Evidence map›Paper›PMID 24447148›Full record

ArticleNutrition and cancer2014

Methylseleninic acid suppresses pancreatic cancer growth involving multiple pathways.

Lei Wang, Hongbo Hu, Zhe Wang, Hua Xiong, Yan Cheng, Joshua Dezhong Liao, Yibin Deng, Junxuan Lü

Abstract read
In one paragraph

Article in Nutrition and cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. THE MAIN CYTOTOXIC EFFECTS OF METHYLSELENINIC ACID ON VARIOUS CANCER CELLS.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Role of AQP9 in transport of monomethyselenic acid and selenite.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2017
    Article
  11. Review
  12. 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

8 authors at 3 institutions in 1 country.

Lei Wanga Hormel Institute , University of Minnesota , Austin , Minnesota , USA.
Hongbo Hu
Zhe Wang
Hua Xiong
Yan Cheng
Joshua Dezhong Liao
Yibin Deng
Junxuan Lü
Hormel (United States) · USUniversity of Minnesota · USTexas Tech University Health Sciences Center · US

Funding

PREVENTION OF PROSTATE CARCINOGENESIS BY NEXT-GENERATION SELENIUMR01CA172169 · NCI · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI LU, JUNXUAN · 2013 to 2018
$1.6M
Methyl-selenium for prostate cancer chemopreventionR01CA126880 · NCI · UNIVERSITY OF MINNESOTA · PI LU, JUNXUAN · 2007 to 2011
$1.4M
Prevention of PTEN deletion driven prostate cancer by seleniumR21CA155522 · NCI · UNIVERSITY OF MINNESOTA · PI DENG, YIBIN, LU, JUNXUAN · 2011 to 2012
$365k
NCI NIH HHS R01 CA126880NCI NIH HHS R01CA126880NCI NIH HHS R01 CA172169NCI NIH HHS R21 CA155522NCI NIH HHS R21CA155522
6 · The paper itself

Abstract

As a potential novel agent for treating pancreatic cancer, methylseleninic acid (MSeA) was evaluated in cell culture and xenograft models. Results showed that MSeA induced G1 cell cycle arrest and apoptosis in a majority of human and mouse pancreatic cancer cell lines, but G2 arrest in human PANC-1 and PANC-28 cell lines. In contrast to our previous finding in human prostate cancer LNCaP cells having a lack of P53 activation by MSeA, induction of G2 arrest in PANC-1 cells was accompanied by increased mutant P53 Ser15 phosphorylation, upregulation of P53-targets P21Cip1 and GADD45 and G2 checkpoint kinase (Chk2) activation, suggestive of DNA damage responses. A rapid inhibition of AKT phosphorylation was followed by reduced mTOR signaling and increased autophagy in PANC-1 cells attenuating caspase-mediated apoptosis execution. Furthermore, daily oral treatment with MSeA (3 mg Se/kg body weight) significantly suppressed growth of subcutaneously inoculated PANC-1 xenograft in SCID mice. Immunohistochemical analyses detected increased p-Ser15 P53, P21Cip1, pS139-H2AX (DNA damage responses), and caspase-3 cleavage and decreased pSer473AKT and Ki67 proliferative index and reduced intratumor vascular density in MSeA-treated xenograft. These results provide impetus for further research of MSeA in the therapy and/or chemoprevention of pancreatic cancer.

Indexed as

AnimalsApoptosisCaspase 3Cell Line, TumorCell ProliferationDNA DamageG1 Phase Cell Cycle CheckpointsHumansMiceMice, SCIDOrganoselenium CompoundsPancreatic NeoplasmsPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesCASP3 protein, humanCaspase 3methylselenic acidMTOR protein, humanOrganoselenium CompoundsProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID24447148
PMCPMC6812653
OpenAlexW2094566855

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.