ArticleBioResearch open access2015
The PTB-Associated Splicing Factor/Peroxisome Proliferator-Activated Receptor Gamma Axis Regulates Autophagosome Formation in Human Pancreatic Cancer Cells.
Article in BioResearch open access, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Splicing alterations in pancreatic ductal adenocarcinoma: a new molecular landscape with translational potential.Journal of experimental & clinical cancer research : CR · 2023Review
- The Dysregulated MAD in Mad: A Neuro-theranostic Approach Through the Induction of Autophagic Biomarkers LC3B-II and ATG.Molecular neurobiology · 2023Review
- Prognostic Significance of Autophagy-Relevant Gene Markers in Colorectal Cancer.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor that plays a major regulatory role in metabolic function. It is overexpressed in many types of cancer cells, suggesting that regulation of PPARγ may also affect carcinogenesis. Our previous study suggested that PTB-associated splicing factor (PSF) is a PPARγ-interacting protein and growth regulator of colon cancer cells. In addition, PSF has been shown to be involved in several important regulatory steps of cancer cell proliferation. In this study, we aimed to investigate the relationships between PSF and PPARγ in pancreatic cancer by evaluating the effects of PSF expression in pancreatic cancer cell lines. PSF expression affected the expression of PPARγ, and knockdown of PSF using specific small-interfering RNA (siRNA) significantly suppressed the proliferation of pancreatic cancer cells. Furthermore, PSF knockdown induced cell growth inhibition and autophagosome formation through inhibition of PPARγ. Interestingly, Panc-1 cells were more susceptible to PSF knockdown-induced autophagy than MIA-PaCa-2 cells. Thus, our data indicated that PSF was an important regulator of autophagy and played critical roles in the survival and growth of pancreatic cancer cells. The PSF-PPARγ axis may play a role in the control of pancreatic cancer pathogenesis. This study is the first to describe the effects of PSF on pancreatic cancer cell growth and autophagy associated with PPARγ.
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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.