MiR-361-3p regulates ERK1/2-induced EMT via DUSP2 mRNA degradation in pancreatic ductal adenocarcinoma

Hu, Jisheng; Li, Le; Chen, Hongze; Zhang, Guangquan; Liu, Huan; Kong, Rui; Chen, Hua; Wang, Yongwei; Li, Yilong; Fengyu, Tian; Lv, Xinjian; Li, Guanqun; Sun, Bei

doi:10.1038/s41419-018-0839-8

Cited by 74 publications

(67 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…miRNAs act as oncogenes or tumor suppressors in tumors dependent on special conditions. miR-361-3p has been reported upregulated in various human tumors, including breast cancer, oral squamous cancer and pancreatic cancer (16,17,27). However, miR-361-3p functions in liver T-ICs have never been investigated before.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

Zhang

Fan

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Increasing evidence shows that liver tumor-initiating cells (T-ICs) closely associated with the progression, metastasis, recurrence and chemo-resistance of hepatocellular carcinoma (HCC). However, the underlying mechanism for the propagation of liver T-ICs remains unclear. The purpose of our study was to explore the role of miR-361-3p in the expansion of liver T-ICs and the potential molecular mechanism.Results: Flow cytometry analysis was performed to isolate CD24+, CD133+ or EpCAM+ cells from primary HCC cells or HCC cell lines. Real-time PCR was used to detect the expression of miR-361-3p in liver T-ICs. The impact of miR-361-3p on liver T-ICS expansion was investigated both in vivo and in vitro. The correlation between miR-361-3p expression and TACE (transcatheter arterial chemoembolization) or sorafenib benefits in HCC was evaluated in patient cohorts. miR-361-3p expression is upregulated in liver T-ICs. Knockdown of miR-361-3p impairs the self-renewal and tumorigenicity liver T-ICs. Conversely, forced miR-361-3p expression enhances the self-renewal and tumorigenicity liver T-ICs. Mechanistically, miR-361-3p directly targets SOX1 via binding its 3’-UTR in liver T-ICs. Moreover, miR-361-3p knockdown hepatoma cells are more sensitive to cisplatin or sorafenib treatment. Clinical cohort analysis demonstrates that miR-361-3p low HCC patients are benefited from TACE or sorafenib treatment. Conclusions: Our findings revealed the crucial role of the miR-361-3p in liver T-IC expansion and TACE or sorafenib response, rendering miR-361-3p an optimal target for the prevention and intervention in HCC.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Previous studies found that miR-361-3p promotes human breast cancer cell viability by inhibiting the E2F1/P73 signaling pathway (16). Moreover, miR-361-3p regulates ERK1/2-induced EMT via DUSP2 mRNA degradation in pancreatic ductal adenocarcinoma (17). However, the function of miR-361-3p in liver T-ICs is unclear.…”

Section: Introductionmentioning

confidence: 97%

miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

Zhang

Fan

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…It is a prognostic biomarker in cutaneous leishmaniasis caused by L. braziliensis (Lago et al, 2018). Its expression was associated with better survival outcomes in cervical cancer (Hu et al, 2018). It also functions as an oncomiR in pancreatic ductal adenocarcinoma (Hu et al, 2018) and acts as a novel tumor suppressor for non-small cell lung cancer (Chen et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Inhibition of miR-206 increased the level of brain-derived neurotrophic factor (BDNF) improved memory of AD mice (Lee et al, 2012). Particularly, miR-361-3p, an important miRNA in the regulation of non-small cell lung cancer (Chen et al, 2016), pancreatic ductal adenocarcinoma (Hu et al, 2018), cervical cancer (Hu et al, 2018) and cutaneous leishmaniasis lesions (Lago et al, 2018), have been reported to be downregulated in AD (Wang et al, 2011). However, the pathological effect of miR-361-3p in AD and the possible molecular mechanisms are still poorly investigated.…”

Section: Introductionmentioning

confidence: 99%

MiR-361-3p inhibits β-amyloid accumulation and attenuates cognitive deficits through targeting BACE1 in Alzheimer's disease

