Low expression of miR-381 is a favorite prognosis factor and enhances the chemosensitivity of osteosarcoma

Li, Yunchao; Chun-hua, Zhao; Yu, Zhibin; Chen, Jiarui; She, Xiaoling; Li, Peiyao; Liu, Changhong; Zhang, Yan; Feng, Jianbo; Fu, Haijuan; Wang, Bing; Kuang, Lei; Li, Lei; Lv, Guohua; Wu, Minghua

doi:10.18632/oncotarget.11861

Cited by 38 publications

(40 citation statements)

References 34 publications

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“…It is reported that miR-93 can repress apoptosis after cerebral ischemia via interleukin-1 [38]. Similarly, a previous study proved that miR-381 was overexpressed in the mature brain and normal hippocampal neurons [13], and decreasing miR-381 expression inhibited cell proliferation and invasion [39, 40], from which we inferred that up-regulation of miR-381 inhibited neuronal apoptosis.…”

Section: Discussionsupporting

confidence: 62%

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

Piao¹,

Wu²,

Yang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Acute cerebral ischemia is a manifestation of cerebral vascular insufficiency and has a high mortality. However, the therapy for acute cerebral ischemia is still limited. This study aimed to investigate the effect of microRNA-381 (miR-381) on the repair of nerve injury in rats with acute cerebral ischemia after cerebral lymphatic blockage (CLB) by targeting leucine-rich repeat C4 protein (LRRC4) through the Stromal cell-derived factor-1/CXC chemokine receptor-4 signaling pathway. Methods: Rat models of CLB and middle cerebral artery occlusion (MCAO) were established, and 56 Wistar rats were divided into sham, MCAO, CLB + MCAO, CLB + MCAO + miR-381 inhibitor, CLB + MCAO + miR-381 mimic, CLB + MCAO + AMD3100 and CLB + MCAO + miR-381 mimic + AMD3100 groups. Modified neurological severity score (mNSS was used to determine nerve injury, TTC staining to measure infarction volume, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and flow cytometry to evaluate cell apoptosis, immunofluorescence to measure BrdU-positive cell number, enzyme-linked immunosorbent assay (ELISA) to determine contents of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), nerve growth factor (NGF) and neurite outgrowth inhibitor -A (Nogo-A), Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting to evaluate expression of miR-381, LRRC4, SDF-1, CXCR4, pERK, Slit2 and vascular endothelial growth factor (VEGF). Results: LRRC4 was a target gene of miR-381. Compared with the results in the CLB + MCAO group, mNSS, infarction volume, apoptosis rate and TNF-α, IL-1β, IL-6 and Nogo-A contents as well as LRRC4 expression in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups were increased (those in the CLB + MCAO + AMD3100 group > those in the CLB + MCAO + miR-381 mimic + AMD3100 group), while BrdU-positive cell number, contents of NGF and IL-10, and expression of SDF-1, CXCR4, pERK, Slit2 and VEGF in brain tissues were decreased (those in the CLB + MCAO + AMD3100 group < those in the CLB + MCAO + miR-381 mimic + AMD3100 group). The results in the CLB + MCAO + mimic group were opposite of those in the CLB + MCAO + miR-381 inhibitor and CLB + MCAO + AMD3100 groups. Conclusion: Taken together, we concluded that up-regulation of miR-381 promoted nerve injury repair in acute cerebral ischemia rats after CLB by negatively regulating LRRC4 through activating the SDF-1/CXCR4 signaling pathway.

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Section: Discussionsupporting

confidence: 62%

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

Piao¹,

Wu²,

Yang³

et al. 2018

Cell Physiol Biochem

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“…Our results indicated that miR-381 was down-regulated in DDPresistant breast cancer tissues and cells, and miR-381 overexpression could overcome DDP resistance in DDPresistant breast cancer cells (MCF-7/DDP and MDA-MB-231/DDP). Ã P < 0.05. et al, 2013a; Wang et al, 2015;Li et al, 2016). Collectively, our data demonstrated that miR-381 could facilitate the sensitivity of breast cancers to DDP.…”

