Downregulated microRNA‑140‑5p expression regulates apoptosis, migration and invasion of lung cancer cells by targeting zinc finger protein 800

Zhuo, Enqing; Cai, Changqing; Liu, Wenzhe; Li, Kunsong; Zhao, Wenzhen

doi:10.3892/ol.2020.12253

Cited by 14 publications

(14 citation statements)

References 49 publications

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“…Cleaved caspase-3 is an apoptosis-related protein (24). Since mR-616-3p was found to promote apoptosis in HUVECs, western blotting analysis was used to determine whether miR-616-3p affects the expression of cleaved caspase-3 protein.…”

Section: Inhibition Of Mir-616-3p Expression Inhibits the Expression Of Cleaved Caspase-3 Protein In Huvecsmentioning

confidence: 99%

Apoptosis in HUVECs induced by microRNA‑616‑3p via X‑linked inhibitor of apoptosis protein targeting

Chen

Liu

et al. 2021

Exp Ther Med

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Atherosclerosis causes stroke and coronary heart disease and is associated with a high mortality rate worldwide. However, the pathogenesis of atherosclerosis remains unclear. Endothelial cell apoptosis is one of the early changes observed in atherosclerosis. Previous studies have found that microRNA (miR)-616-3p may be involved in the development of atherosclerosis, but the specific mechanism is not clear. The present study aimed to investigate whether miR-616-3p is involved in endothelial cell apoptosis and its underlying mechanism. The present study demonstrated that compared with normal HUVECs, HUVECs treated with oxidized low-density lipoprotein expressed higher miR-616-3p and lower X-linked inhibitor of apoptosis protein (XIAP) levels. In the present study, HUVECs were transfected with miR-616-3p mimic and Cell Counting Kit-8 (CCK-8), flow cytometry and TUNEL staining assays demonstrated that compared with miR-616-3p mimic control, the miR-616-3p mimic promoted HUVEC apoptosis. In addition, using StarBase 3.0 for bioinformatics analysis it was predicted that miR-616-3p may bind to the 3'untranslated region (UTR) of XIAP mRNA. The present study performed the CCK-8, flow cytometry, TUNEL staining and dual-luciferase reporter assays and demonstrated that miR-616-3p binds to the 3'UTR of the XIAP mRNA and inhibits its expression and that this further promotes apoptosis in HUVECs. In addition, western blotting demonstrated that compared with miR-616-3p mimic control, the miR-616-3p mimic increases the level of cleaved caspase-3 in HUVECs. In summary, the present study demonstrated that miR-616-3p can directly inhibit the expression of XIAP mRNA by targeting its 3'UTR which promoted apoptosis in HUVECs. miR-616-3p and XIAP may be used as therapeutic targets of atherosclerosis in the future.

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Section: Inhibition Of Mir-616-3p Expression Inhibits the Expression Of Cleaved Caspase-3 Protein In Huvecsmentioning

confidence: 99%

Apoptosis in HUVECs induced by microRNA‑616‑3p via X‑linked inhibitor of apoptosis protein targeting

Chen

Liu

et al. 2021

Exp Ther Med

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“…These findings may contribute to further understanding the mechanism of liver I/R injury and may provide novel insights into liver I/R. miR-140-5p has been extensively studied in tumor and non-tumor diseases and has exhibited favorable results (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)38). There is still a large gap in applying miR-140-5p research results to benefit patients clinically.…”

Section: Discussionmentioning

confidence: 95%

“…Other miRNAs, such as miR-125b, miR-128-3b and miR-450b-5p ( 5 , 6 , 8 ), are reportedly involved in liver I/R. miR-140-5p has been investigated extensively in tumor research, including glioma, breast and lung cancer, and hepatocellular carcinoma ( 13 , 14 , 17 , 18 ). miR-140-5p has also been extensively studied in non-tumor diseases.…”

Section: Discussionmentioning

confidence: 99%

“…In 2009, Miyaki et al revealed that miR-140-5p was highly expressed in differentiated human articular chondrocytes (12), while later studies reported that miR-140-5p was also expressed in other human tissues. miR-140-5p has been revealed to be expressed at low levels in various tumor tissues and play an antitumor role (13)(14)(15)(16)(17)(18). miR-140-5p has been revealed to inhibit inflammatory response (19)(20)(21) and miR-140-5p alleviates mouse liver ischemia/reperfusion injury by targeting CAPN1…”

Section: Introductionmentioning

confidence: 99%

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miR‑140‑5p alleviates mouse liver ischemia/reperfusion injury by targeting CAPN1

