Background: FK506, also named tacrolimus, a new macrolide immunosuppressive agent, has been shown to possess anti-proliferation activities in some cancer cells. The aim of this study was to investigate the effect of FK506 on the cell proliferation and migration of lung cancer cell lines and its mechanism.
Methods: A549 and H1299 cell lines were cultured in vitro. The effect of FK506 on cell viability and DNA synthesis ability of A549 and H1299 were measured by CCK-8 assay and EDU-labeling assay, respectively. Flow cytometry assay was used to detect the cell cycle. The in vitro migration of lung cancer cells was detected by Boyden chamber assay and wound-healing assay after the treatment of FK506. The expression of p27, RB1, CDK4, CDK6 and MMP9 were detected using Western blot.
Results: FK506 inhibited cell growth and induced cell cycle arrest in G0/G1 phase in A549 and H1299 cells in a dose- and time-dependent manner. Compared to the control groups, the migration of A549 and H1299 cells treated with FK506 were decreased obviously. Moreover, FK506 increased the expression of P27 and RB1, and reduced the expression of CDK4, CDK6 and MMP9.
Conclusions: FK506 inhibit the cell growth and migration of lung cancer cells in vitro. The inhibitive effects may be associated with the up-regulation of p27 expression and inhibition CDK4, CDK6 and MMP9 expression.
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http://dx.doi.org/10.3779/j.issn.1009-3419.2017.07.02 | DOI Listing |
Front Immunol
December 2024
Department of Otolaryngology, the Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu, China.
Background: B-cell receptor-associated protein 31 (BCAP31) is a widely expressed transmembrane protein primarily located in the endoplasmic reticulum (ER), including the ER-mitochondria associated membranes. Emerging evidence suggests that BCAP31 may play a role in cancer development and progression, although its specific effects across different cancer types remain incompletely understood.
Methods: The raw data on BCAP31 expression in tumor and adjacent non-tumor (paracancerous) samples were obtained from the Broad Institute Cancer Cell Line Encyclopedia (CCLE) and UCSC databases.
Cytojournal
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Department of Respiratory and Critical Care Medicine, Wuyi County First People's Hospital, Jinhua, Zhejiang, China.
Objective: Epithelial-mesenchymal transition (EMT) and metastasis are the primary causes of mortality in non-small-cell lung cancer (NSCLC). 5'-3' exoribonuclease 2 (XRN2) plays an important role in the process of tumor EMT. Thus, this investigation mainly aimed to clarify the precise molecular pathways through which XRN2 contributes to EMT and metastasis in NSCLC.
View Article and Find Full Text PDFCytojournal
November 2024
Medical College, Ningbo University Health Science Center, Ningbo, China.
Objective: Patients with non-small cell lung cancer (NSCLC) have poor prognoses. Sulfatase 1 (SULF1) is an extracellular neutral sulfatase and is involved in multiple physiological processes. Hence, this study investigated the function and possible mechanisms of SULF1 in NSCLC.
View Article and Find Full Text PDFCytojournal
November 2024
Department of Gynaecology and Obstetrics, The 960th Hospital of the Joint Logistics Support Force of the People`s Liberation Army of China, Jinan, China.
Objective: Endometrial cancer (EC) is a common gynecological malignancy, and its metastasis is one of the primary causes of treatment failure. Immunoglobulin superfamily member 1 (IGSF1), a membrane protein, has been associated with the aggressiveness and metastatic capability of various cancers. However, the role and mechanism of this protein in EC remains unclear.
View Article and Find Full Text PDFACS Chem Biol
December 2024
Department of Urology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
MicroRNAs (miRNAs) play a significant role in tumor progression, and regulating miRNA expression with small molecules may offer a new approach to cancer therapy. Among them, miRNA-20b has been found to be dysregulated in several cancers, including nonsmall cell lung cancer (NSCLC). Herein, an in silico high-throughput computer screen was conducted to identify small molecules that downregulate miR-20b using the three-dimensional structure of the Dicer binding site on pre-miR-20b.
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