Introduction: A trypsin inhibitor, the serine peptidase inhibitor, Kazal type 1 (SPINK1), a secreted protein, has been identified in recent years as contributing to the advancement of specific cancer types. Lung cancer is a common class of malignant tumors. However, the role of SPINK1 in lung cancer is unknown. This study aimed to investigate the profound mechanism of SPINK1 in lung cancer. Methods: In this study, we used bioinformatics methods to select lung cancer samples for single-cell sequencing analysis, including CNV analysis, GSVA analysis, mimetic timing analysis, and intercellular communication, to identify potential molecular targets and pathways. We selected A549 cells and SPC-A1 cells to evaluate the role of SPINK1 in tumorigenesis in vitro. Results: The study indicated that SPINK1 expression was significantly elevated in tumor tissue compared with normal tissue, and higher levels correlated with poorer patient prognosis. Moreover, when SPINK1 was overexpressed, both BEAS-2B and SPC-A1 cells formed dense cell clusters, and SPINK1 overexpression significantly promoted the formation of cell clones. Discussion: Amlodipine (AML) treatment decreases mRNA and protein expression of CDK1, BCL-2, CyclinE1, and CCND1 in A549 and SPC-A1 cells by targeting SPINK1, which regulates glycolytic metabolism Conclusion: The present study suggests that SPINK1 may modulate glycolytic metabolism in lung cancer cells, inhibiting their growth and proliferation, and potentially providing therapeutic insights.
Yue et al. (Thu,) studied this question.