Publications by authors named "Chien-Fei Lee"

Article Synopsis
  • Small-cell lung cancer (SCLC) is a very dangerous type of lung cancer that doesn't usually respond well to standard treatments.
  • A new drug called lurbinectedin was recently approved for patients whose cancer came back, but doctors think using it with other treatments might work better.
  • Researchers found that combining lurbinectedin with a special drug called berzosertib may help more patients by making cancer cells grow uncontrollably and die, and they are now testing this combination in a clinical trial.
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Bromodomain-containing protein 4 (BRD4) is a cancer therapeutic target in ongoing clinical trials disrupting primarily BRD4-regulated transcription programs. The role of BRD4 in cancer has been attributed mainly to the abundant long isoform (BRD4-L). Here we show, by isoform-specific knockdown and endogenous protein detection, along with transgene expression, the less abundant BRD4 short isoform (BRD4-S) is oncogenic while BRD4-L is tumor-suppressive in breast cancer cell proliferation and migration, as well as mammary tumor formation and metastasis.

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Adenosine regulates important pathophysiological functions via four distinct adenosine receptor subtypes (A1, A2A, A2B, and A3). The A1 and A2A adenosine receptors (A1R and A2AR) are major targets of caffeine and have been extensively investigated. Huntington's disease (HD) is a dominant neurodegenerative disease caused by an abnormal CAG expansion in the Huntingtin gene.

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Adenosine is a naturally occurring nucleoside that is distributed ubiquitously throughout the body as a metabolic intermediary. In the brain, adenosine functions as an important upstream neuromodulator of a broad spectrum of neurotransmitters, receptors, and signaling pathways. By acting through four G-protein-coupled receptors, adenosine contributes critically to homeostasis and neuromodulatory control of a variety of normal and abnormal brain functions, ranging from synaptic plasticity, to cognition, to sleep, to motor activity to neuroinflammation, and cell death.

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Background: Developing retinas display retinal waves, the patterned spontaneous activity essential for circuit refinement. During the first postnatal week in rodents, retinal waves are mediated by synaptic transmission between starburst amacrine cells (SACs) and retinal ganglion cells (RGCs). The neuromodulator adenosine is essential for the generation of retinal waves.

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The A2A adenosine receptor (A2AR) is a G protein-coupled receptor and a major target of caffeine. The A2AR gene encodes alternative transcripts that are initiated from at least two independent promoters. The different transcripts of the A2AR gene contain the same coding region and 3'-untranslated region and different 5'-untranslated regions that are highly conserved among species.

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The A2A adenosine receptor (A2AR) is a G-protein-coupled receptor. We previously reported that the C terminus of the A2AR binds to translin-associated protein X (TRAX) and modulates nerve growth factor (NGF)-evoked neurite outgrowth in PC12 cells. Herein, we show that neuritogenesis of primary hippocampal neurons requires p53 because blockage of p53 suppressed neurite outgrowth.

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