ArticleInternational journal of clinical and experimental pathology2019
FAM129A promotes invasion and proliferation by activating FAK signaling pathway in non-small cell lung cancer.
Article in International journal of clinical and experimental pathology, 2019. 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, 10 citations in OpenAlex.
- Cyclin-Dependent Kinase 5 Contributes to Bruton's Tyrosine Kinase Inhibitor Resistance via the IRE1α/XBP1 Axis in Mantle Cell Lymphoma.Research square · 2026Article
- Translating tumor epigenetic subtyping into methylome network-based prognostic models in early-stage NSCLC: results from the prospective MOBIT study.Journal of translational medicine · 2026Article
- The complex role and molecular mechanism of family with sequence similarity genes in cancer: a comprehensive review.Discover oncology · 2025Review
- Identification of renal cyst cells of type I Nephronophthisis by single-nucleus RNA sequencing.Frontiers in cell and developmental biology · 2023Article
- A Screening of Epigenetic Therapeutic Targets for Non-Small Cell Lung Cancer Reveals PADI4 and KDM6B as Promising Candidates.International journal of molecular sciences · 2022Review
- MiR-4521 plays a tumor repressive role in growth and metastasis of hepatocarcinoma cells by suppressing phosphorylation of FAK/AKT pathway via targeting FAM129A.Journal of advanced research · 2022Article
- Review
- The Regulatory Role of GBF1 on Osteoclast Activation Through EIF2a Mediated ER Stress and Novel Marker FAM129A Induction.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Family with sequence similarity 129, member A (FAM129A), also called Niban or C1orf24, was initially identified from a rat model of hereditary renal carcinoma. FAM129A inhibited apoptosis and promoted migration and proliferation in human cancers. However, little is known about the downstream signaling during tumor progression. Our data showed that FAM129A played an oncogenic role in non-small cell lung carcinoma (NSCLC), which upregulated the protein levels of MMP2 and Cyclin D1 through activating the FAK signaling pathway. Treatment by FAK inhibitor counteracted the increase of MMP2 and Cyclin D1 expression following by FAM129A transfection through attenuating the phosphorylation of FAK. Results of immunohistochemistry revealed that the expression of FAM129A was significantly associated with larger tumor size (P=0.036), advanced TNM stage (P<0.001), and lymph node metastasis (P=0.001). Subsequent Kaplan-Meier analysis indicated that patients with FAM129A expression presented with poorer clinical outcome (P=0.001). Taken together, our results suggested that FAM129A may promote tumor proliferation and invasion of NSCLC through facilitating the phosphorylation of FAK and upregulated MMP2 and Cyclin D1. Overexpression of FAM129A may be a prognostic predictor in NSCLC patients.
Indexed as
Identifiers
31933898PMC6945167W3006675673What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.