Related Experiment Video
Updated: Jul 6, 2026
Induction of Mouse Lung Injury by Endotracheal Injection of Bleomycin
Published on: April 30, 2019
Induction of premature senescence in human lung cancer by fungal immunomodulatory protein from Ganoderma tsugae
Chien-Huang Liao1, Yi-Min Hsiao, Ching-Hsiung Lin
1Institute of Medical and Molecular Toxicology, Chung Shan Medical University, Taichung, Taiwan, ROC.
Abstract:
Purified recombinant fungal immunomodulatory protein from Ganoderma tsugae (reFIP-gts) has anti-telomerase effects in human lung adenocarcinoma A549 cells. However, how reFIP-gts affects cancer cell fates remains unclear. Here, we demonstrated that reFIP-gts-treated lung cancer cells are arrested at G1 phase by flow cytometry and possess morphological phenotype consistent with cellular senescence. The senescent nature of these cells was supported by positive staining for senescence-associated beta-galactosidase activity and increased lysosomal content in A549 and CaLu-1 lung cancer cells. Arrest of cells at G1 appears to be the key means through which reFIP-gts induces premature cellular senescence in A549 cells. Finally, reFIP-gts- treated A549 cells grew more slowly and formed significantly fewer cell colonies in soft agar than untreated A549 cells. In an in vivo mouse model, A549 cells treated with reFIP-gts grew significantly slower than cells treated with PBS alone, confirming that lung tumor can be inhibited by reFIP-gts. The use of reFIP-gts may be a powerful new strategy for chemoprevention and antineoplastic therapy.
Insights
Recombinant fungal immunomodulatory protein from Ganoderma tsugae (reFIP-gts) induces cellular senescence and G1 cell cycle arrest in lung cancer cells. This protein inhibits lung tumor growth, offering a potential new strategy for cancer therapy.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Recombinant fungal immunomodulatory protein from Ganoderma tsugae (reFIP-gts) exhibits anti-telomerase activity.
- The precise mechanisms by which reFIP-gts influences cancer cell fate are not fully understood.
Purpose of the Study:
- To investigate the effects of reFIP-gts on lung cancer cell cycle progression and senescence.
- To evaluate the in vitro and in vivo anti-tumor efficacy of reFIP-gts.
Main Methods:
- Flow cytometry analysis to assess cell cycle distribution.
- Senescence-associated beta-galactosidase staining and lysosomal content assessment.
- Soft agar colony formation assays and in vivo mouse xenograft models.
Main Results:
- reFIP-gts induced G1 cell cycle arrest and morphological features of cellular senescence in A549 and CaLu-1 lung cancer cells.
- Senescence was confirmed by increased beta-galactosidase activity and lysosomal content.
- reFIP-gts treatment significantly inhibited A549 cell proliferation, colony formation in soft agar, and in vivo tumor growth.
Conclusions:
- G1 cell cycle arrest is a primary mechanism for reFIP-gts-induced premature cellular senescence.
- reFIP-gts demonstrates significant potential as a chemopreventive and antineoplastic therapeutic agent for lung cancer.