miR-331-3p functions as an oncogene by targeting ST7L in pancreatic cancer

Carcinogenesis
Xiaoli ChenXiaodong Huang

Abstract

Pancreatic cancer (PC) is a highly invasive tumor with early metastasis and poor prognosis, yet the mechanisms for tumor progression have not been fully elucidated. Emerging evidence indicates that microRNA-331-3p (miR-331-3p) plays an important role in the progression of diverse human cancers. Here, we found that miR-331-3p was significantly upregulated in tumor specimens of PC patients and PC cell lines. Functional studies showed that downregulation of miR-331-3p inhibited PC cell proliferation and epithelial-mesenchymal transition (EMT)-mediated metastasis in vitro. Furthermore, suppression of tumorigenicity 7 like (ST7L) was identified as a novel target gene of miR-331-3p. Tumor promotion effects of miR-331-3p were partially reversed by ST7L re-expression. In addition, miR-331-3p antagomir suppressed PC tumor growth and metastasis via upregulation of ST7L in xenograft mice. In summary, these results demonstrate that miR-331-3p is a tumor-promoting microRNA (miRNA) in PC cells and a promising biomarker for PC.

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Citations

Jul 23, 2019·Analytical Sciences : the International Journal of the Japan Society for Analytical Chemistry·Young-Jin KimMizuo Maeda
Mar 17, 2020·Technology in Cancer Research & Treatment·Mingchuan ZhaoXichun Hu
Sep 15, 2020·Technology in Cancer Research & Treatment·Ting ZhanXiaodong Huang
Dec 5, 2019·International Journal of Molecular Sciences·Ewelina HermytAndrzej Witek
Sep 29, 2019·World Journal of Gastrointestinal Oncology·Lei-Ying YangMing-Shun Zhou
Jan 9, 2021·Journal of Veterinary Internal Medicine·Lucia UngerEman Hamza
Jul 22, 2018·Biochemical and Biophysical Research Communications·Tongmiao LiuYanling Gai
Aug 21, 2020·Oncology Research and Treatment·Fuguo JiangHonggang Wang
Nov 20, 2021·Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology·Qing-Hai ZhuJinHai Ye

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