Knockdown of ANXA1 suppresses the biological behavior of human NSCLC cells in vitro

Fāng, Yīng; Guan, Xiaoying; Cai, Tonghui; Long, Jie; Wang, Hongyan; Xie, Xiaobin; Zhang, Yajie

doi:10.3892/mmr.2016.5022

Cited by 27 publications

(34 citation statements)

References 28 publications

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“…In colon and gastric cancers, ANXA1 interacts with formyl peptide receptors to promote cell migration and invasion (20,21). In non-small cell lung cancer, ANXA1 knockdown suppressed cell proliferation and metastasis (22). However, ANXA1 acts as a tumor suppressor by reducing cell proliferation and attenuating the metastatic potential in breast cancer (23).…”

Section: Introductionmentioning

confidence: 99%

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

et al. 2017

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Abstract. Annexin A1 (ANXA1) acts either as a tumor suppressor or an oncogene in different tumor types. Several clinical studies revealed that the expression of ANXA1 is associated with the pathologic differentiation grade in oral squamous cell carcinoma (OSCC) patients. However, the direct function of ANXA1 in OSCC progression has remained to be fully clarified. The present study was designed to investigate the role of ANXA1 in OSCC cell proliferation and invasion in vitro. Furthermore, whether ANXA1 was involved in transforming growth factor β1 (TGFβ1)/epidermal growth factor (EGF)-induced epithelial-mesenchymal transition (EMT) in OSCC was explored. Tca-8113 and SCC-9 cells were transfected with ANXA1-pcDNA3.1 plasmid to overexpress ANXA1. Subsequently, cell proliferation and invasion were examined using MTT and Transwell-Matrigel invasion assays. TGFβ1 and EGF were used to induce EMT in Tca-8113 and SCC-9 cells, and the expression of epithelial (E)-cadherin, neural (N)-cadherin and vimentin was determined by western blot analysis. The results demonstrated that ANXA1 overexpression induced a significant decrease of cell growth and invasiveness in Tca-8113 and SCC-9 cells. The expression of E-cadherin was significantly increased, while the expression of vimentin and N-cadherin was significantly decreased in ANXA1-overexpressing Tca-8113 and SCC-9 cells. ANXA1 expression was significantly decreased in TGFβ1/EGF-treated cells. Furthermore TGFβ1/EGF-induced EMT in OSCC cell lines was attenuated by ANXA1 overexpression. In conclusion, to the best of our knowledge, the present study was the first to evidence that ANXA1 inhibits OSCC cell proliferation and invasion in vitro. TGFβ1/EGF-induced EMT was reversed by ANXA1 in OSCC. ANXA1 was suggested to be a potential marker for OSCC as well as a novel treatment.

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Section: Introductionmentioning

confidence: 99%

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

et al. 2017

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“…Data presented from our previous work showed that the expression of ANXA1 was significantly upregulated in eight matched cancer tissues and five NSCLC cell lines, compared with the normal tissues and cell lines . ANXA1 was detected at a higher expression level in the A549 cells than in human bronchial epithelial cells (16HBE).…”

Section: Resultsmentioning

confidence: 94%

“…The expression of ANXA1 has been reported to be reduced or increased in many types of cancer. We and others have recently reported that the expression of ANXA1 is upregulated in lung cancer . Of importance, ANXA1 has been shown to activate nuclear factor (NF)‐κB in T cells, and T cells from ANXA1‐deficient mice showed decreased NF‐κB activation, indicating that ANXA1 may somehow regulate NF‐κB .…”

Section: Introductionmentioning

confidence: 99%

“…In breast cancer, co‐immunoprecipitation confirmed that ANXA1 can bind to inhibitor of NF‐κB kinase (IKK)γ or NEMO, which may be important for the activation of NF‐κB to promote metastasis capability . Interestingly, ANXA1 enhanced cells proliferation, invasion, and migration ability in NSCLC . However, the mechanism behind this regulation remains obscure.…”

