miR-206/133b Cluster: A Weapon against Lung Cancer?

Pan, Jingyu; Sun, Chengcao; Bi, Zhuoyue; Chen, Zhenlong; Li, Shujun; Li, Qing-Qun; Wang, Yuxuan; Bi, Yang; Li, Dejia

doi:10.1016/j.omtn.2017.06.002

Cited by 46 publications

(29 citation statements)

References 76 publications

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“…Recent investigation on head and neck squamous cell carcinoma reported that miR‐206 inhibits cell invasion and migration via downregulating MMP‐2 . An increasing body of studies have demonstrated the role of miR‐206 as a tumor‐inhibiting factor in a variety of cancers, including TC …”

Section: Discussionmentioning

confidence: 99%

“…9 An increasing body of studies have demonstrated the role of miR-206 as a tumor-inhibiting factor in a variety of cancers, including TC. 6,8,16,18 RAP1B is a member of the small GTPase Ras family, functioning as a molecular switch and plays a crucial role in cell activities, including cell proliferation, migration, and invasion. Recent studies have revealed the abnormal occurrence of RAP1B in several malignancies.…”

Section: Discussionmentioning

confidence: 99%

“…They also play critical roles in essential biological processes, including cell proliferation, cell differentiation, and apoptosis . An increasing number of investigations have reported aberrant expression of miR‐206 in multiple cancers, including breast cancer, lung cancer, and colon cancer, and established that miR‐206 functions as a suppressor in tumor progression. For instance, elevated miR‐206 expression inhibited proliferation and invasion via decreasing expression of NAMPT and coronin 1C in breast cancer, and HDAC6 in head and neck squamous cell carcinoma .…”

Section: Introductionmentioning

confidence: 99%

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miR‐206 inhibits thyroid cancer proliferation and invasion by targeting RAP1B

Wang

et al. 2019

J of Cellular Biochemistry

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Thyroid cancer (TC) is one of the primary tumors arisen from endocrine system. The purpose of this study was to investigate the underlying mechanism by which RAP1B (Ras‐related protein Rap‐1b) modulates microRNA (miR)‐206 related effects on TC cells. Expression of miR‐206 and RAP1B was analyzed in cells and tissues. miR‐206 mimics or inhibitors and RAP1B vector were used in functional experiments to investigate the effects of miR‐206 and RAP1B on cell activities including proliferation, migration, and invasion. Luciferase assay was performed to explore the association between miR‐206 and RAP1B. The influence of miR‐206 on tumorigenesis of TC cells was investigated using an ex vivo model. Our results demonstrated the reduce of miR‐206 in TC tissues and cell lines in which RAP1B was increased. Overexpression of miR‐206 significantly inhibited the functional capacities of TPC‐1 cells including proliferation, invasion, and migration, most likely, through reducing the expression of RAP1B. Xenograft experiment showed that increased miR‐206 could effectively inhibit the tumorigenesis of TC cells. Our study showed that miR‐206 negatively regulated cell activities of proliferation, invasion, and migration in TC via suppressing RAP1B expression, suggesting that miR‐206 exerts a vital role in TC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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miR‐206 inhibits thyroid cancer proliferation and invasion by targeting RAP1B

Wang

et al. 2019

J of Cellular Biochemistry

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“…Among these miRNAs, miR-206 was identified to have protective effects on the development of coronary artery disease and cancers. 15,16 In particular, studies revealed that miR-206 participated in the progression of glioma by functioning as a tumor inhibitor to regulate cellular biological processes, and decreased miR-206 expression was associated with poor prognosis in glioma. [17][18][19] Further, miR-206 knockdown was shown to protect human embryonic stem cells (hESCs) against propofol-induced cell apoptosis, thereby inhibiting neurotoxicity.…”

