miR-30 family promotes migratory and invasive abilities in CD133+ pancreatic cancer stem-like cells

Tsukasa, Koichiro; Ding, Qiang; Miyazaki, Yasuhiro; Matsubara, Shigeo; Natsugoe, Shoji; Takao, Sonshin

doi:10.1007/s13577-016-0137-7

Cited by 39 publications

(40 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, the inconsistency on the role of miR-30a/c-5p in tumor cell sensitivity to other chemo-therapeutics also exists in various cancers. For example, miR-30a-5p was inversely correlated with gemcitabine [40] and paclitaxel [41] sensitivity, while high expression of miR-30a/b/c-5p was resistant to gemcitabine in CD133+ pancreatic cancer stem-like cells [42]. Here, the downregulation of miR-30a/c-5p was found in cisplatin-resistant ovarian cancer cells, and miR-30a/c-5p overexpression re-sensitized cells to cisplatin.…”

Section: Discussionmentioning

confidence: 99%

A Feedback Loop Between miR-30a/c-5p and DNMT1 Mediates Cisplatin Resistance in Ovarian Cancer Cells

Han¹,

Zhen²,

Ye³

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Many microRNAs (miRs) are dysregulated in cancers, and aberrant miR expression patterns have been suggested to correlate with chemo-resistance of cancer cells. We aim to study the role of miR-30 family members in cisplatin-resistance of ovarian cancer cells. Methods: qRT-PCR was used to compare differential expression levels of miR-30 family members in ovarian cancer cell line A2780 and its cisplatin-resistant derivative CP70. Changes of cisplatin-sensitivity in miR-30a-5p- and miR-30c-5p-overexpressed-CP70 cells and miR-30a-5p- and miR-30c-5p-inhibited-A2780 cells were examined by CCK8 assay and apoptosis analysis using flow cytometry; targets of miR-30a/c-5p were analyzed by western blotting and luciferase reporter assay; methylation regulation of pre-miR-30a/c-5p was examined by methylation specific PCR. Results: miR-30a-5p and miR-30c-5p, in contrast to other miR-30 family members, dramatically decreased in cisplatin-resistant CP70 cells due to overexpressed-DNMT1 induced aberrant methylation. miR-30a/c-5p in turn directly inhibited DNMT1 as well as Snail. Forced expression of miR-30a/c-5p or knocking down of DNMT1 and Snail promoted cisplatin susceptibility and partially reversed epithelial-mesenchymal transition (EMT) in CP70 cells, while inhibition of miR-30a/c-5p or ectopic expression of DNMT1 and Snail induced cisplatin resistance and partial EMT in cisplatin-sensitive A2780 cells. Conclusions: A feedback loop between miR-30a/c-5p and DNMT1 is a potent signature for cisplatin-resistance and EMT in ovarian cancer, promising a potential target for improved anti-cancer treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

A Feedback Loop Between miR-30a/c-5p and DNMT1 Mediates Cisplatin Resistance in Ovarian Cancer Cells

Han¹,

Zhen²,

Ye³

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…The downstream regulatory pathway of miR-30 in pancreatic CSCs is still unknown. Further investigations should be carried out to understand the effects of miR-30 on pancreatic cancer [165].…”

Section: Mir-30mentioning

confidence: 99%

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Jiao

Qian

et al. 2019

Cells

View full text Add to dashboard Cite

Cancer ranks as the second leading cause of death worldwide, causing a large social and economic burden. However, most anti-cancer treatments face the problems of tumor recurrence and metastasis. Therefore, finding an effective cure for cancer needs to be solved urgently. Recently, the discovery of cancer stem cells (CSCs) provides a new orientation for cancer research and therapy. CSCs share main characteristics with stem cells and are able to generate an entire tumor. Besides, CSCs usually escape from current anti-cancer therapies, which is partly responsible for tumor recurrence and poor prognosis. microRNAs (miRNAs) belong to small noncoding RNA and regulate gene post-transcriptional expression. The dysregulation of miRNAs leads to plenty of diseases, including cancer. The aberrant miRNA expression in CSCs enhances stemness maintenance. In this review, we summarize the role of miRNAs on CSCs in the eight most common cancers, hoping to bridge the research of miRNAs and CSCs with clinical applications. We found that miRNAs can act as tumor promoter or suppressor. The dysregulation of miRNAs enhances cell stemness and contributes to tumor metastasis and therapeutic resistance via the formation of feedback loops and constitutive activation of carcinogenic signaling pathways. More importantly, some miRNAs may be potential targets for diagnosis, prognosis, and cancer treatments.

show abstract

“…Among all miRNAs, the miR-30 family consists of five members (miR-30a, miR-30b, miR-30c, miR-30d, and miR-30e) that are highly conserved between human and mouse2425, and has been widely investigated in a variety of human diseases24252627. Recent studies have shown that miR-30c targets PAI-1 in human cells2128.…”

mentioning

confidence: 99%

Hyperglycaemia-induced reciprocal changes in miR-30c and PAI-1 expression in platelets

Luo

Ren

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Type 2 diabetic mellitus (DM2) is associated with accelerated thrombotic complications and is characterized by high levels of plasminogen activator inhibitor-1 (PAI-1). Recent studies show that human platelets have high levels of miR-30c and synthesize considerable active PAI-1. The underlying mechanism of how PAI-1 expression is upregulated in DM2 is poorly understood. We now report that hyperglycaemia-induced repression of miR-30c increases PAI-1 expression and thrombus formation in DM2. Bioinformatic analysis and identification of miRNA targets were assessed using luciferase assays, quantitative real-time PCR and western blots in vitro and in vivo. The changes in miR-30c and PAI-1 levels were identified in platelets from healthy and diabetic individuals. We found that miR-30c directly targeted the 3′ UTR of PAI-1 and negatively regulated its expression. miR-30c was negatively correlated with glucose and HbA1c levels in DM2. In HFD-fed diabetic mice, increasing miR-30c expression by lenti-miR-30c significantly decreased the PAI-1 expression and prolonged the time to occlusion in an arterial thrombosis model. Platelet depletion/reinfusion experiments generating mice with selective ablation of PAI-1 demonstrate a major contribution by platelet-derived PAI-1 in the treatment of lenti-miR-30c to thrombus formation. These results provide important implications regarding the regulation of fibrinolysis by platelet miRNA under diabetic mellitus.

show abstract

miR-30 family promotes migratory and invasive abilities in CD133+ pancreatic cancer stem-like cells

Cited by 39 publications

References 38 publications

A Feedback Loop Between miR-30a/c-5p and DNMT1 Mediates Cisplatin Resistance in Ovarian Cancer Cells

A Feedback Loop Between miR-30a/c-5p and DNMT1 Mediates Cisplatin Resistance in Ovarian Cancer Cells

microRNA: The Impact on Cancer Stemness and Therapeutic Resistance

Hyperglycaemia-induced reciprocal changes in miR-30c and PAI-1 expression in platelets

Contact Info

Product

Resources

About