Related Experiment Video For Long ncRNAs (lncRNAs)
Updated: Jan 21, 2026

Identification of Coding and Non-coding RNA Classes Expressed in Swine Whole Blood
Published on: November 28, 2018
Long non-coding RNA MACC1-AS1 promoted pancreatic carcinoma progression through activation of PAX8/NOTCH1 signaling
Chen Qi1, Chen Xiaofeng1, Li Dongen1
1Department of Hepatobiliary & Pancreatic Surgery, Ningbo First Hospital, No. 59 Liuting Street, Haishu District, Ningbo, 315000, Zhejiang Province, China.
Background:
Accumulated evidences have demonstrated that long non-coding RNAs (lncRNAs) are dysregulated and correlate with the pathophysiological basis of malignant tumors. The objective of this research is to uncover the possible molecular mechanism of MACC1-AS1 regarding the regulation of pancreatic carcinoma (PC) metastasis.
Methods:
lncRNA microarray and qRT-PCR were applied to identify differentially expressed lncRNA profile in PC. The function and role of MACC1-AS1 in PC were assessed via in vitro as well as in vivo assays. Luciferase analyses, RNA immunoprecipitation, and RNA pull-down were performed to determined the underlying MACC1-AS1 mechanisms.
Results:
Numbers of differentially expressed lncRNAs in PC were identified via lncRNA microarrays, among which MACC1-AS1 was revealed as the most abundant lncRNA. The upregulation of MACC1-AS1 in PC was further confirmed in two expanded PC cohorts, which showed that MACC1-AS1 expression was upregulated in those PC patients with poor survival. Functionally, knockdown of MACC1-AS1 inhibited the proliferation as well as metastasis of PC cells. Meanwhile, MACC1-AS1 upregulated the expression of PAX8 protein, which promoted aerobic glycolysis and activated NOTCH1 signaling. Additionally, PAX8 was upregulated in PC tissues, which was correlated with the expression of MACC1-AS1 and the overall survival of PC patients.
Conclusions:
Together, our findings indicate a critical role of MACC1-AS1/PAX8/NOTCH1 signaling, which may be an alternative treatment target in PC therapy.
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