ArticlePPAR research2014
Synergistic Antiproliferative Effects of Combined γ -Tocotrienol and PPAR γ Antagonist Treatment Are Mediated through PPAR γ -Independent Mechanisms in Breast Cancer Cells.
Article in PPAR research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed, 15 citations in OpenAlex.
- Synergistic Anticancer Effect of Tocotrienol Combined with Chemotherapeutic Agents or Dietary Components: A Review.International journal of molecular sciences · 2016Review
- Anti-proliferative effects of γ-tocotrienol are associated with suppression of c-Myc expression in mammary tumour cells.Cell proliferation · 2015Article
Corrections and comments
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous findings showed that the anticancer effects of combined γ -tocotrienol and peroxisome proliferator activated receptor γ (PPAR γ ) antagonist treatment caused a large reduction in PPAR γ expression. However, other studies suggest that the antiproliferative effects of γ -tocotrienol and/or PPAR γ antagonists are mediated, at least in part, through PPAR γ -independent mechanism(s). Studies were conducted to characterize the role of PPAR γ in mediating the effects of combined treatment of γ -tocotrienol with PPAR γ agonists or antagonists on the growth of PPAR γ negative +SA mammary cells and PPAR γ -positive and PPAR γ -silenced MCF-7 and MDA-MB-231 breast cancer cells. Combined treatment of γ -tocotrienol with PPAR γ antagonist decreased, while combined treatment of γ -tocotrienol with PPAR γ agonist increased, growth of all cancer cells. However, treatment with high doses of 15d-PGJ2, an endogenous natural ligand for PPAR γ , had no effect on cancer cell growth. Western blot and qRT-PCR studies showed that the growth inhibitory effects of combined γ -tocotrienol and PPAR γ antagonist treatment decreased cyclooxygenase (COX-2), prostaglandin synthase (PGDS), and prostaglandin D2 (PGD2) synthesis. In conclusion, the anticancer effects of combined γ -tocotrienol and PPAR γ antagonists treatment in PPAR γ negative/silenced breast cancer cells are mediated through PPAR γ -independent mechanisms that are associated with a downregulation in COX-2, PGDS, and PGD2 synthesis.
Identifiers
What OpenQuestion holds
Registered trials
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.