Dataset Information

MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.

ABSTRACT: Mortality factor 4-like 1 (MORF4L1) is a member of a subgroup of histone acetyltransferases and belongs to the mortality factor on chromosome 4 (MORF4) class of proteins. However, the role of MORF4L1 in cancers is largely unknown. Using reverse transcription-quantitative polymerase chain reaction and published datasets, the present study demonstrated that the expression of MORF4L1 is decreased in several cancers, including nasopharyngeal carcinoma (NPC). Additionally, the methylation rate of the promoter of MORF4L1 was identified to be significantly higher in tumour cells than in normal cells. The ectopic expression of MORF4L1 was also revealed to inhibit cell proliferation, colony formation, migration and invasion in NPC, whereas the knockdown of MORF4L1 promoted cell proliferation, colony formation, migration and invasion. Mechanistically, the present study demonstrated that MORF4L1 functions as a tumour suppressor by increasing p21 and E-cadherin levels. These findings may be useful novel targets for treating patients with NPC.

SUBMITTER: Sang Y

PROVIDER: S-EPMC6313188 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Publications

MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.

Sang Yi Y Zhang Ruhua R Sun Longhua L Chen Kaddie Kwok KK Li Si-Wei SW Xiong Longxin L Peng Yongjian Y Zeng Lei L Huang Guofu G

Oncology letters 20181016 1

Mortality factor 4-like 1 (MORF4L1) is a member of a subgroup of histone acetyltransferases and belongs to the mortality factor on chromosome 4 (MORF4) class of proteins. However, the role of MORF4L1 in cancers is largely unknown. Using reverse transcription-quantitative polymerase chain reaction and published datasets, the present study demonstrated that the expression of MORF4L1 is decreased in several cancers, including nasopharyngeal carcinoma (NPC). Additionally, the methylation rate of the ...[more]

PMID: 30655767

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Project description:The authors' previous study revealed that the serum levels of microRNA (miR)-663b are significantly increased in patients with nasopharyngeal carcinoma (NPC), and are associated with NPC progression and poor prognosis. However, the molecular mechanism of underlying NPC growth and metastasis remains unclear. In the present study, quantitative polymerase chain reaction and western blot analyses were performed to examine changes to mRNA and protein expression, respectively. MTT, wound healing and Transwell assays were used to examine cell proliferation, migration and invasion, respectively. Luciferase reporter gene assays were performed to identify target genes of miR-663b. It was demonstrated that miR-663b was significantly upregulated in NPC tissue compared with non-tumor nasopharyngeal epithelial tissue samples. Furthermore, miR-663b expression gradually increased with advancing stages of NPC, with the highest expression being observed in the latest stage IV. The increased expression of miR-663b was associated with advanced clinical stage and lymph node metastasis. In addition, miR-663b expression was increased in NPC cell lines compared with normal nasopharyngeal epithelial NP69 cells. Knockdown of miR-663b resulted in a significant reduction in the proliferation, migration and invasion of NPC CNE1 cells. Tumor suppressor candidate 2 (TUSC2) was identified as a novel target gene of miR-663b. It was further demonstrated that TUSC2 was significantly downregulated in NPC tissue samples and cell lines. miR-663b negatively regulated the expression of TUSC2 at the post-transcriptional level in CNE1 cells. Additionally, inhibition of TUSC2 expression attenuated the suppressive effects of miR-663b downregulation on the proliferation, migration and invasion of CNE1 cells. To the best of our knowledge, this is the first study to demonstrate that miR-663b, which is upregulated in NPC, promotes the proliferation, migration and invasion of NPC cells, partially through the inhibition of TUSC2 expression. Therefore, it is suggested that miR-663b is a promising therapeutic target for the treatment of patients with NPC.

Dataset Information

MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.

Publications

MORF4L1 suppresses cell proliferation, migration and invasion by increasing p21 and E-cadherin expression in nasopharyngeal carcinoma.

Similar Datasets

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