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首页> 外文期刊>BioResearch open access. >The PTB-Associated Splicing Factor/Peroxisome Proliferator-Activated Receptor Gamma Axis Regulates Autophagosome Formation in Human Pancreatic Cancer Cells
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The PTB-Associated Splicing Factor/Peroxisome Proliferator-Activated Receptor Gamma Axis Regulates Autophagosome Formation in Human Pancreatic Cancer Cells

机译：PTB相关的剪接因子/过氧化物酶体增殖物激活受体γ轴调节人类胰腺癌细胞中自噬体的形成。

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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.
机译：过氧化物酶体增殖物激活受体γ（PPARγ）是一种核受体，在代谢功能中起主要调节作用。它在许多类型的癌细胞中过表达，表明PPARγ的调节也可能影响癌变。我们先前的研究表明，PTB相关剪接因子（PSF）是一种PPARγ相互作用蛋白，是结肠癌细胞的生长调节剂。此外，已证明PSF参与癌细胞增殖的几个重要调控步骤。在这项研究中，我们旨在通过评估胰腺癌细胞系中PSF表达的影响来研究胰腺癌中PSF和PPARγ之间的关系。 PSF的表达影响PPARγ的表达，使用特异性小干扰RNA（siRNA）抑制PSF可以显着抑制胰腺癌细胞的增殖。此外，PSF抑制通过抑制PPARγ诱导细胞生长抑制和自噬体形成。有趣的是，Panc-1细胞比MIA-PaCa-2细胞更容易受到PSF敲低诱导的自噬。因此，我们的数据表明PSF是自噬的重要调节剂，并且在胰腺癌细胞的存活和生长中起着关键作用。 PSF-PPARγ轴可能在胰腺癌发病机理的控制中起作用。这项研究首次描述了PSF对胰腺癌细胞生长和与PPARγ相关的自噬的影响。

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