LAUSR.org creates dashboard-style pages of related content for over 1.5 million academic articles. Sign Up to like articles & get recommendations!

Methyltransferase‐like 3 promotes cervical cancer metastasis by enhancing cathepsin L mRNA stability in an N6‐methyladenosine‐dependent manner

Photo from wikipedia

N6‐methyladenosine (m6A) is a highly abundant RNA modification in eukaryotic cells. Methyltransferase‐like 3 (METTL3), a major protein in the m6A methyltransferase complex, plays important roles in many malignancies, but its… Click to show full abstract

N6‐methyladenosine (m6A) is a highly abundant RNA modification in eukaryotic cells. Methyltransferase‐like 3 (METTL3), a major protein in the m6A methyltransferase complex, plays important roles in many malignancies, but its role in cervical cancer metastasis remains uncertain. Here, we found that METTL3 was significantly upregulated in cervical cancer tissue, and its upregulation was associated with a poor prognosis in cervical cancer patients. Knockdown of METTL3 significantly reduced cervical cancer cell migration and invasion. Conversely, METTL3 overexpression markedly promoted cervical cancer cell metastasis in vitro and in vivo. Furthermore, METTL3 mediated the m6A modification of cathepsin L (CTSL) mRNA at the 5′‐UTR, and the m6A reader protein insulin‐like growth factor 2 mRNA‐binding protein 2 (IGF2BP2) bound to the m6A sites and enhanced CTSL mRNA stability. Our results indicated that METTL3 enhanced CTSL mRNA stability through an m6A‐IGF2BP2‐dependent mechanism, thereby promoting cervical cancer cell metastasis. These findings provide insights into a novel m6A modification pattern involved in cervical cancer development.

Keywords: cervical cancer; metastasis; mrna stability; m6a; cancer

Journal Title: Cancer Science
Year Published: 2022

Link to full text (if available)


Share on Social Media:                               Sign Up to like & get
recommendations!

Related content

More Information              News              Social Media              Video              Recommended



                Click one of the above tabs to view related content.