Knockdown of lncRNA ZFAS1‐suppressed non–small cell lung cancer progression via targeting the miR‐150‐5p/HMGA2 signaling

Zeng, Z.; Zhao, Guofang; Rao, Chuangzhou; Hua, Gang; Yang, Minglei; Miao, Xiaobo; Ying, Jingjing; Nie, Liangqin

doi:10.1002/jcb.29542

Cited by 28 publications

(22 citation statements)

References 31 publications

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“…1A , P < 0.05). The results are consistent with previous studies 19 , 20 . We also examined the ZFAS1 expression level in A549, HCC827, and 16HBE cells.…”

Section: Resultssupporting

confidence: 94%

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Long Noncoding RNA ZFAS1 Promotes Progression of NSCLC via Regulating of miR-590-3p

Zhou

Liu

et al. 2020

Cell Transplant

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The incidence and mortality rate of nonsmall cell lung cancer (NSCLC) are continuously increasing. Recently, the important roles of long noncoding ribonucleic acid (lncRNA) zinc finger antisense1 (ZFAS1) in the development of many disease have been proved. However, the roles of ZFAS1 in NSCLC are still not completely understood. Thus, this study aimed to explore the potential roles and underlying mechanisms of lncRNA ZFAS1 in the progression of NSCLC. Our results demonstrated that lncRNA ZFAS1 expression was significantly upregulated in NSCLC tissues and cell lines. Loss-of-function experiments revealed that lncRNA ZFAS1 inhibition could remarkably suppress NSCLC cells proliferation in vitro. Bioinformatic analysis and luciferase reporter assay revealed that lncRNA ZFAS1 directly interacted with miR-590-3p. Rescue experiments showed that miR-590-3p inhibitor reversed the cell proliferation function of lncRNA ZFAS1 knockdown in vitro. Furthermore, we confirmed that lncRNA ZFAS1 inhibited cell division cycle 42 (Cdc42) expression by regulating of miR-590-3p in NSCLC cells. Therefore, our study indicates that lncRNA ZFAS1/miR-590-3p axis is involved in NSCLC cell proliferation. It also suggests that lncRNA ZFAS1 is a putative tumor oncogene in NSCLC.

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“…1A , P < 0.05). The results are consistent with previous studies 19 , 20 . We also examined the ZFAS1 expression level in A549, HCC827, and 16HBE cells.…”

Section: Resultssupporting

confidence: 94%

“…RIP assays were carried out to determine the interaction between ZFAS1 and miR-590-3p as in the previous study 19 , 20 . We used EZMagna RIP RNA-binding protein immunoprecipitation kit (Millipore, Chengdu, Sichuan, China) according to the manufacturer’s protocol.…”

Section: Methodsmentioning

confidence: 99%

Long Noncoding RNA ZFAS1 Promotes Progression of NSCLC via Regulating of miR-590-3p

Zhou

Liu

et al. 2020

Cell Transplant

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“…Moreover, ZFAS1 attenuates the rate of cholesterol efflux and facilitates inflammatory responses in atherosclerosis (25). Additionally, ZFAS1 has been found to be dysregulated in various types of cancer and to serve an oncogenic role in the onset and development of malignant tumors, such as ovarian cancer and glioma, by promoting cancer metastasis, growth and epithelial-to-mesenchymal transition (26)(27)(28). However, the functional effect of ZFAS1 on cell migration and the proliferation of VSMCs has yet to be fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

lncRNA ZFAS1 promotes the ox‑LDL induced proliferation, invasion and migration of vascular smooth muscle cells

