Can SDH1 in Chinese Medicine target ALK for NSCLC remission?
Purpose: This study aims to investigate whether SDH1, the active ingredient of the Chinese medicine compound Selaginella Doederleinii Hieron, can effectively inhibit anaplastic lymphoma kinase (ALK) activity in non-small cell lung cancer (NSCLC). NSCLC is a significant and challenging disease, which has limited treatment options with widely existing adverse events (AEs). The research will involve both in vitro and in vivo experiments to assess the potential of SDH1 to target and restrain ALK kinase activity, potentially leading to the remission of NSCLC. Methods: Materials for this study included human NSCLC cell lines cultured in specific conditions and various reagents. In vitro, the level of protein is pressured by Western blot, and cell growth is assessed by MTT assay. In vivo, experiments used a xenograft tumor mouse model injected with NSCLC cells and treated with different reagents, with tumor growth and other observations recorded. Possible Results: There are three most possible results: (1)SDH1 can inhibit ALK kinase to control the growth of NSCLC cells; (2) SDH1 cannot target ALK kinase but it can control the growth of NSCLC cells; (3) SDH1 cannot restrain the activity of ALK kinase neither in vitro nor in vivo, thus it cannot kill NSCLC cells. Conclusion: The result of our study investigates the impact of SDH1 on anaplastic lymphoma kinase (ALK) and A549 NSCLC. The findings could reveal the potential of targeting ALK to induce remission in non-small cell lung cancer both in laboratory and animal models, which tends to provide a possible avenue for future clinical and pharmaceutical approaches to combat NSCLC.
Authors
- Senlin Xu (ORCID: https://orcid.org/0000-0001-6625-5370)
Institutions
- University of Alberta (CA)
Publication Details
- Journal
- Theoretical and Natural Science
- Published
- 2025-01-09
- DOI
- https://doi.org/10.54254/2753-8818/2024.19975
- Primary Topic
- Lung Cancer Treatments and Mutations
- Type
- article
- Field-Weighted Citation Impact
- 0.00