miR-204 suppresses the development and progression of human glioblastoma by targeting ATF2

Song, Shiwei; Fajol, Abul; Tu, Xian-kun; Ren, Baogang; Shu, Shi

doi:10.18632/oncotarget.11732

Cited by 40 publications

(33 citation statements)

References 25 publications

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“…Several researchers have reported that miR-204-5p is down-regulated and functions as a tumor suppressor in various types of human tumors. For example, miR-204-5p is down-regulated in glioblastoma, and suppresses the development and progression of glioblastoma by targeting ATF2 16. miR-204-5p suppresses NSCLC invasion and migration by targeting JAK2 17.…”

Section: Discussionmentioning

confidence: 99%

miR-204-5p acts as a tumor suppressor by targeting matrix metalloproteinases-9 and B-cell lymphoma-2 in malignant melanoma

Luan¹,

Yao²,

Ni³

et al. 2017

OTT

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An increasing number of microRNAs have been found to be involved in tumorigenesis, including melanoma tumorigenesis. miR-204-5p is down-regulated and functions as a tumor suppressor in many human malignant tumors. miR-204-5p expression is also decreased in melanoma tissues, but its biological roles and molecular mechanisms in malignant melanoma remain unclear. In this study, the aberrant down-regulation of miR-204-5p was detected in melanoma, especially in metastatic melanoma. miR-204-5p also served as a protective factor for the prognosis of melanoma patients. We determined that miR-204-5p suppresses cell proliferation, migration and invasion, and promotes cell apoptosis in melanoma. Matrix metalloproteinases-9 and B-cell lymphoma-2 are the functional targets of miR-204-5p, through which it plays an important biological role in malignant melanoma. The effect of miR-204-5p on malignant melanoma is verified using a xenograft model. We also determined that miR-204-5p increases 5-fluorouracil and cisplatin (DDP) chemosensitivity in malignant melanoma cells. This finding elucidates new functions and mechanisms for miR-204-5p in melanoma development, and provides potential therapeutic targets for the treatment of melanoma.

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Section: Discussionmentioning

confidence: 99%

miR-204-5p acts as a tumor suppressor by targeting matrix metalloproteinases-9 and B-cell lymphoma-2 in malignant melanoma

Luan¹,

Yao²,

Ni³

et al. 2017

OTT

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“…For example, the RNA-binding protein ELAV-like protein 1 (ELAVL1, HuR) can stabilize ATF2 transcripts via binding to the 3′-untranslated region (3′-UTR) (22). In contrast, a number of microRNAs, including miR-26a/b, miR-204, miR-451, and miR-622, have been shown to bind to the 3′-UTR of ATF2 transcripts to promote their degradation (23–27). The miRNA-mediated regulation of ATF2 is important for both biological stress- and tumor-related signaling.…”

Section: Transcriptional and Post-transcriptional Regulation Of Atf2mentioning

confidence: 99%

ATF2, a paradigm of the multifaceted regulation of transcription factors in biology and disease

Watson

Ronai

Lau

2017

Pharmacological Research

112

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Summary Stringent transcriptional regulation is crucial for normal cellular biology and organismal development. Perturbations in the proper regulation of transcription factors can result in numerous pathologies, including cancer. Thus, understanding how transcription factors are regulated and how they are dysregulated in disease states is key to the therapeutic targeting of these factors and/or the pathways that they regulate. Activating transcription factor 2 (ATF2) has been studied in a number of developmental and pathological conditions. Recent findings have shed light on the transcriptional, post-transcriptional, and post-translational regulatory mechanisms that influence ATF2 function, and thus, the transcriptional programs coordinated by ATF2. Given our current knowledge of its multiple levels of regulation and function, ATF2 represents a paradigm for the mechanistic complexity that can regulate transcription factor function. Thus, increasing our understanding of the regulation and function of ATF2 will provide insights into fundamental regulatory mechanisms that influence how cells integrate extracellular and intracellular signals into a genomic response through transcription factors. Characterization of ATF2 dysfunction in the context of pathological conditions, particularly in cancer biology and response to therapy, will be important in understanding how pathways controlled by ATF2 or other transcription factors might be therapeutically exploited. In this review, we provide an overview of the currently known upstream regulators and downstream targets of ATF2.

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“…Wu et al [22] found that ATF2 in renal cell carcinoma can regulate the expression of cell cycle protein B1, cell cycle protein D1, vimentin expression, thereby regulating cell proliferation and metastasis. In addition, previous studies [23] have confirmed that miR-204 can specifically inhibit the expression of ATF2 protein and regulate the proliferation, migration and invasion of human brain keratinocytoma tumour cells. In this study, after transfecting ATF2 siRNA into C33A cells, the expression level of autophagy-related protein LC3I/II was significantly decreased (p < .05), cell viability decreased (p < .05) and apoptosis rate increased (p < .05).…”

Section: Discussionmentioning

confidence: 67%

Molecular mechanism of miR-204 regulates proliferation, apoptosis and autophagy of cervical cancer cells by targeting ATF2

Guo

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Objective: To investigate the regulatory mechanism of miR-204 on proliferation, apoptosis and autophagy of cervical cancer cells. Methods: The expression of miR-204 in cervical cancer tissues and cell lines was detected by real-time PCR. Cell viability and apoptosis were detected by MTT and flow cytometry, respectively. Protein expression of Bcl-2, Bax, Caspase-3 and LC3I/II in C33A cells after transfection was detected by Western blot assay. The interaction between miR-204 and ATF2 was verified by Targetscan online prediction, dual-luciferase assay and Western blot. Results: The expression of miR-204 was significantly down-regulated in cervical cancer tissues and cell lines (p < .05). Cell viability was suppressed while apoptosis was enhanced in C33A cells transfected with miR-204. In addition, overexpression of miR-204 reduced protein expression of Bcl-2 and LC3I/II and elevated protein expression of Bax and Caspase-3 in C33A cells (p < .05). The results of Targetscan online prediction, dual-luciferase assay and Western blot indicted that miR-204 could regulate the expression of ATF2. Cell viability was increased (p < .05) and the expression of ATF2 and LC3I/II was down-regulated (p < .05) in C33A cells after silencing of ATF2. Ectopic expression of ATF2 could restore miR-204 mediated inhibition on proliferation of C33A cells. Conclusions: miR-204 could inhibit proliferation and autophagy and induce apoptosis of cervical cancer cells by targeting ATF2, representing promising target for cervical cancer treatment.

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miR-204 suppresses the development and progression of human glioblastoma by targeting ATF2

Cited by 40 publications

References 25 publications

miR-204-5p acts as a tumor suppressor by targeting matrix metalloproteinases-9 and B-cell lymphoma-2 in malignant melanoma

miR-204-5p acts as a tumor suppressor by targeting matrix metalloproteinases-9 and B-cell lymphoma-2 in malignant melanoma

ATF2, a paradigm of the multifaceted regulation of transcription factors in biology and disease

Molecular mechanism of miR-204 regulates proliferation, apoptosis and autophagy of cervical cancer cells by targeting ATF2

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