MicroRNA‐127 is Downregulated by Tudor‐SN Protein and Contributes to Metastasis and Proliferation in Breast Cancer Cell Line MDA‐MB‐231

Zhao, Xiujuan; Duan, Zhongchao; Liu, Xin; Wang, Baoya; Wang, Xinting; He, Jian‐Qing; Yao, Zhi; Yang, Jie

doi:10.1002/ar.22823

Cited by 21 publications

(13 citation statements)

References 33 publications

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“…In breast cancer cell lines, Wu et al (36) suggested that miR-339-5p may inhibit the expression of BCL6 mRNA, which was associated with suppressed migration and invasion of cells. Zhao et al (37) identified that the downregulation of miR-127 expression may promote metastasis and proliferation, and that BCL6 was a target of miR-127. Pinto et al (38) demonstrated that, in metastatic lymph nodes, the expression of BCL6 protein was significantly lower compared with that in the corresponding primary breast cancer.…”

Section: Discussionmentioning

confidence: 99%

miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

Zhang

Yang

et al. 2017

Oncol Lett

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Abstract. Metastasis is a common event in cancer pathology, and represents the primary cause of cancer-associated mortality. Metastasis, which is the process in which cancer cells at the primary tumor site spread to a different location in the body and form a new tumor, is regulated by multiple factors and includes a number of steps and stages. In our previous study, it was demonstrated miR-339-5p inhibits cell migration and invasion in vitro and is associated with the tumor-node-metastasis stage and the lymph node metastasis status of non-small cell lung cancer. In the present study, expression of miR-339-5p was first determined in the tissues and peripheral blood of patients with non-small cell lung cancer (NSCLC) and in NSCLC cell lines. It was then demonstrated that miR-339-5p inhibits A549 and H1299 cell invasion. The underlying molecular events of miR-339-5p action in NSCLC were also explored. By luciferase assay and western blot analysis, B-cell CLL/lymphoma 6 (BCL6) was verified as the direct target gene of miR-339-5p. miR-339-5p may inhibit lung cancer cell invasion and migration by regulating the epithelial-to-mesenchymal transition via BCL6 in vitro. It was also demonstrated that the relative expression of miR-339-5p in the peripheral blood is associated with cancer metastasis in patients with non-small cell lung cancer.

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Section: Discussionmentioning

confidence: 99%

miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

Zhang

Yang

et al. 2017

Oncol Lett

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“…Tudor-SN is a type of multi-functional protein that is widely expressed in tumor cells. Tudor-SN has the ability to activate various transcription factors, including NF-κB, and is involved in adjusting the expression of miRNAs (11).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have indicated that Tudor-SN has a close association with lipid metabolism, and that the expression of lipoprotein in liver cells can be affected through adjustment of lipid metabolism-associated genes (11,12). Inactivation of alkylglycerone phosphate synthase (AGPS) can lower the ether ester level in the tumor cell and cancer pathogenicity, while overexpression of AGPS can increase the ether ester level, viability and migration potential of various tumor cells, including 231MFP, C8161 melanoma, PC3 prostate cancer and primary breast cancer cells, and advance the growth and migration of the tumor cells (13,14).…”

Section: Introductionmentioning

confidence: 99%

Tudor‑staphylococcal nuclease regulates the expression and biological function of alkylglycerone phosphate synthase via nuclear factor‑κB and microRNA‑127 in human glioma U87MG cells

