MicroRNA-6809-5p mediates luteolin-induced anticancer effects against hepatoma by targeting flotillin 1

Yang, Peiwei; Liu, Zhengyu; Pan, Qing; Chen, Tingting; Feng, Xiaohai; Wang, Shou‐Mei; Pan, Yun-Cui; Zhu, Min; Zhang, Shuhui

doi:10.1016/j.phymed.2018.10.027

Cited by 43 publications

(37 citation statements)

References 32 publications

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“…18 Yang et al found that miR-6809-5p mediated luteolin-induced anticancer effects by targeting flotillin 1 in hepatoma. 23 In our previous studies, we have identified several miRNAs as tumor suppressors in glioma, including miR-124-3p, 24 miR-137, 25 miR-181b-5p, 26 and miR-454-3p, 21 and we would like to examine whether these four miRNAs are involved in luteolin's anticancer activity in glioma. In the present study, the glioma cell lines LN229 and U251 were chosen.…”

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confidence: 99%

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

You¹,

Wang²,

Shao

et al. 2019

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Purpose Glioma is a malignant tumor that originates in the brain and spine and is difficult to be completely removed. Though glioma patients receive active treatment, the survival rate is still poor. Therefore, it is urgent to discover a new medicine to treat glioma patients in order to improve the survival rate. In this study, we explored the anticancer effect and the potential mechanism of luteolin on glioma in vitro. Materials and methods Cell viability was determined by Cell Counting Kit-8 (CCK-8) assay. Fluorescent microscopy and flow cytometry analysis were used to determine the cellular apoptosis. Western blot analysis was performed to explore the changes in protein expression. Quantitative reverse transcription-PCR (qRT-PCR) analysis was utilized to evaluate the expression level of the tumor suppressor miR-124-3p. Results CCK-8 assays indicated that luteolin significantly inhibited glioma cell proliferation in a time- and dose-dependent manner. Fluorescent microscopy and flow cytometry analysis confirmed that luteolin induced glioma cell apoptosis. Western blot analysis showed that luteolin induced cellular apoptosis in glioma cells via MAPK activation (JNK, ERK, and p38). Luteolin stimulated the death receptor (FADD) to regulate the apoptosis proteins (Caspase-8, Caspase-3, and PARP). Luteolin increased the expression levels of LC3B II/I and downregulated the level of p62 that promotes cell autophagy. Finally, qRT-PCR confirmed that luteolin upregulated the expression levels of miR-124-3p. Conclusion These findings illustrate that luteolin may be a potential drug for glioma treatment.

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confidence: 99%

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

You¹,

Wang²,

Shao

et al. 2019

OTT

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“…These miRNAs are consistent with known characteristics of ZZ individuals with liver disease such as HSCs activation, brosis and cirrhosis, and HCC which shows the possibility of using EVs as a potential source of biomarkers for early diagnosis of disease progression. Importantly, we identi ed that of the 44 miRNAs whose levels change in the plasma EVs of AATD individuals, 5 which were higher in AATD individuals (miR-125a, miR-125b1, miR-125b2, miR-128 and miR-130b) and 1 lower (miR-6809) appear to play important roles in liver brosis (41)(42)(43)(44)(45). A large body of evidence supports the implication of the miR-125 family and miR-130b (46) in different liver diseases, including ALF (47), nonalcoholic fatty liver disease (48), cholestasis (49), and HCC (50).…”

Section: Discussionmentioning

confidence: 99%

Alpha-1 antitrypsin deficient individuals have circulating extracellular vesicles with profibrogenic cargo 

