Abstract
BackgroundColorectal cancer (CRC) arises in a multistep molecular network process, which is from either discrete genetic perturbation or epigenetic dysregulation. The long non-coding RNAs (lncRNAs), emerging as key molecules in human malignancy, has become one of the hot topics in RNA biology. Aberrant O-glycosylation is a well-described hallmark of many cancers. GALNT7 acts as a glycosyltransferase in protein O-glycosylation, involving in the occurrence and development of CRC.MethodsThe microarrays were used to survey the lncRNA and mRNA expression profiles of primary CRC cell line SW480 and metastatic CRC cell line SW620. Cell proliferation, migration, invasion, and apoptosis were assayed. Xenograft mouse models were used to determine the role of lncRNA-SNHG7 in CRC in vivo. In addition, CNC analysis and competing endogenous analysis were used to detect differential SNHG7 and relational miRNAs expression in CRC cell lines.ResultsSNHG7 expression showed a high fold (SW620/SW480) in CRC microarrays. The CRC patients with high expression of SNHG7 had a significantly poor prognosis. Furthermore, SNHG7 promoted CRC cell proliferation, metastasis, mediated cell cycle, and inhibited apoptosis. SNHG7 and GALNT7 were observed for co-expression by CNC analysis, and a negative correlation of SNHG7 and miR-34a were found by competing endogenous RNA (ceRNA) analysis. Further results indicated that SNHG7 facilitated the proliferation and metastasis as a competing endogenous RNA to regulate GALNT7 expression by sponging miR-34a in CRC cell lines. SNHG7 also played the oncogenic role in regulating PI3K/Akt/mTOR pathway by competing endogenous miR-34a and GALNT7.ConclusionThe CRC-related SNHG7 and miR-34a might be implicated in CRC progression via GALNT7, suggesting the potential usage of SNHG7/miR-34a/GALNT7 axis in CRC treatment.
Highlights
Colorectal cancer (CRC) arises in a multistep molecular network process, which is from either discrete genetic perturbation or epigenetic dysregulation
The results showed that high levels of p-PI3K, p-Akt, and p-mTOR were observed in SW480 cells transfected with Small nucleolar RNA host gene 7 (SNHG7) or GALNT7 than control groups, respectively
We explored the possible mechanism of long non-coding RNAs (lncRNAs)-SNHG7, as competing endogenous RNA, modulating GALNT7 by sponging miR-34a in human CRC cell lines
Summary
Colorectal cancer (CRC) arises in a multistep molecular network process, which is from either discrete genetic perturbation or epigenetic dysregulation. The long non-coding RNAs (lncRNAs), emerging as key molecules in human malignancy, has become one of the hot topics in RNA biology. GALNT7 acts as a glycosyltransferase in protein O-glycosylation, involving in the occurrence and development of CRC. Colorectal cancer (CRC), a high-risk digestive tract tumor, is one of the most frequent malignant tumors worldwide [1]. The pathogenesis of CRC involves multiple factors, including environmental and genetic variables, while detailed molecular mechanisms remain unclear [2]. Long non-coding RNAs (lncRNAs) are over 200 nucleotides in length without protein-coding capacity. Mounting evidence demonstrates that lncRNAs may be emerged as essential regulators in many biological processes [3]. Recent literature has documented that lncRNAs enrich in the cytoplasm typically participate in post-transcriptional regulation by interacting with miRNAs or mRNAs [5], and play an active role in regulating miRNA availability within the cell and form regulatory networks [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
