MicroRNA‑216b reduces growth, migration and invasion of pancreatic ductal adenocarcinoma cells by directly targeting ρ‑associated coiled‑coil containing protein kinase 1

Liu, Yang-an; Zhang, Yue; Zheng, Zhi; Li, Kai; Wu, Xinhua; Xiao, Yuanhua; Wang, Lili; Zhu, Ling

doi:10.3892/ol.2018.8109

Cited by 13 publications

(12 citation statements)

References 41 publications

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“…Accumulating evidence reveals that miRNA dysfunction influences the metastasis, chemo-radioresistance and overall survival time of patients with cancer, including patients with PDAC (7)(8)(9)(10). Previous reports have revealed miRNA involvement in PDAC progression, including roles of miR-216b (11), miR-10a-5p (10), miR-374b-5p (12), miR-1271 (13), miR-7-5p (14), miR-4295 (15) and miR-185 (16). However, the molecular mechanisms underlying the involvement of miRNAs in PDAC progression remain unclear.…”

Section: Introductionmentioning

confidence: 99%

miR‑212 regulated by HIF‑1α promotes the progression of pancreatic cancer

2019

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MicroRNA-212 (miR-212) is dysregulated in numerous tissues and cancer types and serves a role in the progression of human cancer. However, the function and mechanism of miR-212 in the development of pancreatic ductal adenocarcinoma (PDAC) remain unknown, particularly in a hypoxic microenvironment. In the present study, miR-212 expression was observed to be significantly upregulated in PDAC tissues compared with normal tissues. Clinical data analysis indicated that miR-212 was positively associated with a large tumor size, Tumor-Node-Metastasis stage, lymph node metastasis and vessel invasion, and influenced the overall survival time. Notably, there was a positive association between the expression of hypoxia-inducible factor-1α (HIF-1α) and miR-212 in vivo and in vitro in hypoxic conditions. Mechanistically, HIF-1α bound directly to a hypoxia response element in the miR-212 promoter region and activated miR-212 expression in PDAC cells. Collectively, these results demonstrated that HIF-1α positively regulated miR-212 expression and resulted in PDAC progression.

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Section: Introductionmentioning

confidence: 99%

miR‑212 regulated by HIF‑1α promotes the progression of pancreatic cancer

2019

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“…miRNA-155-5p promotes autophagy in cervical cancer cells by targeting PDK1 and further inhibits the tumor progression in cervical cancers. Further, miRNA-216b increases growth, migration, and invasion, and serves as a tumor suppressor in pancreatic ductal adenocarcinoma (10). In addition, miRNA-1269 promotes cell survival and accelerates the proliferative ability of lung cancer cells by inhibiting its target gene TP53 (11).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-374b inhibits the tumor growth and promotes apoptosis in non-small cell lung cancer tissue through the p38/ERK signaling pathway by targeting JAM-2

Wang¹,

Yu²,

Wang³

2018

J. Thorac. Dis

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Background: MicroRNAs (miRNAs) are reportedly involved in various cancers. The present study aimed to investigate the role of miRNA-374b in cell viability, proliferation, apoptosis, and tumor formation in nonsmall cell lung cancer (NSCLC) in humans. Methods: The expression level of miRNA-374b in blood and tumor tissues from NSCLC patients was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to assess the viability of NSCLC cells after transfection with miRNA-374b. Colony formation assay was performed to assess the proliferation of cells pretreated with miRNA-374b. The terminal deoxynucleotidyl transferase-dUTP nick-end labeling (TUNEL) assay was performed to determine the role of miRNA-374b in apoptosis in NSCLC cells. A tumor formation assay was performed to assess the effects of miRNA-374b on tumorigenesis in NSCLC. Results: miRNA-374b was markedly downregulated in the blood and tumor tissues from NSCLC patients. Furthermore, overexpression of miRNA-374b markedly reduced the viability of NSCLC cells, but miRNA-374b inhibitor increased the viability of NSCLC cells compared with that in negative controls. Moreover, miRNA-374b decreased the number of colonies; however, its corresponding anti-miRNA oligonucleotide (AMO) markedly increased colony formation by NSCLC cells. Also, miRNA-374b promoted the apoptosis and inhibited tumor formation in NSCLC; however, this inhibition was reversed upon treatment with the AMO. Western blot analysis revealed that miRNA-374b regulates tumor progression through the p38/ERK signaling pathway by inhibiting JAM-2 in NSCLC. Conclusions: The present results indicate that miRNA-374b inhibits tumor growth and promotes apoptosis in NSCLC through the p38/ERK signaling pathway by targeting JAM-2.

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“…In keeping with these data, Liu et al [33] have recently reported that the level of miR-216b in PDAC cells (Panc-1, BxPC3 and SW 1990) is 3-to 4-fold lower than in non-cancer cells. The targets of miR-216b in PDAC cells include TPT1, a gene encoding for the translationally-controlled tumor protein [34], and ROCK1, the ρ-associated coiled-coil containing protein kinase 1 [33]. In addition, miR-216b targets the KRAS oncogene in nasopharyngeal tumor cells [35].…”

Section: Resultsmentioning

confidence: 56%

MicroRNA therapeutics: design of single-stranded miR-216b mimics to target KRAS in pancreatic cancer cells

et al. 2018

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Datasets reporting microRNA expression profiles in normal and cancer cells show that miR-216b is aberrantly downregulated in pancreatic ductal adenocarcinoma (PDAC). We found that KRAS, whose mutant G12D allele drives the pathogenesis of PDAC, is a target of miR-216b. To suppress oncogenic KRAS in PDAC cells, we designed single-stranded (ss) miR-216b mimics with unlocked nucleic acid (UNA) modifications to enhance their nuclease resistance. We prepared variants of ss-miR-216b mimics with and without a 5ʹ phosphate group. Both variants strongly suppressed oncogenic KRAS in PDAC cells and inhibited colony formation in pancreatic cancer cells. We observed that the designed ss-miR-216b mimics engaged AGO2 to promote the silencing of KRAS. We also tested a new delivery strategy based on the use of palmityl-oleyl-phosphatidylcholine (POPC) liposomes functionalized with ss-miR-216b conjugated with two palmityl chains and a lipid-modified cell penetrating peptide (TAT). These versatile nanoparticles suppressed oncogenic KRAS in PDAC cells.

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MicroRNA‑216b reduces growth, migration and invasion of pancreatic ductal adenocarcinoma cells by directly targeting ρ‑associated coiled‑coil containing protein kinase 1

Cited by 13 publications

References 41 publications

miR‑212 regulated by HIF‑1α promotes the progression of pancreatic cancer

miR‑212 regulated by HIF‑1α promotes the progression of pancreatic cancer

MicroRNA-374b inhibits the tumor growth and promotes apoptosis in non-small cell lung cancer tissue through the p38/ERK signaling pathway by targeting JAM-2

MicroRNA therapeutics: design of single-stranded miR-216b mimics to target KRAS in pancreatic cancer cells

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