miR-331-3p Suppresses Cell Proliferation in TNBC Cells by Downregulating NRP2

Zhao, Ming; Zhang, Mengmeng; Tao, Zhonghua; Cao, Ji; Wang, Leiping; Hu, Xichun

doi:10.1177/1533033820905824

Cited by 25 publications

(16 citation statements)

References 47 publications

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“…NRP2 was previously reported as a member of the membrane protein neuropilin family. Increased expression of NRP2 was found in invasive and TNBC and was correlated with lymph node metastasis [9,10]. In our study, dual-luciferase reporter assay revealed the interaction between miR-149- LRP11-AS1 exhibited the malignant behavior in TNBC by sponging miR-149-3p and regulating the miR-149-3p/NRP2 axis.…”

Section: Discussionsupporting

confidence: 56%

LRP11-AS1 Promotes the Malignant Behavior of Triple Negative Breast Cancer Cells via the MiR-149-3p/NRP2 Axis

Zeng

Chen

Huang

et al. 2021

Preprint

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Background: Breast cancer is the most commonly diagnosed cancer in women. Triple negative breast cancer (TNBC) is the most difficult subtype of breast cancer to treat due to the deficiency in drug-targetable receptors. LRP11-AS1, a newly identified oncogenic long noncoding RNA (lncRNA) was found to be significantly overexpressed in TNBC cells. The aim of this study is to investigate the malignant roles and the oncogenic mechanisms of LRP11-AS1 in TNBC. Methods: CCK-8, colony formation, transwell migration and transwell invasion assays were performed to study the functions of LRP11-AS1. Quantitative PCR and western blot were used to determine the gene expression. Bioinformatics analysis and dual-luciferase reporter assay were conducted to study lncRNA and miRNA interactions. Results: LRP11-AS1 was found to be significantly overexpressed in TNBC cells compared to the non-TNBC cells and normal mammary epithelial cells. Knockdown of LRP11-AS1 could inhibit the growth and metastasis of TNBC cells and regulate cell cycle. Mechanistically, LRP11-AS1 was found to act as a competing endogenous RNA (ceRNA) to sponge miR-149-3p. Silencing of LRP11-AS1 increased the expression of miR-149-3p and overexpression of miR-149-3p suppressed the expression of LRP11-AS1. Inhibition of miR-149-3p could reverse the anticancer effect of LRP11-AS1 deficiency in TNBC cells. Moreover, Neuropilin-2 (NRP2) was found to be the target of miR-149-3p. Rescue experiments revealed that NRP2 overexpression could rescue the anticancer effect of LRP11-AS1 deficiency in TNBC cells. Conclusion: LRP11-AS1 overexpressed in TNBC showed the oncogenic effects possibly by sponging miR-149-3p and regulating the miR-1493p/NRP2 axis, which indicated LRP11-AS1 as a potential diagnostic biomarker and therapeutic target in TNBC.

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Section: Discussionsupporting

confidence: 56%

LRP11-AS1 Promotes the Malignant Behavior of Triple Negative Breast Cancer Cells via the MiR-149-3p/NRP2 Axis

Zeng

Chen

Huang

et al. 2021

Preprint

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“…For example, the inhibitory effects of fentanyl on tumor growth and cell invasion in colorectal cancer may be realized by downregulation of miR-182 through β-catenin. 25 In a recent miRNA array in primary cultures of rat hippocampal neurons, fentanyl was proved to increase miR-331-3p level, 20 which functions as a tumor suppresser in numerous cancers including lung cancer, e.g., miR-331-3p inhibits proliferation and migration in hepatocellular carcinoma Bel-7402 cell line by targeting E2F1, 26 miR-331-3p suppresses proliferation and metastasis in ovarian cancer through regulation of RCC2, 27 miR-331-3p reduces cell proliferation in breast cancer through targeting NRP2, 28 Circular RNA circ_0001649 represses cell proliferation and invasion of NSCLC by sponging miR-331-3p, 29 miR-331-3p suppresses cell proliferation and invasion of NSCLC by targeting ErbB2 and VAV2. 21 Furthermore, in 2020, Tian et al reported that miR-331-3p inhibits cell proliferation and invasion of NSCLC cells by targeting MLLT10; 30 circulating miR-331-3p was identified as a novel biomarker for early diagnosis and monitoring of lung cancer.…”

Section: Discussionmentioning

confidence: 99%

Fentanyl Inhibits Lung Cancer Viability and Invasion via Upregulation of miR-331-3p and Repression of HDAC5

