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Identification and Exploration of Serine Peptidase Inhibitor Kazal Type I (SPINK1) as a Potential Biomarker Correlated with the Progression of Non-Small Cell Lung Cancer.

Abstract
Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Although significant advances have been achieved in the treatment of NSCLC during the past two decades, the 5-year survival rate of patients with NSCLC remains <20%. Thus, there is an urgent requirement to further understand the molecular mechanisms that promote NSCLC development and to identify novel therapeutic targets. In the present study, the gene expression profiles of patients with NSCLC from The Cancer Genome Atlas database were carefully analyzed and SPINK1 was identified as a tumor-inducing factor. SPINK1 expression level was found to be increased in both NSCLC tissues and cell lines. Moreover, SPINK1 promoted cell proliferation in A549 and H1299 cells. Knockdown of SPINK1 could activate cell autophagy and apoptosis. Mechanistically, SPINK1 was demonstrated to induce the proliferation of NSCLC via activating the MEK/ERK signaling pathway. In conclusion, these findings suggested that SPINK1 may serve as a potential biomarker in NSCLC.
AuthorsDingyi Li, Xinxin Zhang, Zhiqiang Ding, Rongshuang Ai, Luyao Shi, Zimeng Wang, Qian He, Yilin Dong, Yiting Zhu, Wenzhong Ouyang, Yujuan He
JournalCell biochemistry and biophysics (Cell Biochem Biophys) Vol. 80 Issue 4 Pg. 807-818 (Dec 2022) ISSN: 1559-0283 [Electronic] United States
PMID36194314 (Publication Type: Journal Article)
Copyright© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Chemical References
  • Biomarkers
  • Protease Inhibitors
  • SPINK1 protein, human
  • Serine
  • Trypsin Inhibitor, Kazal Pancreatic
  • Mitogen-Activated Protein Kinase Kinases
Topics
  • Biomarkers
  • Carcinoma, Non-Small-Cell Lung (genetics)
  • Cell Line, Tumor
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lung Neoplasms (genetics)
  • Mitogen-Activated Protein Kinase Kinases (genetics, metabolism)
  • Protease Inhibitors
  • Serine (metabolism)
  • Trypsin Inhibitor, Kazal Pancreatic (genetics, metabolism)

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