miR-5100 promotes tumor growth in lung cancer by targeting Rab6

Huang, Haili; Jiang, Yun; Wang, Yahong; Chen, Ting; Yang, Liting; He, Huijuan; Lin, Ziying; Liu, Tie; Teng, Yan; Kamp, David W.; Wu, Bin; Liu, Gang

doi:10.1016/j.canlet.2015.03.004

Cited by 57 publications

(61 citation statements)

References 27 publications

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“…Western blot was performed as previously described [25]. Briefly, the proteins were separated by 10% SDS-PAGE and subsequently transferred onto a nitrocellulose membrane (Bio-Rad).…”

Section: Methodsmentioning

confidence: 99%

“…For quantitative real-time reverse transcription PCR (qRT-PCR), total RNA was extracted from the cells using TRIzol reagent (Ambion®), as described in the manufacturer’s protocol [25]. Next, the RNA samples were reverse transcribed into cDNA using the FastQuant RT kit (with gDNase) (Tiangen, China), in a total volume of 20 μL, according to the manufacturer’s protocol.…”

Section: Methodsmentioning

confidence: 99%

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The Impact of Cysteine-Rich Intestinal Protein 1 (CRIP1) on Thyroid Carcinoma

Zhao

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: CRIP1 (cysteine-rich intestinal protein 1) has been found in several tumor types; however, its prognostic impact and role in cellular processes, particularly in thyroid carcinoma, are still unclear. Methods: To elucidate the prognostic impact of CRIP1, we analyzed tissues from 58 primary invasive thyroid carcinomas using immunohistochemistry. Western blotting was performed to investigate CRIP1 protein expression in the thyrocyte cell line Nthy-ori 3-1 and four different thyroid carcinoma cell lines, K1, TPC-1, TT, and SW579. Endogenous expression of CRIP1 was suppressed using a siRNA (si-CRIP1). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to investigate cell viability. Flow cytometric analysis was used to detect cell cycle progression and cell apoptosis. The effects of silencing CRIP1 on cell migration and invasion were detected using the transwell assay. Results: The immunohistochemistry results showed that CRIP1 was overexpressed in thyroid carcinoma. CRIP1 expression was associated with tumor size, TNM stage, and lymphatic metastasis, but not with age, gender, and tumor location. In addition, the expression of CRIP1 in K1, TPC-1, TT, and SW529 cells was higher than that in the Nthy-ori 3-1 cells. The highest expression was observed in the SW579 and TT cells. Furthermore, silencing CRIP1 inhibited the proliferation, migration, and invasion of thyroid carcinoma cell lines SW579 and TT. We also found that silencing CRIP1 induced G1 arrest and apoptosis of thyroid carcinoma cell lines SW579 and TT. Conclusion: In conclusion, CRIP1 acts as an oncogene in the cell proliferation, migration, and invasion processes of thyroid carcinoma. CRIP1 may serve well as an independent prognostic marker with significant predictive power for use in thyroid carcinoma therapy.

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“…Western blot was performed as previously described [25]. Briefly, the proteins were separated by 10% SDS-PAGE and subsequently transferred onto a nitrocellulose membrane (Bio-Rad).…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The Impact of Cysteine-Rich Intestinal Protein 1 (CRIP1) on Thyroid Carcinoma

Zhao

Zhang

et al. 2017

Cell Physiol Biochem

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“…Western blot analysis was performed according to standard western blot procedures as previously described [32]. Briefly, proteins were separated by 10% SDS-PAGE and then transferred to nitrocellulose membrane (Bio-Rad).…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was extracted from clinical samples using the TRIzol reagent (Ambion®) according to the manufacturer’s protocol as previously described [32]. For OGG1 detection, RNA samples were then reverse transcribed into cDNA using a FastQuant RT Kit (with gDNase) (TIANGEN, CHINA) in a total volume of 20 µl according to the manufacturer’s protocol.…”

Section: Methodsmentioning

confidence: 99%

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MiR-4673 Modulates Paclitaxel-Induced Oxidative Stress and Loss of Mitochondrial Membrane Potential by Targeting 8-Oxoguanine-DNA Glycosylase-1

Huang

Shi

Huang

et al. 2017

Cell Physiol Biochem

Self Cite

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Background: Our previous study identified a novel microRNA, miR-4673, which is upregulated in A549 cells exposed to paclitaxel (PTX). In this study, we investigated the role of miR-4673 in PTX-induced cytotoxicity. Methods: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, apoptosis assay, 5,5’,6,6’-Tetrachloro-1,1’,3,3’-tetraethyl-imidacarbocyanine iodide (JC-1) staining and 2’,7’-Dichlorofluorescein (DCFH) staining were used to evaluate cell viability, apoptosis, mitochondrial membrane potential (MMP) loss and reactive oxygen species (ROS) generation in A549 and H1299 cells. Bioinformatics analysis and Luciferase reporter assay were used to explore whether 8-oxoguanine-DNA glycosylase-1 (OGG1) is a target gene of miR-4673. Results: Enforced expression of miR-4673 decreased cell viability and increased PTX-induced apoptosis, MMP loss and reactive oxygen species (ROS) generation in A549 and H1299 cells. Bioinformatics analysis, which was used to identify potential target of miR-4673, revealed a binding site of miR-4673 in 3’UTR of OGG1. Luciferase reporters assays showed that miR-4673 specifically binds to ‘CUGUUGA’ in 3’UTR of OGG1. Enforced expression of miR-4673 decreased accumulation of OGG1. In addition, silencing OGG1 enhanced inhibitory effects of PTX on apoptosis, MMP loss and ROS generation, which is similar to effects of miR-4673. Moreover, enforced expression of OGG1 compromised promoting effects of miR-4673 on PTX-induced apoptosis, MMP loss and ROS generation. Conclusion: miR-4673 modulates PTX-induced apoptosis, MMP loss and ROS generation by targeting OGG1.

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Form and function of the Golgi apparatus: scaffolds, cytoskeleton and signalling

2019

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In addition to the classical functions of the Golgi in membrane transport and glycosylation, the Golgi apparatus of mammalian cells is now recognised to contribute to the regulation of a range of cellular processes, including mitosis, DNA repair, stress responses, autophagy, apoptosis and inflammation. These processes are often mediated, either directly or indirectly, by membrane scaffold molecules, such as golgins and GRASPs which are located on Golgi membranes. In many cases, these scaffold molecules also link the actin and microtubule cytoskeleton and influence Golgi morphology. An emerging theme is a strong relationship between the morphology of the Golgi and regulation of a variety of signalling pathways. Here, we review the molecular regulation of the morphology of the Golgi, especially the role of the golgins and other scaffolds in the interaction with the microtubule and actin networks. In addition, we discuss the impact of the modulation of the Golgi ribbon in various diseases, such as neurodegeneration and cancer, to the pathology of disease.

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miR-5100 promotes tumor growth in lung cancer by targeting Rab6

Cited by 57 publications

References 27 publications

The Impact of Cysteine-Rich Intestinal Protein 1 (CRIP1) on Thyroid Carcinoma

The Impact of Cysteine-Rich Intestinal Protein 1 (CRIP1) on Thyroid Carcinoma

MiR-4673 Modulates Paclitaxel-Induced Oxidative Stress and Loss of Mitochondrial Membrane Potential by Targeting 8-Oxoguanine-DNA Glycosylase-1

Form and function of the Golgi apparatus: scaffolds, cytoskeleton and signalling

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