial CellsFemaleHumansCellular Apoptosis Susceptibility Protein

Identifiers

PMID27521996
PMCPMC5222983
OpenAlexW2507807202

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.