ArticleCell biochemistry and function2021
S100A6 represses Calu-6 lung cancer cells growth via inhibiting cell proliferation, migration, invasion and enhancing apoptosis.
Article in Cell biochemistry and function, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Multifaceted roles of S100A6 in neurological disorders: expression, interaction networks, and clinical implications.Frontiers in pharmacology · 2026Review
- Exploring the expression and prognostic roles of LAD1 in lung adenocarcinoma.Scientific reports · 2025Article
- Host S100A6 inhibits ZIKV replication by degrading NS3 through lysosomal pathway.Frontiers in cellular and infection microbiology · 2025Article
- Overexpression of PRDM16 attenuates acute kidney injury progression: genetic and pharmacological approaches.MedComm · 2024Article
- S100A6 Regulates nucleus pulposus cell apoptosis via Wnt/β-catenin signaling pathway: an in vitro and in vivo study.Molecular medicine (Cambridge, Mass.) · 2024Article
- S100A6 could not promote the differentiation of Calu-6 lung cancer cell line.Annals of medicine and surgery (2012) · 2024Article
- S100A6: molecular function and biomarker role.Biomarker research · 2023Review
- The Role of S100A6 in Human Diseases: Molecular Mechanisms and Therapeutic Potential.Biomolecules · 2023Review
- From bench to bedside: Calprotectin (S100A8/S100A9) as a biomarker in rheumatoid arthritis.Frontiers in immunology · 2022Review
- S100A6 represses Calu-6 lung cancer cells growth via inhibiting cell proliferation, migration, invasion and enhancing apoptosis.Cell biochemistry and function · 2021Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100 calcium binding protein A6 (S100A6) has been reported to involve in many kinds of cancers through regulating intracellular calcium homeostasis. Previous studies found that S100A6 increased in lung cancer patients' plasma and pleural effusion. This study focused on its function in Calu-6 lung cancer cells. S100A6 gene was transferred into Calu-6 lung cancer cell line by lentivirus vector, the empty vector transfected cells and the blank cells were set as control groups. MTT was evaluating cell proliferation. The transwell assay was reflecting cell migration and cell invasion. The flow cytometric analysis was detecting cell apoptosis and cell cycle of three groups (Calu-6, Calu-6/neo, Calu-6/S100A6). Nude mouse tumorigenicity was then applied to evaluate S100A6's effect on cellular tumorigenicity. Compared with control groups, Calu-6/S100A6 cells showed a weakening trend in the cell behaviours of proliferation, migration and invasiveness, while had an enhancement of cell apoptosis, with all P < .05. The cell cycle of Calu-6/S100A6 cells had a reduction of S phase and an increase of G1 phase (P < .05). In animal study, after 5 weeks of cell injection, the tumour bulk of Calu-6/S100A6 group was smaller than controls, with P < .05. Our results demonstrate S100A6 inhibits the growth of Calu-6 lung cancer cells, as well as impairs Calu-6's ability in tumorigenesis. At cellular level, S100A6 is supposed to act as a tumour suppressor gene in lung cancer.
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