MiR-107 inhibits proliferation of lung cancer cells through regulating TP53 regulated inhibitor of apoptosis 1 (TRIAP1)

Wang, Bing; Zuo, Zhili; Lv, Fang; Lu, Zhao; Du, Minjun; Gao, Yushun

doi:10.1515/biol-2017-0023

Cited by 3 publications

(4 citation statements)

References 24 publications

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“…Evidence has indicated that the expression of TRIAP1 mRNA correlates with myelomas and breast cancer [40, 41]. TRIAP1 is up-regulated in drug-resistant breast cancer cells, and regulates breast cancer cells’ sensitivity to doxorubicin [10, 39, 40]. In the present study, it was demonstrated that TRIAP1 is the direct target of miR-107.…”

Section: Discussionsupporting

confidence: 62%

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Effects of miR-107 on the Chemo-drug sensitivity of breast cancer cells

et al. 2019

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AbstractBackgroundA growing body of evidence indicates that aberrant expression of miR-107 plays a core role in cancers. This study aims to demonstrate the function of miR-107 and its roles in chemo-drug resistance in breast cancer cells.MethodologyCCK-8 assays were carried out to test the effect of miR-107 mimics on the proliferation of MCF-7 cells. The apoptosis level of each group was detected by flow cytometry. miR-107 level, mRNA levels of Bcl-2/Bax and TRIAP1 were detected by quantitative real-time Polymerase Chain Reaction (qRT-PCR) analysis. Protein levels of Bcl-2/Bax, p-Akt/Akt in MCF-7 cells were detected by using Western Blot. Lastly, the dual luciferase reporter gene assay system was used to confirm interaction between miR-107 and its target gene TRIAP1.ResultsCCK-8 assays indicated that miR-107 mimics augmented Taxol-induced cell viability inhibition. Flow cytometry showed that miR-107 mimics augmented Taxol-induced elevation of cell apoptosis. qRT-PCR analysis revealed that miR-107 mimics inhibited the mRNA expression of Bcl-2 and induced the mRNA level of Bax. Western Blotting indicated that miR-107 mimics inhibited the expression of proteins Bcl-2 and p-Akt, and induced the expression of Bax, while showing no significant effects on Akt. The relative luciferase activity revealed that oncogene TRIAP1 is a potential target gene of miR-107.ConclusionsmiR-107 plays a role in regulating chemo-drug sensitivity in mammary cancer cell by targeting TRIAP1.

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Section: Discussionsupporting

confidence: 62%

“…Among them, over 200 have been identified in humans [9]. miRNAs can negatively modulate gene expression by targeting mRNAs and trigger either translation repression or RNA degradation [10, 11]. Normally, conserved miRNAs have critical functions across many processes, such as cell proliferation, apoptosis, and metabolism [12, 13, 14, 15].…”

Section: Introductionmentioning

confidence: 99%

Effects of miR-107 on the Chemo-drug sensitivity of breast cancer cells

et al. 2019

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“…miRNAs regulate cell proliferation and apoptosis by targeting specific genes during cellular processes (22). According to previous studies, TRIAP1 was predicted to be a candidate oncogene in various types of cancer, including ovarian cancer (23), nasopharyngeal carcinoma (24) and lung cancer (25). In the present study, TRIAP1 was revealed to be upregulated in lung cancer tumor tissues compared with adjacent non-tumor tissue.…”

