ArticleTranslational cancer research2019
FAM46B suppresses proliferation, migration and invasion of non-small cell lung cancer via β-catenin/MMP7 signaling.
Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Integration of CRISPR/dCas9-Based methylation editing with guide positioning sequencing identifies dynamic changes of mrDEGs in breast cancer progression.Cellular and molecular life sciences : CMLS · 2025Article
- Dissecting the Puzzling Roles of FAM46C: A Multifaceted Pan-Cancer Tumour Suppressor with Increasing Clinical Relevance.Cancers · 2024Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study investigated the functions of FAM46B in non-small cell lung cancer (NSCLC) cells and determined the role of β-catenin/matrix metalloproteinase 7 (MMP7) signaling in mediating these functions.
methodsHuman paracancerous and cancer tissues were collected from lung cancer patients. Cell proliferation was assessed by cell counting kit-8 (CCK-8) assay while migration and invasion were examined by transwell chamber assays. Relative mRNA expression and protein levels were determined by quantitative reverse transcription (q-RT) polymerase chain reaction (PCR) and western blot, respectively.
resultsFAM46B displayed reduced expression in lung cancer tissues compared with paired paracancerous tissues. In contrast, β-catenin protein levels were elevated in lung cancer tissues compared with paired paracancerous tissues. FAM46B over-expression reduced proliferation, migration and invasion of A549 and H292 cells, as well as decreased the protein levels of β-catenin, MMP7 and vascular endothelial growth factor (VEGF). On the other hand, FAM46B knockdown by shRNA in H1975 cells enhanced proliferation, migration and invasion, as well as increased the protein levels of β-catenin and MMP7. These enhanced effects were ameliorated by treatment with the Wnt/β-catenin inhibitor XAV939, suggesting a role for Wnt signaling in mediating the functions of FAM46B in NSCLC.
conclusionsFAM46B functions as a tumor suppressor by inhibiting β-catenin/MMP7 signaling.
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