Background: This 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.
Methods: Human 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.
Results: FAM46B 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.
Conclusions: FAM46B functions as a tumor suppressor by inhibiting β-catenin/MMP7 signaling.
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http://dx.doi.org/10.21037/tcr.2019.07.27 | DOI Listing |
Trends Cancer
December 2024
Herbert Irving Comprehensive Cancer Center, New York, NY, 10032, USA; Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY, 10032, USA; Division of Digestive and Liver Diseases, Vagelos College of Physicians and Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA. Electronic address:
Metastasis is responsible for most cancer-related deaths. Different cancers have their own preferential sites of metastases, a phenomenon termed metastatic organotropism. The mechanisms underlying organotropism are multifactorial and include the generation of a pre-metastatic niche (PMN), metastatic homing, colonization, dormancy, and metastatic outgrowth.
View Article and Find Full Text PDFTrends Cancer
December 2024
Charité - Universitätsmedizin Berlin, Institute of Pathology, Berlin, Germany; German Cancer Consortium (DKTK), Partner Site Berlin, German Cancer Research Center (DKFZ), Heidelberg, Germany; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. Electronic address:
In 1982, the RAS genes HRAS and KRAS were discovered as the first human cancer genes, with KRAS later identified as one of the most frequently mutated oncogenes. Yet, it took nearly 40 years to develop clinically effective inhibitors for RAS-mutant cancers. The discovery in 2013 by Shokat and colleagues of a druggable pocket in KRAS paved the way to FDA approval of the first covalently binding KRAS inhibitors, sotorasib and adagrasib, in 2021 and 2022, respectively.
View Article and Find Full Text PDFHematol Oncol Clin North Am
December 2024
Department of Radiation Oncology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA. Electronic address:
Circulating tumor DNA (ctDNA) is emerging as a transformative biomarker in the management of non-small cell lung cancer (NSCLC). This review focuses on its role in detecting minimal residual disease (MRD), predicting treatment response, and guiding therapeutic decision-making in radiation oncology and immunotherapy. Key studies demonstrate ctDNA's prognostic value, particularly in identifying relapse risk and refining patient stratification for curative-intent and consolidative treatments.
View Article and Find Full Text PDFCancer Lett
December 2024
Department of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong; Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong. Electronic address:
J Thorac Oncol
December 2024
Division of Medical Oncology, Yonsei Cancer Center, Yonsei University College of Medicine, Seoul, Republic of Korea. Electronic address:
Introduction: Treatment with adjuvant osimertinib for three years is the standard-of-care for resected stage IB-IIIA non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR)-mutations. The role of neoadjuvant osimertinib in the perioperative setting is yet to be elucidated in the NeoADAURA study (NCT04351555).
Methods: This is a single center, pilot study of patients with clinical stage IA-IIIA NSCLC (AJCC 8th edition) harboring an activating EGFR mutation (Exon 19 deletion, L858R) (NCT04816838).
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