MicroRNA-223 Increases the Sensitivity of Triple-Negative Breast Cancer Stem Cells to TRAIL-Induced Apoptosis by Targeting HAX-1

Sun, Xu; Li, Yongqing; Zheng, Min; Zuo, Wenqi; Wen-zhu, Zheng

doi:10.1371/journal.pone.0162754

Cited by 73 publications

(68 citation statements)

References 36 publications

(35 reference statements)

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“…In our study, miR-223 was identified as a regulator of STIM1 via qRT-PCR, western blot analysis and luciferase reporter assay. Additionally, HAX-1 [27] and Caprin-1 [22] have also been identified as the target genes of miR-223 in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Upregulation of miR-223 could inhibit breast cancer cell proliferation and migration, in contrast, downregulation of miR-223 caused decreased abilities of cell proliferation and migration. Besides STIM1, previous study uncovered two other target genes of miR-223, Caprin-1 [22] and HAX-1 [27], which also contributed to breast cancer proliferation, migration, and invasion. Moreover, we showed that miR-223 expression levels were significantly lower in breast cancer tissues than in the adjacent tissues, and that miR-223 was negatively correlated with some poor prognostic factors.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

Yang¹,

Jiang

Ma³

et al. 2018

Cell Physiol Biochem

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Background/Aims: To investigate the cellular effects and clinical significance of microRNA-223 (miR-223) in breast cancer by targeting stromal interaction molecule1 (STIM1). Methods: Breast cancer cell lines (T47D, MCF-7, SKB-R3, MDA-MB-231 and MDA-MB-435) and a normal breast epithelial cell line (MCF-10A) were prepared for this study. MiR-223 mimics, anti-miR-223 and pcDNA 3.1-STIM1 were transiently transfected into cancer cells independently or together, and then RT-qPCR was performed to detect the expressions of miR-223 and STIM1 mRNA, dual-luciferase reporter assay was conducted to examine the effects of miR-223 on STIM1, Western blotting was used to measure the expressions of the STIM1 proteins, MTT and Trans-well assays were performed to detect cell proliferation and invasion. Finally, the correlation of miR-223 and STIM1 was investigated by detecting with ISH and IHC in breast cancer specimens or the corresponding adjacent normal tissues. Results: Compared with normal cells and tissues, breast cancer tissues and cells exhibited significantly lower expression of miR-223, but higher expression of STIM1. MiR-223 could inhibit the proliferation and invasiveness of breast cancer cells by negatively regulating the expressions of STIM1. Reimplantation with STIM1 partially rescued the miRNA-223-induced inhibition of breast cancer cells. Clinical data revealed that high expression of STIM1 and miR-223 was respectively detrimental and beneficial factor impacting patient’s disease-free survival (DFS) rather than overall survival (OS). Moreover, Pearson correlation analysis also confirmed that STIM1 was inversely correlated with miR-223. Conclusion: MiR-223 inhibits the proliferation and invasion of breast cancer by targeting STIM1. The miR-223/STIM1 axis could possibly be a potential therapeutic target for treating breast cancer patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

Yang¹,

Jiang

Ma³

et al. 2018

Cell Physiol Biochem

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“…These results indicated that overexpression of miR-382 was able to increase the anti-tumor effect of γδ T cells on HCC in vivo. [23][24][25]. Among these miRNAs, miR-382 which acts as a tumor suppressor is reported to inhibit tumor growth and sensitize cancer cells to anti-tumor drugs.…”

Section: Mir-382-overexpressed Hcc Model Is Sensitive To γδ T Cells Tmentioning

confidence: 99%

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

Hou¹,

Chen²,

Zheng³

et al. 2018

Oncotarget

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“…TRAIL binds to death receptors 5 (DR5) located on the surface of cancer cells, and thus activates caspase-8-dependent apoptosis [7][8][9]. By contrast, treatment with TRAIL has no effect on normal tissues [10].…”

Section: Introductionmentioning

confidence: 99%

miR-128 Targets the SIRT1/ROS/DR5 Pathway to Sensitize Colorectal Cancer to TRAIL-Induced Apoptosis

Liu

Yang

Liu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an ideal anti-tumor drug because it exhibits selective cytotoxicity against cancer cells. However, certain cancer cells are resistant to TRAIL, and the potential mechanisms are still unclear. The aim of this study was to reduce the resistance of colorectal cancer (CRC) cells to TRAIL. Methods: Quantitative real-time PCR analysis was performed to detect the expression of microRNA-128 (miR-128) in tissues from patients with CRC and CRC cell lines. MTT assays were used to evaluate the effect of miR-128 on TRAIL-induced cytotoxicity against CRC cell lines. The distribution of death receptor 5 (DR5) and the production of reactive oxygen species (ROS) were detected by flow cytometry analysis. Western blot, flow cytometry, and luciferase reporter assays were performed to evaluate the potential mechanism and pathway of miR-128-promoted apoptosis in TRAIL-treated CRC cells. Results: MiR-128 expression was downregulated in tumor tissues from patients with CRC as well as in CRC cell lines in vitro. The enforced expression of miR-128 sensitized CRC cells to TRAIL-induced cytotoxicity by inducing apoptosis. Mechanistically, bioinformatics, western blot analysis, and luciferase reporter assays showed that miR-128 directly targeted sirtuin 1 (SIRT1) in CRC cells. miR-128 overexpression suppressed SIRT1 expression, which promoted the production of ROS in TRAIL-treated CRC cells. This increase of ROS subsequently induced DR5 expression, and thus increased TRAIL-induced apoptosis in CRC cells. Conclusion: The combination of miR-128 with TRAIL may represent a novel approach for the treatment of CRC.

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MicroRNA-223 Increases the Sensitivity of Triple-Negative Breast Cancer Stem Cells to TRAIL-Induced Apoptosis by Targeting HAX-1

Cited by 73 publications

References 36 publications

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

MicroRNA-223 Targeting STIM1 Inhibits the Biological Behavior of Breast Cancer

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

miR-128 Targets the SIRT1/ROS/DR5 Pathway to Sensitize Colorectal Cancer to TRAIL-Induced Apoptosis

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