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OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1.

ABSTRACT: INTRODUCTION:Lymph node metastasis is the primary cause of death in oral squamous-cell carcinoma (OSCC) patients, so understanding the underlying molecular mechanism is critical for treating metastatic OSCC. OVOL1, a transcription factor, functions as a "break" to repress metastasis in breast cancer and prostate cancer. AIMS:To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis. RESULTS:The OVOL1 level was increased significantly in non-metastatic OSCC tissues and negatively correlated with ZEB1 level. OVOL1 repressed ZEB1 expression by directly binding to the promoter region of ZEB1. OVOL1 functioned as a tumor suppressor, and suppressed SCC-152 cells proliferation, migration, and invasion and promoted apoptosis. ZEB1 almost fully rescued the overexpressed OVOL1 function in SCC-152 cells. CONCLUSION:OVOL1 overexpression contributes to the progression of OSCC through inhibiting ZEB1, which may provide a marker for prognosis in OSCC.

SUBMITTER: Xu C

PROVIDER: S-EPMC6949574 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1.

Xu Chunfeng C Yan Tingyuan T Yang Jianrong J

International journal of clinical and experimental pathology 20190701 7

<h4>Introduction</h4>Lymph node metastasis is the primary cause of death in oral squamous-cell carcinoma (OSCC) patients, so understanding the underlying molecular mechanism is critical for treating metastatic OSCC. OVOL1, a transcription factor, functions as a "break" to repress metastasis in breast cancer and prostate cancer.<h4>Aims</h4>To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis.<h4>Results</h4>The OVOL1 level was increased significantly in non-meta ...[more]

PMID: 31934116

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Project description:Background and aim: Understanding the molecular biological mechanisms underlying laryngeal squamous cell carcinoma (LSCC) invasion and metastasis is crucial for diagnosis, treatment, and prognosis. We aimed to examine the expression of the tumor suppressor microRNA-204-5p (miR-204-5p) and its target gene, forkhead box C1 (FOXC1), in human LSCC and explore their roles in the malignant behaviors of LSCC Hep-2 and TU-177 cells. Methods: The regulatory effects of miR-204-5p on the 3' untranslated region of FOXC1 predicted by bioinformatics were tested by dual-luciferase reporter assay. Quantitative RT-PCR was used to detect mRNA expression in 43 fresh samples of LSCC and corresponding adjacent normal mucosa (ANM). FOXC1 protein expression was examined by immunohistochemistry. miR-204-5p mimics and FOXC1 siRNA were transfected into LSCC cell lines Hep-2 and TU-177 to observe malignant behavior. miR-204-5p mimics were injected into Hep-2 or TU-177 xenograft tumors in nude mice to examine tumor growth.Results: The miR-204-5p mRNA level was lower in all 43 LSCC samples than in the ANM samples, but the FOXC1 level was higher in the LSCC samples than in the ANM samples. The miR-204-5p level was lower for stage III and IV cancer and lymph node N+ status samples than for stage I and II cancer and N0 status samples. FOXC1 mRNA and protein levels were higher for N+ than for N0 LSCC. The miR-204-5p mRNA levels were lower in Hep-2 and TU-177 cells than in ANM tissues, but FOXC1 mRNA levels were higher in Hep-2 and TU-177 cells than in ANM tissues. Dual-luciferase reporter assays demonstrated the targeted regulatory effects of miR-204-5p on the FOXC1 3' UTR. Cell proliferation and colony formation was facilitated with miR-204-5p mimics and FOXC1 siRNA, with weaker cell migration and invasion than the controls. Moreover, miR-204-5p overexpression or FOXC1 knockdown inhibited the EMT process in LSCC cells. In vivo experiments demonstrated that injection of miR-204-5p into Hep-2 and TU-177 xenograft tumors in nude mice significantly inhibited tumor growth. Conclusions: miR-204-5p is involved in the invasion and metastasis of LSCC. It has a targeted regulatory effect on FOXC1 expression; malignant LSCC behaviors, including cell proliferation, invasion, and metastasis, are suppressed, and tumor growth in vivo is inhibited. This suggests that miR-204-5p may be a target for molecular therapy of LSCC in the future.

Dataset Information

OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1.

Publications

OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1.

Similar Datasets

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