Zhang

Jia

et al. 2018

Oncol Lett

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Abstract. Glioma is one of the malignant tumor types detrimental to human health; therefore, it is important to find novel targets and therapeutics for this tumor. The downregulated expression of Tudor-staphylococcal nuclease (SN) and alkylglycerone phosphate synthase (AGPS) can decrease cancer malignancy, and the overexpression of them can the increase viability and migration potential of various tumor cell types; however, the role of AGPS in the proliferation and migration of glioma, and the association of Tudor-SN and AGPS in human glioma is not clear. In the present study, it was determined that AGPS silencing suppressed the proliferation and migration potential of glioma U87MG cells, and suppressed the expression of the circular RNAs circ-ubiquitin-associated protein 2, circ-zinc finger protein 292 and circ-homeodomain-interacting protein kinase 3, and the long non-coding RNAs H19 imprinted maternally expressed transcript (non-protein coding), colon cancer-associated transcript 1 (non-protein coding) and hepatocellular carcinoma upregulated long non-coding RNA. Furthermore, Tudor-SN silencing suppressed the expression of AGPS; however, nuclear factor (NF)-κB and microRNA (miR)-127 retrieval experiments partially reduced the expression of AGPS. Additionally, it was determined that Tudor-SN silencing suppressed the activity of the mechanistic target of rapamycin (mTOR) signaling pathway, and NF-κB and miR-127 retrieval experiments partially reduced the activity of mTOR. Therefore, it was considered that NF-κB and miR-127 may be the mediators of Tudor-SN-regulated AGPS via the mTOR signaling pathway. These results improve on our knowledge of the mechanisms underlying Tudor-SN and AGPS in human glioma. IntroductionGliomas are a type of tumor formed by neoplastic transformation of neural stem cells, progenitor cells and differentiated glial cells, including astrocytes, oligodendrocytes and ependymal cells (1). Neoplastic cells may spread diffusely to normal brain tissues and damage normal neurological functions, which is the reason why malignant gliomas are detrimental to human health (2). In China, gliomas constitute 44.69% of primary intracranial tumors and 1-3% of generalized malignancies (3). According to the World Health Organization, malignant glioma causes the second highest amount of mortalities in sufferers <34 years old, and the third highest amount of mortalities in sufferers aged 35-54 years old (4). It is estimated that the survival time of the majority of glioma sufferers is ~1 year. Although there are currently various treatments available, including excision, chemotherapy and radiotherapy, the characteristic of strong invasiveness has severely influenced the effectiveness of glioma treatment.MicroRNAs (miRNAs/miRs) are an important molecular mediator of cell genetic changes, and are directly or indirectly associated with the occurrence and development of a number

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“…In terms of its link to cancer progression, Tudor-SN has been shown to promote resistance to apoptosis and to be induced by NF-κB, which as mentioned above, was increased in the CD-induced tissues through potentially decreased miR-146a and 146b expression (Figure 5) [45, 49]. Amongst the miRNAs influenced by Tudor-SN, is miR-127, and studies have shown that Tudor-SN triggers miR-127 downregulation in breast cancer cells [50]. Our western blot results illustrate that Tudor-SN was significantly increased in the CD-induced tissues (Figure 6).…”

Section: Discussionmentioning

confidence: 99%

Circadian disruption-induced microRNAome deregulation in rat mammary gland tissues

et al. 2015

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Breast cancer is the most common malignancy affecting women worldwide, and evidence is mounting that circadian-disruption-induced breast cancer is a warranted concern. Although studies on the role of epigenetics have provided valuable insights, and although epigenetics has been increasingly recognized in the etiology of breast cancer, relatively few studies have investigated the epigenetic link between circadian disruption (CD) and breast cancer. Using a proven photoperiod-shifting paradigm, differing degrees of CD, various tissue-extraction time points, and Illumina sequencing, we investigated the effect of CD on miRNA expression in the mammary tissues of a rodent model system. To our knowledge, our results are the first to illustrate CD-induced changes in miRNA expressions in mammary tissues. Furthermore, it is likely that these miRNA expression changes exhibit varying time frames of plasticity linked to both the degree of CD and length of reentrainment, and that the expression changes are influenced by the light and dark phases of the 24-hour circadian cycle. Of the differentially expressed miRNAs identified in the present study, all but one have been linked to breast cancer, and many have predicted circadian-relevant targets that play a role in breast cancer development. Based on the analysis of protein levels in the same tissues, we also propose that the initiation and development of CD-induced breast cancer may be linked to an interconnected web of increased NF-κB activity and increased levels of Tudor-SN, STAT3, and BCL6, with aberrant CD-induced downregulation of miR-127 and miR-146b potentially contributing to this dynamic. This study provides direct evidence that CD induces changes in miRNA levels in mammary tissues with potentially malignant consequences, thus indicating that the role of miRNAs in CD-induced breast cancer should not be dismissed.

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MicroRNA‐127 is Downregulated by Tudor‐SN Protein and Contributes to Metastasis and Proliferation in Breast Cancer Cell Line MDA‐MB‐231

Cited by 21 publications

References 33 publications

miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

miR-339-5p inhibits metastasis of non-small cell lung cancer by regulating the epithelial-to-mesenchymal transition

Tudor‑staphylococcal nuclease regulates the expression and biological function of alkylglycerone phosphate synthase via nuclear factor‑κB and microRNA‑127 in human glioma U87MG cells

Circadian disruption-induced microRNAome deregulation in rat mammary gland tissues

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