A frequent somatic mutation in the 3'UTR of GAPDH facilitates the development of ovarian cancer by creating a miR‑125b binding site
- Peisen Liu
- Yumin Zhong
- Ting Cao
- Xiujie Sheng
- Huang Huang
Affiliations: Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510150, P.R. China
- Published online on: June 25, 2020 https://doi.org/10.3892/or.2020.7663
Copyright: © Liu
et al. This is an open access article distributed under the
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Ovarian cancer (OVCA) is one of the most common types of cancer in women worldwide. Recent studies have focused on the presence and effect of somatic mutations in patients with OVCA; however, studies on the roles of mutations located in the untranslated regions (UTR) of genes in OVCA remain limited. In the present study, a frequent somatic mutation in the glyceraldehyde 3‑phosphate dehydrogenase (GADPH) 3'UTR was identified using transcriptome sequencing of 120 pairs of OVCA tissue samples. The mutant GAPDH 3'UTR promoted tumor growth and cell motility. Furthermore, the mutation in the GAPDH 3'UTR significantly downregulated the levels of mature miR‑125b by creating a new miR‑125b binding site. Finally, STAT3 levels were increased in SKOV3 cells stably expressing the mutant GADPH 3'UTR, which is a critical target gene of miR‑125b. In conclusion, the present study demonstrated that the mutation located in GAPDH 3'UTR promoted OVCA growth and development by sponging miR‑125b and thereby affecting STAT3 expression levels.