MicroRNA-30e Functions as a Tumor Suppressor in Cervical Carcinoma Cells through Targeting GALNT7

Abstract

Cervical cancer is the third most common cancer in women worldwide. However, the underlying mechanism of occurrence and development of cervical cancer is obscure. In this study, we observed that miR-30e was downregulated in clinical cervical cancer tissues and cervical cancer cells. Next, overexpression of miR-30e reduced the cervical cancer cell growth through MTT, colony formation, EdU, and Transwell assay in SiHa and Caski cells. Subsequently, UDP-N-acetyl-D-galactosamine: polypeptide N-acetylgalactosaminyltransferase 7 (GALNT7) was identified as a potential miR-30e target by bioinformatics analysis. Moreover, we showed that miR-30e was able to bind to the 3′UTR of GALNT7 by luciferase reporter assay. In addition, the mRNA and protein levels of GALNT7 in cervical cancer cells were downregulated by miR-30e. And we validated that downregulation of GALNT7 repressed the proliferation of SiHa and Caski cells by MTT, colony formation, and Transwell assay. We identified that the restoration of GALNT7 expression was able to counteract the effect of miR-30e on cell proliferation of cervical cancer cells. Furthermore, we found that the expression levels of GALNT7 were frequently upregulated and negatively correlative to those of miR-30e in cervical cancer tissues. In addition, we validated that restoration of GALNT7 rescued the miR-30e–suppressed growth of cervical cancer xenografts in vivo. In conclusion, the current results suggest that miR-30e may function as tumor suppressors in cervical cancer through downregulation of GALNT7. Both miR-30e and its novel target, GALNT7, may play an important role in the process of cervical cancer.

Alterations in the glycome after HDAC inhibition impact oncogenic potential in epigenetically plastic SW13 cells

“…Enzymes affecting metabolism of glycolipids and glycoproteins whose expression levels change in response to HDAC inhibition are grouped according to their affected pathway and whether the protein product is associated with cancer (are in bold) or is the initial step in the biosynthetic pathway (are in italic). References documenting the gene product link to cancer indicated in parenthesesBiosynthetic & other metabolic processesLog2 Fold-changeSymbolGene NameMultiple Pathways −1.26 FUT10 α-(1,3)-fucosyltransferase 10 [46, 47] −1.26 FUT11 α-(1,3)-fucosyltransferase 11 [46, 48, 49] −1.56 B4GALT2 UDP-Gal:β-GlcNAc β-(1,4)-galactosyltransferase 2 [50] 1.07B3GAT2β-(1,3)-glucuronyltransferase 2GlycoproteinEGF Domain −1.04 POGLUT1 Protein O-glucosyltransferase 1 [50–53] 1.30 LFNG O-fucosylpeptide 3-β-GlcNAc transferase [50, 54]N & O-Linked Pathways 1.56 B3GNT2 N-acetyllactosaminide β-(1,3)-GlcNAc transferase 2 [50, 55]Complex N-Linked Pathway −1.10 ALG13 UDP-GlcNAc transferase subunit [50] −1.09 ALG10 α-1,2-glucosyltransferase [56] 5.16 MAN1A1 α-Mannosidase, class 1A, member 1 [8, 52] 1.63 MGAT4A α-(1,3)-mannosyl-glycoprotein 4-β-N-acetylglucosaminyltransferase A [50, 56]Complex O-linked Pathway −1.28 GALNT14 Polypeptide GalNAc transferase 14 [8, 57, 58] 1.00 GALNT6 Polypeptide GalNAc transferase 6 [8, 50] −1.08 GALNT7 GalNAc transferase 7 [8, 50, 59, 60] 1.79 GCNT1 β-(1,3)-galactosyl-O-glycosyl-glycoprotein β-1,6-GlcNAc transferase […”

Long non-coding RNA-SNHG7 acts as a target of miR-34a to increase GALNT7 level and regulate PI3K/Akt/mTOR pathway in colorectal cancer progression

“…MiR-30e regulated GALNT7 transcripts in cervical cancer [ 42 ]. MiR-34a was downregulated in colon cancer specimens compared to normal colonic mucosa [ 43 ]. MiR-30a-5p regulated GALNT7 transcripts in renal cell carcinoma [ 44 ].…”

The potential prognostic and therapeutic application of tissue and circulating microRNAs in cervical cancer

“…Li et al have reported that miR-378 is a novel therapeutic strategy in CC (Li, Yang, Wang, Cao, & Yang, 2017). MiR-30e can suppress the proliferation and invasion of CC cells through targeting mRNA and it can be a new therapeutic target for CC in the future (Wu et al, 2017). Wang et al have shown that overexpression of miR-34a-5p prevented proliferation of CC cells and promoted apoptosis of these cells by downregulating Bcl-2 expression (Wang, Xie, & Wang, 2017).…”