Down-regulation of TIMP-1 inhibits cell migration, invasion, and metastatic colonization in lung adenocarcinoma

Chang, Ying; Chiu, Yi Jen; Cheng, Hsiu Chi; Liu, Fang Ju; Lai, Wu‐Wei; Chang, Hsiao Jen; Liao, Pao Chi

doi:10.1007/s13277-015-3039-5

Cited by 15 publications

(8 citation statements)

References 50 publications

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“…TIMPs appear to inhibit tumor growth and invasion in some tumors, whereas in certain types of malignant tumors high TIMP levels are correlated with more aggressive behavior. Down-regulation of TIMP-1 inhibited cell migration, invasion, and metastatic colonization in lung adenocarcinoma 6 . TIMP-1 promoted the accumulation of cancer associated fibroblasts and cancer progression 43 .…”

Section: Discussionmentioning

confidence: 95%

Simulated microgravity with floating environment promotes migration of non-small cell lung cancers

Ahn

Lee

Han

et al. 2019

Sci Rep

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A migration of cancer is one of the most important factors affecting cancer therapy. Particularly, a cancer migration study in a microgravity environment has gained attention as a tool for developing cancer therapy. In this study, we evaluated the proliferation and migration of two types (adenocarcinoma A549, squamous cell carcinoma H1703) of non-small cell lung cancers (NSCLC) in a floating environment with microgravity. When we measured proliferation of two NSCLCs in the microgravity (MG) and ground-gravity (CONT), although initial cell adhesion in MG was low, a normalized proliferation rate of A549 in MG was higher than that in CONT. Wound healing results of A549 and H1703 showed rapid recovery in MG; particularly, the migration rate of A549 was faster than that of H1703 both the normal and low proliferating conditions. Gene expression results showed that the microgravity accelerated the migration of NSCLC. Both A549 and H1703 in MG highly expressed the migration-related genes MMP-2, MMP-9, TIMP-1, and TIMP-2 compared to CONT at 24 h. Furthermore, analysis of MMP-2 protein synthesis revealed weaker metastatic performance of H1703 than that of A549. Therefore, the simulated microgravity based cancer culture environment will be a potential for migration and metastasis studies of lung cancers.

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Section: Discussionmentioning

confidence: 95%

Simulated microgravity with floating environment promotes migration of non-small cell lung cancers

Ahn

Lee

Han

et al. 2019

Sci Rep

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“…Tissue inhibitor of metalloproteinases (TIMP)-1 is a factor that strongly supports lung cancer progression ( 76 – 79 ) and its expression is elevated in all stages and types of lung cancer particularly in adenocarcinoma ( 73 ). Overexpression of TIMP-1 induces the expression of the tumorigenic miR-210 in lung adenocarcinoma cells and within their derived exosomes under the control of the PI3K/Akt/HIF-1 pathway.…”

Section: Angiogenesis Enhancement By Tex In Lung Cancermentioning

confidence: 99%

The Potential Biomarkers and Immunological Effects of Tumor-Derived Exosomes in Lung Cancer

et al. 2018

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Lung cancer remains the leading cause of cancer-related deaths worldwide. Despite considerable achievements in lung cancer diagnosis and treatment, the global control of the disease remains problematic. In this respect, greater understanding of the disease pathology is crucially needed for earlier diagnosis and more successful treatment to be achieved. Exosomes are nano-sized particles secreted from most cells, which allow cross talk between cells and their surrounding environment via transferring their cargo. Tumor cells, just like normal cells, also secrete exosomes that are termed Tumor-Derived Exosome or tumor-derived exosome (TEX). TEXs have gained attention for their immuno-modulatory activities, which strongly affect the tumor microenvironment and antitumor immune responses. The immunological activity of TEX influences both the innate and adaptive immune systems including natural killer cell activity and regulatory T-cell maturation as well as numerous anti-inflammatory responses. In the context of lung cancer, TEXs have been studied in order to better understand the mechanisms underlying tumor metastasis and progression. As such, TEX has the potential to act both as a biomarker for lung cancer diagnosis as well as the response to therapy.

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“…For example, LUAD patients with high expression of TIMP-1 are prone to lymph node or distant metastasis. The results of the cell showed that the down-regulation of TIMP-1 inhibited the migration, invasion and metastasis of LUAD cells [24] ; While the high level of TIMP-1 in serum or plasma of colon cancer patients is negatively related to the survival of patients. The role of TIMP-1 can be divided into MMPs dependent and MMPs independent.…”

Section: Discussionmentioning

confidence: 95%

FAM83B promotes the invasion of primary lung adenocarcinoma via PI3K/AKT/NF-κB pathway

Zhang

Wang

Yue

et al. 2022

Preprint

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Objects: The family with sequence similarity 83B (FAM83B) is one of the markers for poor prognosis in several carcinomas, but the expression and the mechanism resulted in malignant phenotype in lung adenocarcinoma (LUAD) remain to be elucidated. Methods: Data of RNA-seq in LUAD were downloaded from the cancer genome atlas (TCGA) database for differential expression and survival analysis, and immunohistochemistry was employed to analyze the protein expression of FAM83B in 126 cases of primary LUAD. The LUAD cell lines were collected for the detection of the effects on migration and invasion. Then, western blot was performed to measure the expression of tissue inhibitor of metalloproteinase (TIMP)-1 and activation of PI3K/AKT/ NF-κB pathway. Results: FAM83B was overexpressed in multiple types of carcinomas; The differential expression analysis revealed that the level of FAM83B was higher in LUAD than that in para-carcinoma; The patients with overexpression of FAM83B were with shorter overall survival (OS), disease specific survival (DSS) and progress free interval (PFI); Enrichment analysis suggested it was related to the focal adhesion of LUAD. Immunohistochemistry analysis demonstrated that higher FAM83B expression was positively related to lymph node metastasis in primary. Scratch assay and Borden chamber assay showed that the overexpression of FAM83B promoted migration and invasion activity in vitro. Furthermore, high level of FAM83B accelerated the tumorigenesis in vivo. Western blot showed that TIMP-1 was upregulated in H1299/FAM83B OE cells accompanying by the activation of PI3K/AKT/NF-κB pathway. Conclusions: FAM83B was a marker for poor prognosis of LUAD and it might promote the expression of TIMP-1 by activating PI3K/AKT/NF-κB pathway and then affect the ECM balance, which resulted in the migration and invasion of LUAD.

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Down-regulation of TIMP-1 inhibits cell migration, invasion, and metastatic colonization in lung adenocarcinoma

Cited by 15 publications

References 50 publications

Simulated microgravity with floating environment promotes migration of non-small cell lung cancers

Simulated microgravity with floating environment promotes migration of non-small cell lung cancers

The Potential Biomarkers and Immunological Effects of Tumor-Derived Exosomes in Lung Cancer

FAM83B promotes the invasion of primary lung adenocarcinoma via PI3K/AKT/NF-κB pathway

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