Wang

Zhang

et al. 2019

J. Integr. Neurosci.

View full text Add to dashboard Cite

The role of miR-361-3p in the pathology of Alzheimer's disease is unknown. The target scan was used to screen potential target genes of miR-361-3p, and β-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) was emphasized. Results from western blotting and reverse transcription-quantitative polymerase chain reaction (RT-PCR) showed that down-regulated miR-361-3p was correlated with up-regulated BACE1 in Alzheimer's disease patients' brains. Luciferase assay confirmed that miR-361-3p directly targets BACE1. MiR-361-3p overexpression and knockdown experiments were performed and found that miR-361-3p could regulate the expression of BACE1, and the accumulation of APP-β in APPswe transfected SH-SY5Y cell. A Morris water maze test was performed and showed that overexpression of miR-361-3p improved cognitive deficits in APP/PS1 mice. We found miR-361-3p inhibited β-amyloid accumulation by targeting BACE1, which thus weakened cognitive deficits in Alzheimer's disease.

show abstract

“…Western blot analysis was performed as previously described. 20,23,24 Whole-cell lysates with approximately 30 μg of proteins were resolved on 10% or 12% SDS-PAGE and were subjected to western blot assay using the antibodies listed in Supplementary Materials. After appropriate secondary antibody incubation, the bands were visualized with the Molecular Imager System (BIO-RAD, Hercules, USA) using an enhanced chemiluminescence method (Thermo Fisher Scientific, USA).…”

Section: Western Blot Analysismentioning

confidence: 99%

HYAL‐1‐induced autophagy facilitates pancreatic fistula for patients who underwent pancreaticoduodenectomy

Fengyu

Yuan

et al. 2019

FASEB j.

Self Cite

View full text Add to dashboard Cite

The main mechanism of hyaluronidase 1(HYAL-1) in the development of postoperative pancreatic fistula (POPF) after pancreatoduodenectomy (PD) was unknown. In this study, a comprehensive inventory of pre-, intra-, and postoperative clinical and biological data of two cohorts (62 pancreatic cancer [PCa] and 111 pancreatic ductal adenocarcinoma [PDAC]) which could induce POPF were retrospectively analyzed.Then, a total of 7644 genes correlated with HYAL-1 was predicted in PDAC tissues and the enriched pathway, kinase targets and biological process of those correlated genes were evaluated. Finally, a mouse pancreatic fistula (PF) model was first built and in vitro studies were performed to investigate the effects of HYAL-1 on PF progression. Our data indicated that preoperative serum HYAL-1 level, pancreatic fibrosis score, and pancreatic duct size were valuable factors for detecting POPF of Grade B and C. The serum HYAL-1 level of 2.07 mg/ml and pancreatic fibrosis score of 2.5 were proposed as the cutoff values for indicating POPF. The bioinformatic analysis and in vitro and in vivo studies demonstrated that HYAL-1 facilitates pancreatic acinar cell autophagy via the dephosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK) and signal transducers and activators of transcription 3 (STAT3) signaling pathways, which exacerbate pancreatic secretion and inflammation. In summary, the preoperative serum HYAL-1 was a significant predictor for POPF in patients who underwent PD. Tumor-induced HYAL-1 is one of core risk in accelerating PF and then promoting pancreatic secretion and acute inflammation response through the AMPK and STAT3-induced autophagy. K E Y W O R D Sautophagy, fibrosis, HYAL-1, pancreaticoduodenectomy, pancreatic fistula | 2525 LI et aL.

show abstract

MiR-361-3p regulates ERK1/2-induced EMT via DUSP2 mRNA degradation in pancreatic ductal adenocarcinoma

Cited by 74 publications

References 50 publications

miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

miR-361-3p Regulates Liver Tumor-initiating Cells Expansion and Chemo-resistance

MiR-361-3p inhibits β-amyloid accumulation and attenuates cognitive deficits through targeting BACE1 in Alzheimer's disease

HYAL‐1‐induced autophagy facilitates pancreatic fistula for patients who underwent pancreaticoduodenectomy

Contact Info

Product

Resources

About