Khodayari

Oshins

Holliday

et al. 2020

Preprint

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Background: Alpha-1 antitrypsin deficiency (AATD)-mediated liver disease is a toxic “gain-of-function” inflammation in the liver associated with intracellular retention of mutant alpha-1 antitrypsin. The clinical presentation of the disease includes fibrosis, cirrhosis and liver failure. However, the pathogenic mechanism of AATD-mediated liver disease is not well understood. Here, we investigated the role of plasma extracellular vesicles (EVs) in progression of AATD-mediated liver disease. Methods: EVs were isolated from plasma of AATD individuals with liver disease and healthy controls. Their cytokines and miRNA content were examined by multiplex assay and small RNA sequencing. The bioactivity of EVs was assessed by qPCR, western blot analysis and immunofluorescent experiments using human hepatic stellate cells (HSCs) treated with EVs isolated from control or AATD plasma samples.Results: We have found that AATD individuals have a distinct population of EVs with pathological cytokine and miRNA contents. When HSCs were cultured with AATD plasma derived-EVs, the expression of genes related to the development of fibrosis were significantly amplified compared to those treated with healthy control plasma EVs. Conclusion: AATD individuals have a distinct population of EVs with abnormal cytokine and miRNA contents and the capacity to activate HSCs and mediate fibrosis. Better understanding of the components which cause liver inflammation and fibrogenesis, leading to further liver injury, has the potential to lead to the development of new treatments or preventive strategies to prevent AATD-mediated liver disease.

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“…29,30 Similarly, a series of miRNAs have been reported as tumor suppressor or promoter in cancer progression. [31][32][33] Mechanistically, lncRNAs could act as miRNA spongers to modulate miRNA downstream mRNA via ceRNA network. 34,35 miR-1301-3p has been reported to inhibit cell proliferation, induce cell apoptosis, and regulate cell-cycle progression via directly targeting ICT1 in breast cancer.…”

Section: Discussionmentioning

confidence: 99%

NNT‐AS1 enhances bladder cancer cell growth by targeting miR‐1301‐3p/PODXL axis and activating Wnt pathway

Liu

2019

Neurourology and Urodynamics

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As a tumor involved in the urinary system, bladder cancer (BC) seriously threatens human health. Emerging as crucial biomarkers, long noncoding RNAs (lncRNAs) play an important role in the regulation of many cancers. lncRNA NNT-AS1 has been studied in a series of cancers, whereas its role and potential molecular mechanism was poorly understood in BC. Here, we found that NNT-AS1 was upregulated in BC cells. Functionally, the silencing of NNT-AS1 inhibited cell proliferation, migration, invasion, and endothelial-mesenchymal transition. Furthermore, the apoptosis of BC cells was induced upon NNT-AS1 knockdown. Later, miR-1301-3p, the downstream gene of NNT-AS1, was found at a low level in BC cells. In addition, we found that miR-1301-3p targeted to PODXL. PODXL expression downregulated in NNT-AS1-silenced cells was restored by miR-1301-3p inhibition. Importantly, NNT-AS1 was discovered to activate Wnt pathway, and the treatment of LiCl recovered the repressive role of NNT-AS1 silencing in BC cell growth. Through restoration assays, we observed that PODXL overexpressing countervailed NNT-AS1 depletionmediated suppression on BC cell growth and Wnt pathway. These data suggested that NNT-AS1 enhances BC cell growth and activates Wnt pathway by targeting miR-1301-3p/PODXL axis. K E Y W O R D Sbladder cancer, miR-1301-3p, NNT-AS1, PODXL

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MicroRNA-6809-5p mediates luteolin-induced anticancer effects against hepatoma by targeting flotillin 1

Cited by 43 publications

References 32 publications

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

Alpha-1 antitrypsin deficient individuals have circulating extracellular vesicles with profibrogenic cargo

NNT‐AS1 enhances bladder cancer cell growth by targeting miR‐1301‐3p/PODXL axis and activating Wnt pathway

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MicroRNA-6809-5p mediates luteolin-induced anticancer effects against hepatoma by targeting flotillin 1

Cited by 43 publications

References 32 publications

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

<p>Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma</p>

Alpha-1 antitrypsin deficient individuals have circulating extracellular vesicles with profibrogenic cargo&nbsp;

NNT‐AS1 enhances bladder cancer cell growth by targeting miR‐1301‐3p/PODXL axis and activating Wnt pathway

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Alpha-1 antitrypsin deficient individuals have circulating extracellular vesicles with profibrogenic cargo