Amlodipine Targeting SPINK1 Attenuates Lung Cancer Cell Growth and Proliferation Through Glycolytic Metabolism
Guojun Yue1, Lingyun Yue1, Yan Chen1
1Department of Outpatient Radiotherapy, the Second Affiliated Hospital of Zunyi Medical University, Zunyi, China.
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.
Insights
Serine peptidase inhibitor, Kazal type 1 (SPINK1) is elevated in lung cancer, promoting cell proliferation and potentially regulating glycolytic metabolism for therapeutic insights.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Serine peptidase inhibitor, Kazal type 1 (SPINK1) is implicated in various cancers.
- The specific role of SPINK1 in lung cancer pathogenesis remains largely unexplored.
- This study investigates the functional mechanism of SPINK1 in lung cancer.
Purpose of the Study:
- To elucidate the role and mechanism of SPINK1 in lung cancer.
- To identify SPINK1 as a potential molecular target for lung cancer therapy.
Main Methods:
- Bioinformatic analysis of lung cancer single-cell sequencing data (CNV, GSVA, mimetic timing, intercellular communication).
- In vitro studies using A549 and SPC-A1 cell lines to assess SPINK1's role in tumorigenesis.
- Evaluation of SPINK1 overexpression effects on cell clustering and clone formation.
Main Results:
- SPINK1 expression is significantly upregulated in lung tumor tissues compared to normal tissues.
- Elevated SPINK1 levels correlate with poorer patient prognosis.
- SPINK1 overexpression promotes cell clustering and clone formation in lung cancer cells.
Conclusions:
- SPINK1 may modulate glycolytic metabolism in lung cancer cells.
- SPINK1 inhibition could potentially hinder lung cancer growth and proliferation.
- Findings suggest SPINK1 as a potential therapeutic target for lung cancer.
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