Section: Discussionsupporting

confidence: 56%

miR‐381 overcomes cisplatin resistance in breast cancer by targeting MDR1

Wang

et al. 2018

Cell Biology International

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Increasing evidence suggests the involvement of microRNA-381 (miR-381) in chemoresistance of cancer treatment. However, its function and molecular mechanisms in breast cancer chemoresistance are still not well elucidated. In the present study, we aimed to investigate the functional role of miR-381 in cisplatin (DDP) resistance of breast cancer and discover the underlying molecular mechanism. The expression levels of miR-381 and MDR1 were detected by quantitative real-time PCR (qRT-PCR) and Western blot analysis in breast cancer tissues and cell lines. The DDP sensitivity and cell apoptosis of breast cancer cells were determined by MTT assay and flow cytometric analysis, respectively. The relationship between miR-381 and MDR1 was explored by target prediction and luciferase reporter analysis. miR-381 was decreased in DDP-resistant breast cancer tissues and cell lines. Low miR-381 expression was correlated with poor prognosis of breast cancer patients. miR-381 overexpression improved DDP sensitivity of MCF-7/DDP and MDA-MB-231/DDP cells. Conversely, miR-381 inhibition lowered the response of MCF-7 and MDA-MB-231 to DPP. Moreover, miR-381 could directly suppress multidrug resistance 1 (MDR1) expression. MDR1 knockdown could overcome DDP resistance in MCF-7/DDP and MDA-MB-231/DDP cells, while MDR1 overexpression led to DDP resistance in MCF-7 and MDA-MB-231 cells. Notably, MDR1 overexpression counteracted the inductive effect of miR-381 mimics on DDP sensitivity of MCF-7/DDP and MDA-MB-231/DDP cells. On the contrary, miR-381 inhibition-mediated DDP resistance in MCF-7 and MDA-MB-231 cells was reversed by MDR1 knockdown. In summary, miR-381 could overcome DDP resistance of breast cancer by directly targeting MDR1, providing a novel therapeutic target for breast cancer chemoresistance.

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“…4 There is considerable evidence suggesting that miR-381 functions as a suppressor in cancer proliferation, migration, and invasion. 5 For example, miR-381-inhibited pituitary tumor cell tumorigenesis by targeting PTTG1. 6 However, in other studies, miR-381 was validated to promote glioma cell proliferation and pituitary tumor growth in vitro and in vivo.…”

Section: Introductionmentioning

confidence: 99%

miR‐381‐3p restrains cervical cancer progression by downregulating FGF7

Shang

Zhou

Bian

et al. 2018

J of Cellular Biochemistry

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This study aimed at elucidating the molecular mechanism of miR-381-3p in cervical cancer progression, which may provide a novel therapeutic target for patients with cervical cancer. The expression of miR-381-3p was confirmed by quantitative reverse transcription polymerase chain reaction. Microarray analysis was conducted to screen out differentially expressed genes, and the target gene of microRNA (miRNA) was predicted on TargetScan. Dual-luciferase reporter assay then verified the targeting relationship between miR-381-3p and FGF7. The protein expression of FGF7 was examined via Western blot assay. Colony formation assay was used to detect the cell proliferation, while flow cytometry was used to analyze cell cycle and apoptosis. The influence of miR-381-3p and FGF7 on cell migration and invasion was confirmed by transwell migration/invasion assay. Finally, we demonstrated that miR-381-3p was lowly expressed, while FGF7 was highly expressed in cervical cancer cells. There was a direct target relationship and a negative correlation between miR-381-3p and FGF7. miR-381-3p could downregulate FGF7 expression, inhibiting cell proliferation and metastasis, and inducing cell cycle arrest and apoptosis in cervical cancer.

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Low expression of miR-381 is a favorite prognosis factor and enhances the chemosensitivity of osteosarcoma

Cited by 38 publications

References 34 publications

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

MicroRNA-381 Favors Repair of Nerve Injury Through Regulation of the SDF-1/CXCR4 Signaling Pathway via LRRC4 in Acute Cerebral Ischemia after Cerebral Lymphatic Blockage

miR‐381 overcomes cisplatin resistance in breast cancer by targeting MDR1

miR‐381‐3p restrains cervical cancer progression by downregulating FGF7

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