Section: Introductionmentioning

confidence: 99%

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Wang¹,

Yang²,

Liu³

et al. 2020

OTT

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Background: Propofol has been identified to perform anti-tumor functions in glioma. However, the molecular mechanisms underlying propofol-induced prevention on migration and invasion of glioma cells remain unclear. Methods: Cell proliferation, invasion and migration were measured by 3-(4,5)-dimethylthiahiazo (−z-y1)-3,5-di-phenytetrazoliumromide assay and transwell assay, respectively. The expression of microRNA (miR)-206 and Rho-associated coiled coil-containing protein kinase 1 (ROCK1) was detected by quantitative real-time polymerase chain reaction. Western blot was used to measure the activation of the PI3K/AKT pathway. The interaction between miR-206 and ROCK1 was analyzed using the dual-luciferase reporter assay, RNA immunoprecipitation assay, and pull-down assay. Results: Propofol treatment inhibited the migration, invasion, and PI3K/AKT pathway activation in glioma cells. MiR-206 was decreased in glioma tissues and cells, while propofol exposure induced the upregulation of miR-206 in glioma cells. Besides that, we also found overexpressed miR-206 enhanced propofol-mediated inhibition on the migration, invasion, and PI3K/AKT pathway activation of glioma cells. Subsequently, ROCK1 was confirmed to be a target of miR-206. ROCK1 was elevated in glioma tissues and cells, but was reduced by propofol exposure in glioma cells. The rescue assay indicated that the miR-206/ROCK1 axis was involved in propofol-induced inhibition on the migration, invasion, and PI3K/AKT pathway activation in glioma cells. Conclusion: Propofol inhibited the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through the miR-206/ROCK1 axis, suggesting an effective clinical implication for the anesthetic to prevent the metastasis of glioma.

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“…Several microRNAs (miRNAs) were also reported to modulate VEGF-A expression and to be downregulated in lung cancer cell lines. In particular, miR-126, miR-497, MiR-206, miR-29c, miR-135a, and miR-195 expression inversely correlated with VEGF-A production in different lung cancer cell lines or in patients' tumor samples [86][87][88][89][90][91]. Moreover, interleukin-17 (IL-17) was found to stimulate NSCLC-associated angiogenesis by augmenting the secretion of various angiogenic factors.…”

Section: Lung Cancermentioning

confidence: 99%

Role of VEGFs/VEGFR-1 Signaling and Its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models

Ceci

Atzori

Lacal

et al. 2020

IJMS

162

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The vascular endothelial growth factor (VEGF) family members, VEGF-A, placenta growth factor (PlGF), and to a lesser extent VEGF-B, play an essential role in tumor-associated angiogenesis, tissue infiltration, and metastasis formation. Although VEGF-A can activate both VEGFR-1 and VEGFR-2 membrane receptors, PlGF and VEGF-B exclusively interact with VEGFR-1. Differently from VEGFR-2, which is involved both in physiological and pathological angiogenesis, in the adult VEGFR-1 is required only for pathological angiogenesis. Besides this role in tumor endothelium, ligand-mediated stimulation of VEGFR-1 expressed in tumor cells may directly induce cell chemotaxis and extracellular matrix invasion. Furthermore, VEGFR-1 activation in myeloid progenitors and tumor-associated macrophages favors cancer immune escape through the release of immunosuppressive cytokines. These properties have prompted a number of preclinical and clinical studies to analyze VEGFR-1 involvement in the metastatic process. The aim of the present review is to highlight the contribution of VEGFs/VEGFR-1 signaling in the progression of different tumor types and to provide an overview of the therapeutic approaches targeting VEGFR-1 currently under investigation.

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miR-206/133b Cluster: A Weapon against Lung Cancer?

Cited by 46 publications

References 76 publications

miR‐206 inhibits thyroid cancer proliferation and invasion by targeting RAP1B

miR‐206 inhibits thyroid cancer proliferation and invasion by targeting RAP1B

<p>Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis</p>

Role of VEGFs/VEGFR-1 Signaling and Its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models

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