A long non-coding RNA SCAMP1 induces pancreatic ductal adenocarcinoma progression through miR-106a-5p/AGK signaling.

Long non-coding RNAs (lncRNA) participate in regulation of gene expression and biology manipulation and altered lncRNA expression associated with cancer development and progression. The lncRNA SCAMP1 expression was aberrant and changed various cancer malignant behaviors. This study assessed SCAMP1 expression in pancreatic ductal adenocarcinoma (PDAC) for association with clinicopathological parameters and survival of patients and then explored the underlying molecular events. The data revealed that SCAMP1 expression was significantly upregulated in PDAC tissues, which was associated with a larger tumor size and tumor de-differentiation as well as poor survival of patients. Knockdown of SCAMP1 expression reduced tumor cell growth, invasion, epithelial‑mesenchymal transition (EMT), and improved sensitivity to 5-fluorouracil (5-FU) in vitro and inhibited tumor cell xenograft growth in nude mice. At gene levels, SCAMP1 was able to target miR-106a-5p to in turn upregulate acylglycerol kinase (AGK) expression and promote PDAC malignant behaviors in vitro. The data from the current study demonstrated an oncogenic SCAMP1 activity in PDAC. Further study will investigate SCAMP1 as a tumor biomarker and novel target in control of PDAC clinically.