Objective: To analyze the differentially expressed proteins of the synergy effect of Radix Hedysari polysaccharides (HPS)combined with chemotherapy (Cy) on S180 tumor cells.
Methods: The total proteins extracted from the HPS combined with Cy treated S180 cells in tumor-bearing mice were separated by two dimentional gel electrophoresis (2-DE)and compared with those from Cy treated S180 cells using PDQuest 8.0 software. Mass spectrometry was applied to identify the differentially expressed proteins. Western blot was used to determine the differential expression of one protein.
Results: Twenty-four differentially-expressed proteins in HPS group were discovered. The five differential expressed proteins among twenty-four proteins were later identified by mass spectrometry and Mascot software as heat-shock protein hsp84 (HSP90beta), apolipoprotein A, albumin, heat shock protein beta-1 (HSP27)and unnamed protein product, including one up regulated and four down regulated expressed proteins respectively. Results from Western blot manifested the same trend as from proteomics analysis.
Conclusion: Proteomics technique can be used to discover target proteins associated with the synergy effect of HPS combined with Cy on S180 tumor cells, involving some important proteins related to energy metabolism, oxidative stress and apoptosis induction signal transduction.
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Curr Eye Res
January 2025
Dr. Rolf M. Schwiete Center for Limbal Stem Cell and Congenital Aniridia Research, Saarland University, Saar, Germany.
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Graduate Institute of Nanomedicine and Medical Engineering, College of Medical Engineering, Taipei Medical University, Taipei 11031, Taiwan, R.O.C.
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Department of Biomedical Sciences, Chung Shan Medical University, Taichung 402306, Taiwan, R.O.C.
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Department of Pathology, GROW Research Institute for Oncology and Reproduction, Maastricht University Medical Center, 6229HX Maastricht, The Netherlands.
Human papillomavirus (HPV)‑positive and -negative head and neck squamous cell carcinoma (HNSCC) are often associated with activation of the phosphatidylinositol 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway due to mutations or amplifications in , loss of or activation of receptor tyrosine kinases. In HPV‑negative tumors, (encoding p16 protein) inactivation or (encoding Cyclin D1 protein) amplification frequently results in sustained cyclin‑dependent kinase (CDK) 4/6 activation. The present study aimed to investigate the efficacy of the CDK4/6 inhibitors (CDKi) palbociclib and ribociclib, and the PI3K/Akt/mTOR pathway inhibitors (PI3Ki) gedatolisib, buparlisib and alpelisib, in suppressing cell viability of HPV‑positive and ‑negative HNSCC cell lines.
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