Chen

Tang

et al. 2021

Mol Med Rep

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Ischemia/reperfusion (I/R)-induced liver injury remains a primary concern in liver transplantation and hepatectomy. Previous studies have indicated that microRNAs (miRs) are involved in multiple pathophysiological processes, including liver I/R. miR-140-5p reportedly inhibits inflammatory responses and apoptosis in several diseases; however, the role of miR-140-5p in liver I/R remains unknown. The present study aimed to investigate the potential role and mechanism of miR-140-5p on liver I/R injury. Mouse liver I/R and mouse AML12 cell hypoxia/reoxygenation (H/R) models were established. miR-140-5p mimics, inhibitor or agonists were used to overexpress or inhibit miR-140-5p in vitro and in vivo. Reverse transcription-quantitative polymerase chain reaction was used to detect miR-140-5p expression. Liver and cell injury were evaluated using several biochemical assays. The association between miR-140-5p and calpain-1 (CAPN1) was confirmed using a dual-luciferase reporter assay. The results revealed that miR-140-5p expression was decreased in the mouse model of liver I/R injury and AML12 cells subjected to H/R, while overexpressed miR-140-5p reduced liver injury in vivo and cell injury in vitro. In addition, CAPN1 was determined to be a target of miR-140-5p; overexpressed CAPN1 abrogated the effect of miR-140-5p on H/R-induced cell injury. The present study indicated that miR-140-5p protected against liver I/R by targeting CAPN1, which may provide a novel therapeutic target for liver I/R injury.

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“…However, its role in regulating breast tumor angiogenesis and metastasis in response to hypoxia needs to be evaluated. Several cancers, including breast [ 13 , 14 , 15 ], gastric [ 16 , 17 ], lung [ 18 ], multiple myeloma [ 19 ], retinoblastoma [ 20 ], laryngeal squamous cell carcinoma (LSCC) [ 21 ], and nephroblastoma [ 22 ], have shown reduced expression of miR-140-5p which played a crucial role in cancer progression. In the current study, we observed significant repression of miR-140-5p in BC cells under hypoxia.…”

Section: Introductionmentioning

confidence: 99%

miR-140-5p Attenuates Hypoxia-Induced Breast Cancer Progression by Targeting Nrf2/HO-1 Axis in a Keap1-Independent Mechanism

Mahajan

Sitasawad

2021

Cells

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Hypoxia and oxidative stress significantly contribute to breast cancer (BC) progression. Although hypoxia-inducible factor 1α (Hif-1α) is considered a key effector of the cellular response to hypoxia, nuclear factor erythroid 2–related factor 2 (Nrf2), a master antioxidant transcription factor, is a crucial factor essential for Hif-1α-mediated hypoxic responses. Hence, targeting Nrf2 could provide new treatment strategies for cancer therapy. miRNAs are potential regulators of hypoxia-responsive genes. In a quest to identify novel hypoxia-regulated miRNAs involved in the regulation of Nrf2, we found that miR-140-5p significantly affects the expression of Nrf2 under hypoxia. In our study, miR-140-5p expression is downregulated in BC cells under hypoxic conditions. We have identified Nrf2 as a direct target of miR-140-5p, as confirmed by the luciferase assay. Knockdown of miR-140-5p under normoxic conditions significantly enhanced Nrf2/HO-1 signaling and tumor growth, angiogenesis, migration, and invasion in BC. In contrast, overexpression of miR-140-5p under hypoxic conditions revealed opposite results. Further silencing Nrf2 expression mimicked the miR-140-5p-induced anti-tumor effects. Consistent with the knockdown of miR-140-5p in vitro, mice injected with miR-140-5p-KD cells exhibited dramatically reduced miR-140-5p levels, increased Nrf2 levels, and increased tumor growth. In contrast, tumor growth is potently suppressed in mice injected with miR-140-5p-OE cells. Collectively, the above results demonstrate the importance of the Nrf2/HO-1 axis in cancer progression and, thus, targeting Nrf2 by miR-140-5p could be a better strategy for the treatment of Nrf2-driven breast cancer progression.

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Downregulated microRNA‑140‑5p expression regulates apoptosis, migration and invasion of lung cancer cells by targeting zinc finger protein 800

Cited by 14 publications

References 49 publications

Apoptosis in HUVECs induced by microRNA‑616‑3p via X‑linked inhibitor of apoptosis protein targeting

Apoptosis in HUVECs induced by microRNA‑616‑3p via X‑linked inhibitor of apoptosis protein targeting

miR‑140‑5p alleviates mouse liver ischemia/reperfusion injury by targeting CAPN1

miR-140-5p Attenuates Hypoxia-Induced Breast Cancer Progression by Targeting Nrf2/HO-1 Axis in a Keap1-Independent Mechanism

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