Induction of apoptosis by oridonin in nonfunctioning pituitary adenoma cells

Hui-Tong Chen1, Xing-Yi Yuan1, Zhong-Yu Wang1

  • 1Department of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Guangdong Pharmaceutical University, Guangzhou, China.

PubMed

Insights

Oridonin (ORI) effectively inhibits nonfunctioning pituitary adenoma (NFPA) cell growth by disrupting the cell cycle and inducing apoptosis. This natural compound shows promise as a novel therapeutic agent for NFPA treatment.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Pharmacology

Background:

  • Nonfunctioning pituitary adenomas (NFPA) are common pituitary tumors with limited treatment options beyond surgery.
  • Current surgical interventions often fail to achieve complete tumor resection, necessitating the development of novel therapeutic agents.
  • Oridonin (ORI), a natural compound, has demonstrated antitumor properties in various cancers, but its efficacy against NFPA remains unexplored.

Purpose of the Study:

  • To investigate the therapeutic potential of Oridonin (ORI) against nonfunctioning pituitary adenomas (NFPA).
  • To elucidate the mechanisms by which ORI affects NFPA cell behavior, including proliferation, migration, and apoptosis.

Main Methods:

  • In vitro assays were employed to assess ORI's effects on pituitary-derived folliculostellate (PDFS) cells, including viability (CCK-8), colony formation, proliferation (EdU), migration (wound-healing), and invasion (Transwell).
  • Transcriptome sequencing, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to identify affected signaling pathways.
  • Cell cycle analysis, Annexin V/PI staining for apoptosis, and Western blot for apoptosis-related proteins (Bax, Bcl-2, cleaved Caspase-3) were conducted.

Main Results:

  • Oridonin significantly inhibited PDFS cell viability, proliferation, migration, and invasion.
  • Transcriptome analysis revealed that ORI impacts cell cycle and apoptosis pathways in PDFS cells.
  • ORI treatment led to G2/M phase cell cycle arrest and induced significant apoptosis.

Conclusions:

  • Oridonin effectively suppresses nonfunctioning pituitary adenoma cell growth through combined disruption of the cell cycle and induction of apoptosis.
  • ORI demonstrates significant potential as a novel therapeutic agent for nonfunctioning pituitary adenoma treatment.

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