The aim of this study was to examine the potential role of miRNA (miR)‑200b and miR‑301 in predicting the chemo‑responses to treatment for pancreatic carcinoma.
Overexpression of miR-301a enhances pancreatic cancer cell invasion, angiogenesis and migration, while inhibition of miR-301a suppresses pancreatic cancer cell invasion and reduces orthotopic pancreatic tumor growth and metastasis.
Targeting exosomal miR-301a-3p may provide a potential diagnosis and treatment strategy for pancreatic cancer.<b>Significance:</b> These findings identify an exosomal miRNA critical for microenvironmental cross-talk that may prove to be a potential target for diagnosis and treatment of pancreatic cancer.<b>Graphical Abstract:</b> http://cancerres.aacrjournals.org/content/canres/78/16/4586/F1.large.jpg <i></i>.
Dysregulation of microRNAs (miRNAs) is involved in a variety of biological process including tumorigenesis. miR-301a-3p has been reported to be an onco-miRNA in various types of cancer, like breast cancer, malignant melanoma, and pancreatic cancer.
Taken together, these findings indicate that miR-301a exerts as a critical regulator involved in hypoxia-induced gemcitabine resistance in PC and may have potentials to be a therapeutic target for PC patients.
Based on this evidence, we investigated the contribution of miR-301 to pancreatic carcinoma and the novel target genes of miR-301 in pancreatic carcinoma.
Moreover, miR-301a inhibition or Nkrf up-regulation in pancreatic cancer cells led to reduced NF-κB target gene expression and attenuated xenograft tumour growth, indicating that miR-301a overexpression contributes to NF-κB activation.
One hundred microRNA precursors were aberrantly expressed in pancreatic cancer or desmoplasia (p < 0.01), including microRNAs previously reported as differentially expressed in other human cancers (miR-155, miR-21, miR-221 and miR-222) as well as those not previously reported in cancer (miR-376a and miR-301).