Shouliang¹,

Liang

Fan³

et al. 2020

OTT

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Purpose Non-small cell lung cancer (NSCLC) accounts for more than 80% of lung cancer cases and remains the primary cause of cancer-related deaths worldwide. Fentanyl is a commonly utilized anesthetic during the process of tumor resection, and exhibits inhibitory effects on the progression of numerous cancer types, including pancreatic cancer, colorectal cancer and gastric cancer. However, the effects of fentanyl on the cell viability and invasion of NSCLC has not been investigated. Current study aimed to investigate the effects and the mechanisms underlying the effects of fentanyl on NSCLC. Methods The expression of μ-opioid receptor (MOR) was proved by flow cytometry. The expression of microRNA-331-3p (miR-331-3p) and histone deacetylase 5 (HDAC5) in NSCLC tissues and cell lines are evaluated by reverse transcription-quantitative PCR (RT-qPCR) and Western blot, respectively. Cell viability and invasion are measured by cell counting kit-8 (CCK-8) assay and transwell assay, respectively. The interaction between miR-331-3p and 3ʹ-untranslated region (UTR) of HDAC5 is predicted by TargetScan 7.1 ( http://www.targetscan.org/vert_71/ ), validated by dual luciferase assay, RT-qPCR and Western blot. Results There was lower miR-331-3p expression and higher HDAC5 expression in NSCLC cell lines A549 and CALU-1 compared with BEAS-2B, which was reversed by fentanyl administration. miR-331-3p targeted 3ʹ-UTR of HDAC5 in NSCLC cell lines A549 and CALU-1. miR-331-3p inhibitor partially abrogated the inhibitory effects of fentanyl on NSCLC cell viability and invasion by targeting HDAC5. In addition, there was higher HDAC5 expression and lower miR-331-3p expression in tumor tissues which were isolated from patients with NSCLC compared to the adjacent normal tissues, and miR-331-3p was negatively correlated with HDAC5 in NSCLC tumor tissues. Conclusion Fentanyl inhibits the viability and invasion of NSCLC cells by induction of miR-331-3p and reduction of HDAC5.

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“…Guo et al ( 15 ) reported that miR-331-3p suppresses GC cell growth via inhibiting E2F1. Zhao et al ( 32 ) revealed that miR-331-3p suppresses cell proliferation in triple-negative breast cancer cells via downregulating NRP2 ( 32 ). The current results also supported the regulatory role of miR-331-3p.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA MIAT promotes gastric cancer proliferation and metastasis via modulating the miR‑331‑3p/RAB5B pathway

Jiao

Luan

et al. 2020

Oncol Lett

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Gastric cancer (GC) remains a threat to the health of the global population. The present study investigated the effects and mechanisms of the long non-coding RNA myocardial infarction associated transcript (MIAT) on the proliferation, apoptosis and metastasis of GC (HGC-27 and AGS) cells. The expression levels of MIAT, micoRNA (miR)-331-3p and RAB5B mRNA were analyzed using reverse transcription-quantitative PCR analysis. Cell growth, apoptosis, migration and invasion were measured using 5-ethynyl-2′-deoxyuridine, flow cytometry, wound healing and Transwell assays, respectively. A luciferase assay was used to determine whether miR-331-3p targeted MIAT and RAB5B. The results indicated that MIAT levels were significantly upregulated in GC tissues and cells, correlated with RAB5B levels and inversely associated with miR-331-3p levels. MIAT overexpression promoted proliferation and metastasis, and inhibited the apoptosis of GC cells . MIAT knockdown had the opposite effect on GC cells . The rescue experiments revealed that the effects of MIAT knockdown on the biological behaviour of GC cells were attenuated by RAB5B overexpression. These data suggest that MIAT promotes GC progression via modulating miR-331-3p/RAB5B pathway.

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miR-331-3p Suppresses Cell Proliferation in TNBC Cells by Downregulating NRP2

Cited by 25 publications

References 47 publications

LRP11-AS1 Promotes the Malignant Behavior of Triple Negative Breast Cancer Cells via the MiR-149-3p/NRP2 Axis

LRP11-AS1 Promotes the Malignant Behavior of Triple Negative Breast Cancer Cells via the MiR-149-3p/NRP2 Axis

Fentanyl Inhibits Lung Cancer Viability and Invasion via Upregulation of miR-331-3p and Repression of HDAC5

Long non‑coding RNA MIAT promotes gastric cancer proliferation and metastasis via modulating the miR‑331‑3p/RAB5B pathway

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