miR-124 inhibits cell proliferation, migration and invasion by directly targeting SOX9 in lung adenocarcinoma

Wang, Xiaoying; Li, Yanli; Liu, Xiaoli; Yang, Jingyan; Teng, Guangju; Zhang, Lulu; Zhou, Chengjun

doi:10.3892/or.2016.4648

Cited by 43 publications

(27 citation statements)

References 27 publications

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“…miR-124, located in 8q12.3, is frequently found to be downregulated in multiple human malignancies, such as prostate cancer (12), glioma (13), lung adenocarcinoma (14), breast (15), gastric (16), colorectal (17) and bladder cancer (25), hepatocellular carcinoma (20) and ovarian cancer (26). miR-124 exerted a tumor suppressive role in various cancer cells by negative regulation of cell proliferation, apoptosis, migration and invasion through repressing multiple target genes, such as PACE4 (12), SOx9 (14), CD4 (25), STAT3 (20), SphK1 (26) and PIK3CA (27). However, at present, there is no published study regarding the biological functions of miR-124 in RB.…”

Section: Discussionmentioning

confidence: 99%

“…There is a growing interest particularly toward micro-RNA-124 (miR-124) in context of various types of cancers. miR-124 has been reported to be downregulated and function as a tumor suppressor in a variety of human cancers, such as prostate cancer (12), glioma (13), lung adenocarcinoma (14), breast (15), gastric (16) and colorectal cancer (17). However, the expression of miR-124 in patients with RB, and its biological functions in human RB cells, as well as the molecular mechanisms by which miR-124 exerts its functions, remains largely unclear.…”

Section: Introductionmentioning

confidence: 99%

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miR-124 inhibits proliferation and invasion of human retinoblastoma cells by targeting STAT3

Liu

Wang

et al. 2016

Oncology Reports

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A growing body of evidence suggests that microRNA-124 (miR-124) functions as tumor-suppressor, and involves in tumor initiation, development and metastasis in major classes of human cancers; however, the biological role and underlying molecular mechanism of miR-124 in retinoblastoma (RB) remain unknown. Therefore, we investigated the biological activity and underlying molecular mechanism of miR-124 in human retinoblastoma. In the present study, our results demonstrated the downregulation of miR-124 in RB tissues and RB cell lines compared with normal retinal tissues. The ectopic expression of miR-124 in the RB cell lines (Y79 and SO-RB50) suppresses cell proliferation, migration and invasion, induced cell apoptosis in vitro. Furthermore, signal transducer and activator of transcription 3 (STAT3) was identified as a new target of miR-124, and overexpression of miR-124 decreased STAT3 expression on mRNA level and protein level in human RB cells. We also found that STAT3 mRNA expression was upregulated and inversely correlated with miR-124 expression in the RB tissues (r=-0.683; P<0.001). Restoration of the expression of STAT3 rescues the effects induced by miR-124 in RB cells. The findings of the present study suggested that miR-124 functioned as tumor suppressor in RB, at least in part, by targeting STAT3, and that it could serve as a potential candidate for RB therapeutics.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR-124 inhibits proliferation and invasion of human retinoblastoma cells by targeting STAT3

Liu

Wang

et al. 2016

Oncology Reports

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“…For example, Liu et al (2016) suggested SOX9 promoted cell proliferation and invasion in hepatocellular carcinoma. Wang et al (2016) illustrated SOX9 was associated with cell proliferation, migration and invasion and SOX9 was an important functional mediator of miR-124 in lung adenocarcinoma cells. Zhang et al (2012) found miR-101 suppressed SOX9-dependent tumorigenesis in human hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Transcription Factor SOX9 Promotes Osteosarcoma Cell Growth by Repressing Claudin-8 Expression [Retraction]

Yang

Hao

et al. 2017

Tohoku J. Exp. Med.

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Osteosarcoma is a malignant bone cancer that mainly affects children. SOX9 plays a key role in bone formation and osteosarcoma, and Claudin-8 (CLDN8), a tight junction protein, contributes to proliferation of osteosarcoma cells. The aim of this study was to investigate the relationship between SOX9 and CLDN8 in osteosarcoma. The expression levels of SOX9 and CLDN8 were determined in osteosarcoma specimens (n = 25) by qRT-PCR and Western blot analyses. The levels of SOX9 mRNA and protein were significantly higher in osteosarcoma tissues than those in adjacent non-tumor tissues, whereas the expression levels of CLDN8 mRNA and protein were significantly lower in osteosarcoma tissues. Immunohistochemical analysis showed the high expression of SOX9 in 56 out of 97 osteosarcoma tissues (57.7%). By contrast, the low expression of immunoreactive CLDN8 was observed in 62 of 97 osteosarcoma tissues (63.9%). There was the inverse correlation between the expression levels of SOX9 and CLDN8 proteins (R = −0.633, P < 0.001). The overall survival was poorer in the patients with high SOX9 expression. Subsequently, using two human osteosarcoma cell lines, we showed that knockdown of SOX9 inhibited cell proliferation and migration but promoted cell apoptosis. Importantly, knockdown of SOX9 increased the expression levels of CLDN8 protein. The transient luciferase-reporter assays suggest that SOX9 may inhibit the promoter activity of the CLDN8 gene in osteosarcoma cells. In conclusion, we provide the evidence demonstrating that SOX9 may promote cell growth by repressing the expression of CLDN8. Thus, SOX9 may be a therapeutic target for osteosarcoma.

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“…According to previous studies, miR-124 plays a suppressive role in cancer (15,16). To further investigate the mechanism by which MALAT1 regulates tongue cancer cell growth, we ascertained the association of miR-124 and MALAT1.…”

Section: Mir-124 Is Negatively Correlated With Lncrna-malat1mentioning

confidence: 99%

Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1

et al. 2017

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA), was the earliest discovered to be correlated with cancer and contributes to the initiation and development of several types of tumors. Dysregulation of MALAT1 expression is frequently observed in many types of cancer such as gastric cancer, esophageal squamous cell carcinoma and glioma. To date, the role of MALAT1 and the underlying mechanisms in tongue cancer development remain unclear. In the present study, we studied the influence of MALAT1 on tongue cancer cell lines and clinical tongue cancer samples so as to detect its function and the underlying mechanism. In the present study, lncRNA-MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo. In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. Our data revealed that MALAT1 inhibited tongue cancer cell growth and metastasis through miR-124-dependent JAG1 regulation. In conclusion, we revealed that MALAT1 may play an oncogenic role by increasing proliferation and metastasis of tongue cancer and is a potential therapeutic target in human tongue cancer.

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miR-124 inhibits cell proliferation, migration and invasion by directly targeting SOX9 in lung adenocarcinoma

Cited by 43 publications

References 27 publications

miR-124 inhibits proliferation and invasion of human retinoblastoma cells by targeting STAT3

miR-124 inhibits proliferation and invasion of human retinoblastoma cells by targeting STAT3

Transcription Factor SOX9 Promotes Osteosarcoma Cell Growth by Repressing Claudin-8 Expression [Retraction]

Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1

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