Methyltransferase-like protein 11A promotes migration of cervical cancer cells via up-regulating ELK3

https://doi.org/10.1016/j.phrs.2021.105814Get rights and content
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Highlights

  • METTL11A is positively correlated with progression of cervical cancer.

  • METTL11A serves as a potential target for the diagnosis and prognosis of cervical cancer.

  • METTL11A significantly promotes cell proliferation and cell migration both in vivo and in vitro.

  • METTL11A promotes the migration of cervical cancer cells by up-regulating ELK3.

Abstract

Cervical cancer is one of the common malignancies in women, which is characterized with high invasion and metastatic tendency in its advanced stage. Increasing evidence indicates that methyltransferase-like (METTL) gene family is involved in the progression of various cancers. However, the functional role of methyltransferase-like gene family in cervical cancer remains unclear. In the present study, we found that METTL11A, a member of the methyltransferase-like gene family, was significantly over-expressed in cervical carcinoma by analyzing TCGA database. This finding was further validated in clinical tissue samples. Moreover, ectopic expression of METTL11A in cervical cancer cell lines promoted cell proliferation and migration both in vitro and in vivo. Differential gene expression analysis in the transcriptomic sequencing data indicated that ELK3 was down-regulated in METTL11A-silenced cervical cancer cells, which was further verified at both protein and mRNA levels. Functional experiments identified that METTL11A promoted migration of cervical cancer cells in an ELK3-dependent manner. This study will promote understanding the mechanism of cervical cancer progression and the functional role of methyltransferase-like gene families in cancers.

Abbreviations

METTL
methyltransferase-like
CC
cervical cancer
RCC1
regulator of chromatin condensation 1
RB
retinoblastoma
CCF
Cell colony formation experiment
EMT
epithelial-mesenchymal transition

Keywords

METTL11A
ELK3
Cervical cancer
Cell proliferation
Cell migration

Cited by (0)

1

Jinling Zhang and Huibin Song contributed equally to this work.