Evidence map›Paper›PMID 21343396›Full record

ArticleCancer research2011

CNT1 expression influences proliferation and chemosensitivity in drug-resistant pancreatic cancer cells.

Yangzom D Bhutia, Sau Wai Hung, Bhavi Patel, Dylan Lovin, Rajgopal Govindarajan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Unveiling the resistance to therapies in pancreatic ductal adenocarcinoma.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2024
    Review
  5. Elucidation of the Gemcitabine Transporters ofInternational journal of molecular sciences · 2024
    Article
  6. Impact of genetic variants in the solute carrier (Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

2 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.

Yangzom D BhutiaDepartment of Phamaceutical and Biomedical Sciences, University of Georgia, Athens, Georgia 30602, USA.
Sau Wai Hung
Bhavi Patel
Dylan Lovin
Rajgopal Govindarajan
University of Georgia · US

Funding

TARGETING DEATH RECEPTOR-MEDIATED APOPTOSIS FOR HEAD AND NECK CANCERP50CA128613 · NCI · EMORY UNIVERSITY · PI SHIN, DONG M · 2007 to 2011
$12.0M
NCI NIH HHS 5 P50 CA128613NCI NIH HHS P50 CA128613
6 · The paper itself

Abstract

Overcoming the inherent chemoresistance of pancreatic cancers remains a major goal of therapeutic investigations in this disease. In this study, we discovered a role for the human concentrative nucleoside transporter-1 (hCNT1; SLC28A1), a high-affinity pyrimidine nucleoside transporter, in determining the chemosensitivity of human pancreatic cancer cells to gemcitabine, the drug used presently as a standard of care. Compared with normal pancreas and pancreatic ductal epithelial cells, hCNT1 expression was frequently reduced in pancreatic tumors and tumor cell lines. In addition, hCNT1-mediated (3)H-gemcitabine transport was lower in pancreatic cancer cell lines and correlated with cytotoxic IC(50) estimations of gemcitabine. In contrast to gemcitabine-sensitive pancreatic cancer cell lines, MIA PaCa-2, a gemcitabine-resistant pancreatic cancer cell line, exhibited relatively restrictive, cell cycle-dependent hCNT1 expression and transport. hCNT1 translation was suppressed in the late G1-enriched MIA PaCa-2 cell population possibly in an miRNA-dependent manner, which corresponded with the lowest hCNT1-mediated gemcitabine transport during this phase. Although hCNT1 protein was induced during G1/S transition, increased hCNT1 trafficking resulted in maximal cell surface recruitment and transport-overshoot in the G2/M phase-enriched cell population. hCNT1 protein was directed predominantly to proteasomal or lysosomal degradation in S or G2/M phase MIA PaCa-2 cells, respectively. Pharmacological inhibition of hCNT1 degradation moderately increased cell surface hCNT1 expression and cellular gemcitabine transport in MIA PaCa-2 cells. Constitutive hCNT1 expression reduced clonogenic survival of MIA PaCa-2 cells and steeply augmented gemcitabine transport and chemosensitization. In addition to supporting a putative tumor suppressor role for hCNT1, our findings identify hCNT1 as a potential candidate to render drug-resistant pancreatic cancer cells amenable to chemotherapy.

Indexed as

Cell ProliferationBlotting, WesternCell Line, TumorDrug Resistance, NeoplasmFlow CytometryHumansImmunohistochemistryMembrane Transport ProteinsPancreatic NeoplasmsReverse Transcriptase Polymerase Chain Reactioncif nucleoside transporterMembrane Transport Proteins

Identifiers

PMID21343396
PMCPMC3048166
OpenAlexW2133579393

What OpenQuestion holds

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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.