PT  - JOURNAL ARTICLE
AU  - PRAMOD NEPAL
AU  - YUTO HOZAKA
AU  - TAKAKO TANAKA
AU  - MASUMI WADA
AU  - SHUNICHI ASAI
AU  - CHIKASHI MINEMURA
AU  - TETSUYA IDICHI
AU  - TAKAAKI ARIGAMI
AU  - HIROSHI KURAHARA
AU  - NAOHIKO SEKI
AU  - TAKAO OHTSUKA
TI  - Impact of Oncogenic Targets Controlled by Tumor-Suppressive <em>miR-30a-5p</em> in Pancreatic Ductal Adenocarcinoma
AID  - 10.21873/anticanres.15297
DP  - 2021 Oct 01
TA  - Anticancer Research
PG  - 4821--4836
VI  - 41
IP  - 10
4099  - http://ar.iiarjournals.org/content/41/10/4821.short
4100  - http://ar.iiarjournals.org/content/41/10/4821.full
SO  - Anticancer Res2021 Oct 01; 41
AB  - Background/Aim: Our recent miRNA analyses revealed that miR-30a-5p has tumor-suppressive activity in pancreatic ductal adenocarcinoma (PDAC). Herein, we sought to identify tumor-suppressive genes controlled by miR-30a-5p, emphasizing on genes that are closely involved in the molecular pathogenesis of PDAC. We uncovered several novel findings regarding the pathogenesis of this disease. Materials and Methods: In silico analyses were used to identify the putative target genes of miR-30a-5p and assess their expression levels. Direct regulation of RRM2 by miR-30a-5p and its oncogenic functions were evaluated in PDAC cell lines. Overexpression of RRM2 was demonstrated in clinical samples. Results: A total of 24 putative targets were identified by in silico database analysis. High expression of 4 genes (CBFB, RRM2, AHNAK, and DCBLD1) was significantly associated with shorter survival of patients with PDAC. Functional assays demonstrated that knockdown of RRM2 attenuated the malignant phenotype of PDAC cells. Conclusion: The miR-30a-5p/RRM2 axis facilitated the malignant transformation of PDAC cells.