ArticleOncology letters2021
The effects of BAFF and APRIL signaling on non-small cell lung cancer cell proliferation and invasiveness.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- CCN1 promotes APRIL/BAFF signaling in esophageal squamous cell carcinoma but attenuates it in esophageal adenocarcinoma.Scientific reports · 2025Article
- BAFF overexpression in triple-negative breast cancer promotes tumor growth by inducing IL-10-secreting regulatory B cells that suppress anti-tumor T cell responses.Breast cancer research and treatment · 2025Article
- Sex bias in tumor immunity: insights from immune cells.Theranostics · 2025Review
- Immunomodulatory effects of BAFF and APRIL cytokines in post-pulmonary infection lung cancer: Implications for drug resistance and progression.Saudi medical journal · 2024Review
- Expression of Immune-Related and Inflammatory Markers and Their Prognostic Impact in Colorectal Cancer Patients.International journal of molecular sciences · 2023Article
- The BAFF-APRIL System in Cancer.Cancers · 2023Review
- A Proliferation-Inducing Ligand and B-Cell Activating Factor Are Upregulated in Patients with Essential Thrombocythemia.Journal of clinical medicine · 2022Article
- Binary MoSMikrochimica acta · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer represents the most common type of human malignancy and is the main cause of cancer-associated mortality worldwide. To improve the effectiveness of treatment strategies, a better understanding of the mechanisms of cancer progression and invasiveness is required. Recently, B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL), two relatively newly described cytokines belonging to the tumor necrosis factor superfamily, have been shown to play a role in cancer progression. However, at present, the effects of both cytokines on lung cancer cells remain unclear. The present study aimed therefore to understand the direct effects of BAFF and APRIL on non-small cell lung cancer (NSCLC) progression. To do so, reverse transcription quantitative PCR and western blotting were used to evaluate whether A549 and H2030 NSCLC cells express receptors for both BAFF and APRIL. The results demonstrated that both investigated cell lines expressed BAFF-R (receptor specific to BAFF only) and transmembrane activator and CAML interactor (TACI; shared receptor for both cytokines). In addition, functional experiments were performed to determine the effects of BAFF and APRIL stimulation on cancer cell viability. The results demonstrated no direct effects of BAFF and APRIL on NSCLC cell proliferation and invasiveness. In summary, the present study demonstrated that NSCLC cells possess the ability to respond directly to both BAFF and APRIL. However, activation of BAFF-R and TACI signaling in cancer cells did not increase the proliferative capacity and invasiveness. Further investigation is thus required to better understand the role of BAFF and APRIL on the progression of NSCLC.
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