The microRNA-635 suppresses tumorigenesis in non-small cell lung cancer

Zhang, Yan; Sun, Zongwen; Zhang, Yanqun; Tian, Fei; Liu, Cun; Liu, Yongrui; Lin, Yong

doi:10.1016/j.biopha.2016.10.040

Cited by 26 publications

(20 citation statements)

References 34 publications

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“…Tian et al found that miR‐635 functioned as tumor suppressor to inhibit tumorigenesis of osteosarcoma. Moreover, miR‐635 was shown to inhibit the tumorigenesis of NSCLC by targeting YY1 . However, in the present study, JAK1 and JAK3 were characterized as the potential targets of miR‐635 by means of dual‐luciferase reporter assay.…”

Section: Discussionmentioning

confidence: 64%

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Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

Zhu

Wang

et al. 2019

Cancer Medicine

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Non‐small cell lung cancer (NSCLC), the major type of lung cancer, becomes the greatest threat to the life of people. Growing evidence shows prostate androgen‐regulated transcript 1 (PART1) is considered as effective markers for prostate cancer, and has been shown to be associated with poor prognosis of NSCLC. However, the tumorigenic mechanism of PART1 in NSCLC remains to be investigated. In this study, we found that the expression of PART1 was robustly induced in NSCLC tissues and cell lines. Functional studies established that overexpression of PART1 could promote NSCLC cell proliferation, migration, and invasion, while interference of PART1 inhibited NSCLC progression. Our results also identified miR‐635 as a novel target of PART1, whose expression was inhibited by PART1 in NSCLC cell lines. Moreover, gain‐ and loss‐of‐function studies revealed that PART1 could sponge miR‐635 and increase the expression of Janus kinase (JAK) and signal transducer and activator of transcription proteins (STATs). Finally, we deciphered the molecular mechanism by which PART1 contributed to promotion of NSCLC cell progression via phosphorylation and activation of JAK‐STAT signaling pathway. The animal experiment further confirmed that interference of NSCLC could suppress in vivo tumorigenic ability of NSCLC with favorable pharmacological activity via inactivation of JAK‐STAT signaling pathway. In conclusion, our findings clarified the biologic significance of PART1/miR‐635/JAK‐STAT axis in NSCLC progression and provided novel evidence that PART1 may be a new potential therapeutic target for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 64%

“…MiR‐635 was first identified in colorectal cancer . Moreover, it was reported that miR‐635 could inhibit the tumorigenesis of NSCLC by targeting Ying Yang 1 (YY1) . To date, whether PART1 binds with miR‐635 relevant molecular mechanism still needs to be confirmed by further experiments.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

Zhu

Wang

et al. 2019

Cancer Medicine

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“…In non‐small‐cell lung cancer (NSCLC), miR‐635 reduced endogenous YY1 expression, like YY1 siRNA, and did not influence NSCLC viability but decreased invasion. Nude mice implanted with H522 cells transfected with miR‐635 grew slowly compared with control mIR and reduced ki‐67 staining . Lu et al .…”

Section: Yy1 and Tumor Growthmentioning

confidence: 99%

The Yin and Yang of YY1 in tumor growth and suppression

Khachigian

2018

Intl Journal of Cancer

132

106

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Yin Yang-1 (YY1) is a zinc finger protein and member of the GLI-Kruppel family that can activate or inactivate gene expression depending on interacting partners, promoter context and chromatin structure, and may be involved in the transcriptional control of ∼10% of the total mammalian gene set. A growing body of literature indicates that YY1 is overexpressed in multiple cancer types and that increased YY1 levels correlate with poor clinical outcomes in many cancers. However, the role of YY1 in the promotion or suppression of tumor growth remains controversial and its regulatory effects may be tumor cell type dependent at least in experimental systems. The molecular mechanisms responsible for the apparently conflicting roles of YY1 are not yet fully elucidated. This review highlights recent advances in our understanding of regulatory insights involving YY1 function in a range of cancer types. For example, YY1's roles in tumor growth involve stabilization of hypoxia-inducible factor HIF-1α in a p53 independent manner, negative regulation of miR-9 transcription, control of MYCT1 transcription, a novel miR-193a-5p-YY1-APC axis, intracellular ROS and mitochondrial superoxide generation, p53 reduction and EGFR activation, control of genes associated with mitochondrial energy metabolism and miRNA regulatory networks involving miR-7, miR-9, miR-34a, miR-186, miR-381, miR-584-3p and miR-635. On the other hand, tumor suppressor roles of YY1 appear to involve YY1 stimulation of tumor suppressor BRCA1, increased Bax transcription and apoptosis involving cytochrome c release and caspase-3/-7 cleavage, induction of heme oxygenase-1, inhibition of pRb phosphorylation and p21 binding to cyclin D1 and cdk4, reduced expression of long noncoding RNA of SOX2 overlapping transcript, and MUC4/ErbB2/p38/MEF2C-dependent downregulation of MMP-10. YY1 expression is associated with that of cancer stem cell markers SOX2, BMI1 and OCT4 across many cancers suggesting multidynamic regulatory control and groups of cancers with distinct molecular signatures. Greater understanding of the mechanistic roles of YY1 will in turn lead to the development of more specific approaches to modulate YY1 expression and activity with therapeutic potential.

