ArticleCellular oncology (Dordrecht, Netherlands)2020
FAM83D promotes epithelial-mesenchymal transition, invasion and cisplatin resistance through regulating the AKT/mTOR pathway in non-small-cell lung cancer.
Article in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 58 citations in OpenAlex.
- S100A10 promotes tumorigenesis and metastasis in lung adenocarcinoma by regulating JUND/TNC axis-mediated EMT.Translational oncology · 2026Article
- FAM83D facilitates EMT and metastasis of cervical cancer via interaction with GSK3β and inactivation of GSK3β/stabilization of Snail signaling.Biology direct · 2026Article
- Targeting shared mechanisms of cisplatin resistance and metastasis in lung cancer for novel therapeutic strategies.Discover oncology · 2026Review
- Sub-acute toxicity profiles of Rhoicissus tridentata as used in the traditional prostate cancer managment in the Elgon in Wistar albino rats.Scientific reports · 2025Article
- Identification of the key gene for hepatocellular carcinoma based on bioinformatics and machine learning and experimental verification.Translational cancer research · 2025Article
- HMMR mediates progression of nasopharyngeal carcinoma by inhibiting FAM83D ubiquitination and activating beta-catenin signaling pathway.Scientific reports · 2025Article
- Identification of candidate biomarkers correlated with the pathogenesis of breast cancer patients.Scientific reports · 2025Article
- The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024Review
- The FBXW7-binding sites on FAM83D are potential targets for cancer therapy.Breast cancer research : BCR · 2024Article
- PPIP5K2 Facilitates Proliferation and Metastasis of Non-Small Lung Cancer (NSCLC) through AKT Signaling Pathway.Cancers · 2024Article
- Systematic analysis of the oncogenic role of FAM83D across cancers based on data mining.Cell cycle (Georgetown, Tex.) · 2023Article
- Inositol monophosphatase 1 (IMPA1) promotes triple-negative breast cancer progression through regulating mTOR pathway and EMT process.Cancer medicine · 2023Article
- Suppression of FAM83D Inhibits Glioma Proliferation, Invasion and Migration by Regulating the AKT/mTOR Signaling Pathway.Translational oncology · 2022Article
- Comprehensive analysis of the expression, prognostic significance, and function of FAM83 family members in breast cancer.World journal of surgical oncology · 2022Article
- Article
- Overcoming therapeutic resistance to platinum-based drugs by targeting Epithelial-Mesenchymal transition.Frontiers in oncology · 2022Review
- Pan-cancer and single-cell analysis revealsFrontiers in genetics · 2022Article
- Integrating single-cell RNA sequencing and prognostic model revealed the carcinogenicity and clinical significance of FAM83D in ovarian cancer.Frontiers in oncology · 2022Article
- Immune implication of FAM83D gene in hepatocellular carcinoma.Bioengineered · 2021Article
- Identification of Prognostic and Therapeutic Biomarkers among FAM83 Family Members for Pancreatic Ductal Adenocarcinoma.Disease markers · 2021Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeFAM83D has been proposed to act as an oncoprotein in several types of human cancer. Its role and mode of action in human non-small cell lung cancer (NSCLC) metastasis and its impact on chemotherapy are as yet, however, poorly understood.
methodsFAM83D expression was measured in NSCLC cells and normal lung epithelial cells, as well as in primary NSCLC tissues and corresponding adjacent non-cancerous tissues, using qRT-PCR, Western blotting and immunohistochemistry. FAM83D was stably overexpressed in BEAS2B cells or silenced in A549 and H1299 cells using retroviral or lentiviral vectors. The growth capacity of NSCLC cells was evaluated using MTT and colony formation assays. Epithelial-mesenchymal transition (EMT) was assessed using Western blotting and immunofluorescence. NSCLC cell invasive capacities were assessed using scratch wound healing and Boyden chamber assays. NSCLC cell viability in response to cisplatin treatment was assessed using MTT assays in vitro and a xenograft model in vivo.
resultsWe found that FAM83D expression levels were significantly elevated in NSCLC cells and tissues, and positively correlated with tumor progression and a poor prognosis. Exogenous FAM83D overexpression promoted, while FAM83D silencing inhibited NSCLC cell proliferation, EMT and invasion. FAM83D silencing also reduced cisplatin resistance. Concordantly, we found that NSCLC patients with a low FAM83D expression benefited most from chemotherapy. Mechanistically, we found that FAM83D activated the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. Pharmacological treatment with either AKT or mTOR inhibitors reverted FAM83D-induced tumorigenic phenotypes.
conclusionsOur results suggest a role of FAM83D in NSCLC development. In addition, our results indicate that NSCLC patients exhibiting FAM83D overexpression are likely to benefit from AKT and/or mTOR inhibitor treatment.
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