Wang¹,

Hu²,

Ma³

et al. 2021

Exp Ther Med

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Atherosclerosis is a chronic progressive inflammatory vascular disease. The dysfunction of vascular smooth muscle cells (VSMCs) induced by oxidized low-density lipoprotein (ox-LDL) contributes to the formation of atherosclerotic lesions. Additionally, upregulation of the long non-coding RNA zinc finger antisense 1 (ZFAS1) was observed in the plaques of patients with atherosclerosis. The aim of the present study was to explore the functional role of ZFAS1 in atherosclerosis progression. Reverse transcription-quantitative PCR was performed to analyze ZFAS1 mRNA expression, and western blotting was performed to determine the protein expression levels of Ki67, proliferating cell nuclear antigen (PCNA), matrix metallopeptidase (MMP)2 and MMP9. The Cell Counting Kit-8 assay was used to test cell viability. Finally, wound healing and Transwell chamber assays were performed to evaluate cell migration and invasion, respectively. The current findings demonstrated that ZFAS1 expression was upregulated by ox-LDL stimulation in VSMCs. Moreover, ZFAS1 overexpression promoted the ox-LDL-induced proliferation, migration and invasion of VSMCs, and upregulated the expression levels of proteins associated with cellular proliferation (Ki67 and PCNA), migration and invasion (MMP2 and 9). By contrast, ZFAS1-knockdown inhibited the proliferation, migration and invasion of VSMCs, and suppressed cell proliferation-, migration-and invasion-associated protein expression. In conclusion, ZFAS1 promoted the ox-LDL-induced proliferation, invasion and migration of VSMCs. Thus, ZFAS1 may represent a novel biomarker for dysfunction of VSMCs in the pathological condition of atherosclerosis.

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“…For example, lncRNA long stress-induced non-coding transcript 5 (LSINCT5) interacted with metastasis-associated transcription factor, high-mobility group AT-hook 2 (HMGA2), protecting it from proteasome-mediated degradation and increasing migration of NSCLC cells [ 66 ]. Furthermore, lncRNA ZNFX1 antisense RNA 1 (ZFAS1) acted as a ceRNA for miR-150 to increase HMGA2, resulting in increased NSCLC invasion [ 99 ]. LINC00673 modulated EZH2 epigenetic silencing of HOXA5, a tumor suppressor that inhibited NSCLC metastasis by regulating cytoskeletal remodeling [ 60 ].…”

Section: Lncrna Dysregulation In Nsclcmentioning

confidence: 99%

LncRNAs in Non-Small-Cell Lung Cancer

Ginn

Shi

Montagna

et al. 2020

ncRNA

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Lung cancer is associated with a high mortality, with around 1.8 million deaths worldwide in 2018. Non-small-cell lung cancer (NSCLC) accounts for around 85% of cases and, despite improvement in the management of NSCLC, most patients are diagnosed at advanced stage and the five-year survival remains around 15%. This highlights a need to identify novel ways to treat the disease to reduce the burden of NSCLC. Long non-coding RNAs (lncRNAs) are non-coding RNA molecules longer than 200 nucleotides in length which play important roles in gene expression and signaling pathways. Recently, lncRNAs were implicated in cancer, where their expression is dysregulated resulting in aberrant functions. LncRNAs were shown to function as both tumor suppressors and oncogenes in a variety of cancer types. Although there are a few well characterized lncRNAs in NSCLC, many lncRNAs remain un-characterized and their mechanisms of action largely unknown. LncRNAs have success as therapies in neurodegenerative diseases, and having a detailed understanding of their function in NSCLC may guide novel therapeutic approaches and strategies. This review discusses the role of lncRNAs in NSCLC tumorigenesis, highlighting their mechanisms of action and their clinical potential.

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Knockdown of lncRNA ZFAS1‐suppressed non–small cell lung cancer progression via targeting the miR‐150‐5p/HMGA2 signaling

Cited by 28 publications

References 31 publications

Long Noncoding RNA ZFAS1 Promotes Progression of NSCLC via Regulating of miR-590-3p

Long Noncoding RNA ZFAS1 Promotes Progression of NSCLC via Regulating of miR-590-3p

lncRNA ZFAS1 promotes the ox‑LDL induced proliferation, invasion and migration of vascular smooth muscle cells

LncRNAs in Non-Small-Cell Lung Cancer

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