Section: Introductionmentioning

confidence: 99%

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Annexin 1–nuclear factor‐κB–microRNA‐26a regulatory pathway in the metastasis of non‐small cell lung cancer

et al. 2019

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Background Annexin 1 (ANXA1) expression is associated with the malignant tumor phenotype, making it an attractive therapeutic target. However, little is known about the regulation of ANXA1 in non‐small cell lung cancer (NSCLC). Methods We investigated the biological roles of ANXA1 in tumor growth, migration, and invasion, and explored the possibility of ANXA1 as a potential therapeutic target for the treatment of NSCLC. Results Our findings revealed that ANXA1 enhanced nuclear factor (NF)‐κB activation in NSCLC cells by interaction with inhibitor of NF‐κB kinase complex subunit, IKKγ. We also found that NF‐κB could negatively regulate microRNA (miR)‐26a, and miR‐26a was regulated through the ANXA1–NF‐κB regulatory pathway. NF‐κB activation negatively regulated by miR‐26a was confirmed in NSCLC. Conclusion Together, these results provide evidence of the mechanisms of the ANXA1–NF‐κB–miR‐26a regulatory pathway in the invasion and migration in NSCLC.

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“…The molecular mechanisms underlying ANXA1 modulation of cellular responses have not been fully determined. The previous study revealed that ANXA1 upregulation in lung cancer, and suppressing ANXA1 gene expression by the lentiviral vector LV-ANXA1-RNAi, may inhibit the proliferation, migration and invasion capabilities of lung cancer cells (31).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer

et al. 2018

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Abstract. The aim of the present study was to investigate the expression and role of microRNA-26a (miR-26a) in lung cancer, and to verify whether differentially expressed in adenocarcinoma of the lung (DAL-1) is the target protein of miR-26a. mRNA expression levels of miR-26a and DAL-1 were detected using reverse transcription-quantitative polymerase chain reaction. Protein expression levels of DAL-1 and annexin A1 (ANXA1) were evaluated by western blot analysis. Cell Counting Kit-8, Transwell and wound scratch healing assays were used to characterize the function of miR-26a in lung cancer cells. The association of DAL-1 with miR-26a or ANXA1 was determined by dual-luciferase reporter or two-dimensional gel electrophoresis assays. miR-26a revealed decreased expression levels in lung cancer tissues compared with normal lung tissues, and decreased expression levels in lung cancer cells compared with 16HBE cells. Inhibition of miR-26a promoted lung cancer cell growth, migration and invasion. The DAL-1 protein exhibited downregulated expression levels in lung cancer tissues. DAL-1 was not the direct target gene of miR-26a. The two-dimensional gel electrophoresis assay confirmed that DAL-1 and ANXA1 were associated proteins. Expression levels of the ANXA1 protein were increased following DAL-1 gene silencing. The altered expression level of miR-26a affected the expression of ANXA1, and not of DAL-1. miR-26a demonstrated decreased expression levels in lung cancer cells, and it has an important effect on the biological function of lung cancer cells. However, DAL-1 was not a target gene of miR-26a. As a DAL-1 associated protein, ANXA1 was regulated by miR-26a. IntroductionLung cancer has a high incidence of tumor recurrence and metastasis, and is the most common cause of cancer-associated morality worldwide (1). The overall 5-year survival rate among patients with lung cancer is <15%, and a high rate of metastasis is the primary cause of lung cancer-associated mortality (2). A previous study confirmed that differentially expressed in adenocarcinoma of the lung (DAL-1), a protein that belongs to the membrane-associated cytoskeleton protein 4.1 family, is an efficient suppressor of epithelial-mesenchymal transition (EMT) in lung cancer (3). EMT is a pivotal event in lung cancer metastasis progression (4-6). However, the regulators of DAL-1 in EMT remain unknown.Recently, a novel batch of endogenous small non-coding regulatory RNAs (microRNA's; miRNA's) have received attention in the development of cancer, miRNA's bind complementary sequences in target mRNAs, resulting in selective degradation or selective inhibition of their translation (7). The present study investigated the possible miRNAs of DAL-1 using bioinformatic assays, which included miR-26b, miR-26a, miR-96 and miR-223. Among them, the regulation of DAL-1 by miR-223 has been demonstrated to serve a role in gastric cancer (8). The present study revealed that the gene silencing of DAL-1 induced annexin A1 (ANXA1) protein expression levels to increase in H460 cells...

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Knockdown of ANXA1 suppresses the biological behavior of human NSCLC cells in vitro

Cited by 27 publications

References 28 publications

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

ANXA1 affects cell proliferation, invasion and epithelial‑mesenchymal transition of oral squamous cell carcinoma

Annexin 1–nuclear factor‐κB–microRNA‐26a regulatory pathway in the metastasis of non‐small cell lung cancer

MicroRNA‑26a regulates ANXA1, rather than DAL‑1, in the development of lung cancer

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