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“…YY1 (Yin‐Yang‐1) is a zinc‐finger transcription factor that belongs to the GLI‐Krüppel gene family and abnormally expressed in lots of cancer such as colon cancer , non‐small‐cell lung cancer , and myeloma , indicating that it has key roles in carcinogenesis. However, any information of YY1 in laryngeal carcinogenesis is not reported at present.…”

Section: Introductionmentioning

confidence: 99%

YY1 directly suppresses MYCT1 leading to laryngeal tumorigenesis and progress

Sun

et al. 2017

Cancer Medicine

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Human MYCT1 cDNA was first cloned using in silicon hybridization and molecular methods and previously AbstractYY1 is a key transcription factor and plays different roles in various cancers. However, role and mechanism of YY1 in laryngeal cancer are still unknown. YY1 and MYCT1 mRNA and protein levels were detected by Real-time RT-PCR and Western Blot methods, respectively. Binding of YY1 to MYCT1 promoter was predicted and confirmed by bioinformatics and chromatin immunoprecipitation assays, respectively. MYCT1 promoter activity was assessed by dual luciferase assay system. Laryngeal cancer cell proliferation, migration, and apoptosis were evaluated by cell viability, colony formation, cell scratch assay, transwell assay, and flow cytometry methods, respectively. YY1 and MYCT1 were upregulated and downregulated at transcriptional level in laryngeal cancer, respectively, which showed a negative correlation between YY1 and MYCT1 expression in laryngeal cancer. Significantly higher expression of YY1 and lower expression of MYCT1 were found in laryngeal cancer tissues of patients with lymphatic metastasis than those without metastasis.YY1 directly bound to MYCT1 promoter region and inhibited its promoter activity. YY1 silence had similar biological functions as MYCT1 overexpression in repressiveness of proliferation and migration, and promotion of apoptosis in laryngeal cancer cells. However, the effects of YY1 silence were recovered by MYCT1 knockdown. YY1 promotes proliferation and migration with suppression of apoptosis via directly inhibiting MYCT1 in laryngeal cancer cells, suggesting that YY1 is a useful target as a potential oncogene in laryngeal cancer development and progression. implying that MYCT1 function in cancer is tissue-specific. For example, MYCT1 is downregulated and promotes apoptosis in laryngeal and gastric cancer [1,2]. However, MYCT1 is upregulated and enhances cancer cell viability in acute myeloid leukemia [3]. Therefore, study on MYCT1 regulation network helps us to understand the tissuespecific manner of MYCT1 in cancer.At present, several transcription factors have been reported to be a direct regulator of MYCT1. In our and other studies, C-MYC directly targets MYCT1 promoter region and regulates its expression [1,[4][5][6]. We also found that MYCT1 promoter region including C-MYC binding site is hypermethylated in laryngeal cancer, suggesting that the methylation status interferes with the binding of C-MYC to MYCT1 leading to MYCT1 dysregulation in laryngeal cancer [7]. Liddiard et al. discovered that the fusion protein RUNX-ETO contributes to key aspects of the leukemic phenotypes via targeting MYCT1 [3]. In addition to C-MYC and RUNX-ETO, other transcription factors regulating MYCT1 expression are not reported.YY1 (Yin-Yang-1) is a zinc-finger transcription factor that belongs to the GLI-Krüppel gene family [8] and abnormally expressed in lots of cancer such as colon cancer [9], non-small-cell lung cancer [10], and myeloma [11], indicating that it has key roles in carcinogenesis. Ho...

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The microRNA-635 suppresses tumorigenesis in non-small cell lung cancer

Cited by 26 publications

References 34 publications

Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

Long noncoding RNA PART1 promotes progression of non‐small cell lung cancer cells via JAK‐STAT signaling pathway

The Yin and Yang of YY1 in tumor growth and suppression

YY1 directly suppresses MYCT1 leading to laryngeal tumorigenesis and progress

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