Evidence map›Paper›PMID 19014651›Full record

ArticleJournal of ovarian research2008

ST6Gal-I expression in ovarian cancer cells promotes an invasive phenotype by altering integrin glycosylation and function.

Daniel R Christie, Faheem M Shaikh, John A Lucas, John A Lucas, Susan L Bellis

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

79 citing papers in PubMed, 128 citations in OpenAlex.

  1. Trial
  2. Review
  3. Sialylation in the nervous system: Functions and mechanisms.The Journal of biological chemistry · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. The role ofActa pharmaceutica Sinica. B · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. In SituCancers · 2022
    Article

19 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Daniel R ChristieDepartment of Obstetrics and Gynecology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Faheem M Shaikh
John A Lucas
John A Lucas
Susan L Bellis
University of Alabama at Birmingham · US

Funding

Regulation of beta1 integrin glycosylation by rasR01CA084248 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BELLIS, SUSAN L · 2002 to 2011
$2.4M
NCI NIH HHS R01 CA084248
6 · The paper itself

Abstract

backgroundOvarian adenocarcinoma is not generally discovered in patients until there has been widespread intraperitoneal dissemination, which is why ovarian cancer is the deadliest gynecologic malignancy. Though incompletely understood, the mechanism of peritoneal metastasis relies on primary tumor cells being able to detach themselves from the tumor, escape normal apoptotic pathways while free floating, and adhere to, and eventually invade through, the peritoneal surface. Our laboratory has previously shown that the Golgi glycosyltransferase, ST6Gal-I, mediates the hypersialylation of beta1 integrins in colon adenocarcinoma, which leads to a more metastatic tumor cell phenotype. Interestingly, ST6Gal-I mRNA is known to be upregulated in metastatic ovarian cancer, therefore the goal of the present study was to determine whether ST6Gal-I confers a similarly aggressive phenotype to ovarian tumor cells.

methodsThree ovarian carcinoma cell lines were screened for ST6Gal-I expression, and two of these, PA-1 and SKOV3, were found to produce ST6Gal-I protein. The third cell line, OV4, lacked endogenous ST6Gal-I. In order to understand the effects of ST6Gal-I on cell behavior, OV4 cells were stably-transduced with ST6Gal-I using a lentiviral vector, and integrin-mediated responses were compared in parental and ST6Gal-I-expressing cells.

resultsForced expression of ST6Gal-I in OV4 cells, resulting in sialylation of beta1 integrins, induced greater cell adhesion to, and migration toward, collagen I. Similarly, ST6Gal-I expressing cells were more invasive through Matrigel.

conclusionST6Gal-I mediated sialylation of beta1 integrins in ovarian cancer cells may contribute to peritoneal metastasis by altering tumor cell adhesion and migration through extracellular matrix.

Identifiers

PMID19014651
PMCPMC2584051
OpenAlexW2158941299

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.