Section: Discussionsupporting

confidence: 53%

MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

Cai

Chen

et al. 2020

Oncol Lett

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Lung cancer causes over 1.6 million mortalities worldwide annually. MicroRNAs (miRs) are involved in various types of cancer-associated processes. The present study investigated the possible mechanism of miR-107 in the development of lung cancer in order to identify novel targets for clinical treatment. The expression levels of miR-107 and its putative target gene TP53 regulated inhibitor of apoptosis 1 (TRIAP1) were measured in lung cancer tumor tissues and non-tumor adjacent tissues. Subsequently, the association between TRIAP1 and miR-107 was investigated using a dual-luciferase reporter assay. Following transfection, the effects of miR-107 and TRIAP1 on the proliferation and apoptosis of lung cancer cell lines in vitro were investigated using Cell Counting Kit-8 and flow cytometry assays, respectively. Furthermore, the regulatory effect of miR-107 on the expression levels of TRIAP1 and associated proteins was analyzed using a western blot assay. The results revealed lower expression levels of miR-107 and higher expression levels of TRIAP1 in lung cancer tumor tissues compared with non-tumor adjacent tissues. The dual-luciferase reporter assay demonstrated that TRIAP1 is a target gene of miR-107. Additionally, the results revealed that overexpression of miR-107 resulted in a lower proliferation rate and higher apoptosis rate of A549 cells, compared with the negative control (NC) and control groups (P<0.01). The variation of cell proliferation and apoptosis induced by miR-107 mimics was reversed by co-transfection with pcDNA3.1-TRIAP1. Furthermore, the expression levels of cyclin D1 and proliferating cell nuclear antigen were markedly decreased in the miR-107 mimics group compared with the NC group (P<0.01). The expression levels of BCL2 associated X apoptosis regulator, tumor protein p53 and caspase 3 were upregulated and the expression levels of TRIAP1 and BCL2 apoptosis regulator were significantly reduced in the miR-107 mimics group compared with the NC group (P<0.01). The results of the present study suggested that miR-107 regulates lung cancer cell proliferation and apoptosis by targeting TRIAP1.

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“…Functional Wound Closure miRNA-107 inhibits cell proliferation and migration. [24][25][26][27] Delivery of anti-miR-107 using a commercially available transfection reagent (Dharmafect1) accelerates keratinocyte proliferation and migration (Figures S2A and S2B). However, when anti-miR-107 was delivered using TLN k/anti-miR-107 , a marginal change in cell migration was observed, although cell proliferation was increased (Figures S3A and S3B).…”

Section: In Vivo Targeting Efficiency Of Tln Kmentioning

confidence: 99%

Topical Lyophilized Targeted Lipid Nanoparticles in the Restoration of Skin Barrier Function following Burn Wound

Ghatak

Masry

et al. 2018

Molecular Therapy

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Lyophilized keratinocyte-targeted nanocarriers (TLN) loaded with locked nucleic acid (LNA) modified anti-miR were developed for topical application to full thickness burn injury. TLN were designed to selectively deliver LNA-anti-miR-107 to keratinocytes using the peptide sequence ASKAIQVFLLAG. TLN employed DOTAP/DODAP combination pH-responsive lipid components to improve endosomal escape. To minimize interference of clearance by non-targeted cells, especially immune cells in the acute wound microenvironment, surface charge was neutralized. Lyophilization was performed to extend the shelf life of the lipid nanoparticles (LNPs). Encapsulation efficiency of anti-miR in lyophilized TLN was estimated to be 96.54%. Cargo stability of lyophilized TLN was tested. After 9 days of loading with anti-miR-210, TLN was effective in lowering abundance of the hypoxamiR miR-210 in keratinocytes challenged with hypoxia. Keratinocyte uptake of DiD-labeled TLN was selective and exceeded 90% within 4 hr. Topical application of hydrogel-dispersed lyophilized TLN encapsulating LNA anti-miR-107 twice a week significantly accelerated wound closure and restoration of skin barrier function. TLN application depleted miR-107 and upregulated dicer expression, which accelerated differentiation of keratinocytes. Expression of junctional proteins such as claudin-1, loricrin, filaggrin, ZO-1, and ZO-2 were significantly upregulated following TLN treatment. These LNPs are promising as topical therapeutic agents in the management of burn injury.

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MiR-107 inhibits proliferation of lung cancer cells through regulating TP53 regulated inhibitor of apoptosis 1 (TRIAP1)

Cited by 3 publications

References 24 publications

Effects of miR-107 on the Chemo-drug sensitivity of breast cancer cells

Effects of miR-107 on the Chemo-drug sensitivity of breast cancer cells

MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

Topical Lyophilized Targeted Lipid Nanoparticles in the Restoration of Skin Barrier Function following Burn Wound

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