Objective: Long non-coding RNA (lncRNA) SNHG17 has been shown to modulate the biological behavior of multiple cancers (e.g., colorectal and lung cancers). However, its involvement in pancreatic cancer (PC) has not been explored; therefore, in the present study, we sought to examine this involvement.
Methods: First, the mRNA expression levels of various genes were quantified in PC tissues and cell lines using quantitative reverse-transcription PCR (qRT-PCR). The interaction between SNHG17 and miR-942 was explored by bioinformatics prediction as well as a dual luciferase reporter assay. The proliferation and viability of pancreatic carcinoma cells were examined using cell counting kit-8 and MTT assays, respectively. Cellular migratory and invasive properties were evaluated using transwell migration and wound healing assays. Cell death was measured using flow cytometry. Protein expression was quantified by western blotting.
Results: SNHG17 expression was markedly higher in human PC specimens and cell lines than in normal healthy tissues and pancreatic epithelial cells. MiR-942 expression displayed the opposite trend. Bioinformatics prediction and a dual luciferase reporter assay confirmed that SNHG17 serves as a sponge for miR-942. Loss-of-function assay revealed that SNHG17 silencing reduced the proliferation and viability of PC cells, impaired their migratory and invasive capacities, and led to their apoptosis. All these changes could be reversed by miR-942 inhibition. Further mechanical studies showed that SNHG17 silencing decreased the expression of several tumor modulators, including XXX, and this decrease was countered by miR-942 inhibition.
Conclusion: Our study provides experimental evidence for an interaction between SNHG17 and miR-942, which may unveil a new approach for PC pharmacotherapy.
Keywords: PC; SNHG17; invasion; miR-942; proliferation; tumor phenotypes.
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