MiR-212-3p inhibits cell proliferation and promotes apoptosis by targeting nuclear factor IA in bladder cancer

Wu, Xiaoming; Chen, Hao; Zhang, Gaoyue; Wu, Jianhui; Zhu, Wei; Gu, Yanqin; He, Yi

doi:10.1007/s12038-019-9903-5

Cited by 22 publications

(14 citation statements)

References 31 publications

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“…Meanwhile, although miR-212-3p was reported to be associated with various types of cancers such as bladder cancer, glioma, sarcoma and pancreatic cancers (Wu et al 2019 ; Liu et al 2015 ; Ding et al 2018 ; Xie et al 2018 ), its association with BC was not well understood. One weak association was that the BC resistance protein (BCRP/ABCG2) was under regulation of miR-212-3p in renal cancer cells (Reustle et al 2018 ), the regulation of miR-212-3p in BC was merely mentioned.…”

Section: Discussionmentioning

confidence: 99%

“…MiR-212-3p is another miRNA involved in angiogenesis regulation in various types of cancers. It was reported that miR-212-3p was significantly down-regulated in human bladder cancer tissues and its over expression could inhibit the proliferation of bladder cancer cells (Wu et al 2019 ). It could also inhibit angiogenesis and proliferation of glioblastoma by targeting SGK3 (Liu et al 2015 ).…”

Section: Introductionmentioning

confidence: 99%

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ZLM-7 inhibits the occurrence and angiogenesis of breast cancer through miR-212-3p/Sp1/VEGFA signal axis

Zou

Wen

et al. 2020

Mol Med

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Background Breast cancer (BC) is a common malignant tumor with poor prognosis. Angiogenesis is related to the growth and progression of solid tumors and associated with prognosis. ZLM-7, SP1, VEGFA and miR-212-3p were associated with BC angiogenesis and proliferation, however the detailed mechanism was not clear. This study aimed to reveal the regulatory mechanism of angiogenesis of BC. Methods BC cell lines were treated with 10 nM ZLM-7 for 8 h. We detected protein expression level by western blot and RNA expression level by qRT-PCR. Overexpression or inhibition of miR-212-3p is performed using miR-212-3p mimics or miR-212-3p inhibitor, Sp1 overexpression using pcDNA3.1 vector. Angiogenesis was analyzed by co-culturing BC cell lines and HUVEC cells. To evaluate regulatory relationship between miR-212-3p and Sp1, dual luciferase assay was performed. Besides, the direct interaction between Sp1 and VEGFA was analyzed by ChIP. Migration and invasion were analyzed by transwell assay and proliferation was detected by clone formation assay. In mice xenograft model developed using BC cells, we also detected angiogenesis marker CD31 through immunohistochemistry. Results ZLM-7 up-regulated miR-212-3p and inhibited invasion, migration, proliferation and angiogenesis of BC, while miR-212-3p inhibitor antagonized such effects. Binding sequence was revealed between miR-212-3p and Sp1, and expression of Sp1 was inhibited by miR-212-3p on both protein and mRNA level. Sp1 could interact with VEGFA and promoted its expression. Overexpression of miR-212-3p inhibited migration, invasion, proliferation and angiogenesis of BC cell lines, while Sp1 overexpression showed the opposite effect and could antagonize these effects of miR-212-3p overexpression. ZLM-7 decreased VEGFA expression, which was rescued by co-transfection with miR-212-3p inhibitor. Similar, ZLM-7 could inhibit tumor growth and angiogenesis through the miR-212-3p/Sp1/VEGFA axis in vivo. Conclusions ZLM-7 could directly up-regulate miR-212-3p in BC. MiR-212-3p could inhibit VEGFA expression through Sp1, thereby inhibiting angiogenesis and progression of BC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ZLM-7 inhibits the occurrence and angiogenesis of breast cancer through miR-212-3p/Sp1/VEGFA signal axis

Zou

Wen

et al. 2020

Mol Med

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“…[30][31][32] Moreover, miR-212-3p restrained the tumorigenesis of gastric cancer and bladder cancer by inhibiting the expression of a target, such as SRY-box transcription factor 6 (Sox6) and nuclear factor IA (NFIA). 33,34 A previous document demonstrated the tumor suppressive impact of miR-212-3p in NSCLC malignant progression. 20 Here, we were first to uncover that miR-212-3p was a molecular mediator of circNFIX in regulating NSCLC cell malignant progression, arguing for the "sponge" function of circNFIX, as has been reported.…”

Section: Discussionmentioning

confidence: 99%

<p>CircNFIX Acts as a miR-212-3p Sponge to Enhance the Malignant Progression of Non-Small Cell Lung Cancer by Up-Regulating ADAM10</p>

Lü¹,

Zhu²,

Qin³

et al. 2020

CMAR

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Background: Non-small cell lung cancer (NSCLC) remains the most commonly diagnosed malignancy and the leading cause of cancer death worldwide. Circular RNAs (circRNAs) have been demonstrated to play critical roles in human carcinogenesis, including NSCLC. However, it is still unclear whether circRNA nuclear factor I X (circNFIX) is implicated in the molecular pathogenesis of NSCLC. Methods: The expression levels of circNFIX, miR-212-3p and a disintegrin and metalloproteinases 10 (ADAM10) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot. Cell viability was gauged by the Cell Counting Kit-8 (CCK-8) assay, and cell migration and invasion were determined by transwell assays. Glucose uptake and lactate product were determined using the assay kits. Targeted relationships among circNFIX, miR-212-3p and ADAM10 were verified by dual-luciferase reporter and RNA pulldown assays. Additionally, the xenograft model assays were carried out to analyze the role of circNFIX in tumor growth in vivo. Results: Our data revealed that circNFIX was overexpressed in NSCLC and predicted poor prognosis of NSCLC patients. CircNFIX knockdown suppressed NSCLC cell viability, migration, invasion and glycolysis in vitro and hampered tumor growth in vivo. Mechanistically, CircNFIX acted as a molecular sponge of miR-212-3p, and the repressive effect of circNFIX knockdown on NSCLC cell malignant progression was mediated by miR-212-3p. Moreover, ADAM10 was a direct target of miR-212-3p, and circNFIX influenced ADAM10 expression by sponging miR-212-3p in NSCLC cells. Furthermore, the silencing of ADAM10 hindered NSCLC cell viability, migration, invasion and glycolysis in vitro. Conclusion: Our findings first identified that the knockdown of circNFIX, a highly expressed circRNA in NSCLC, exerted a repressive role in NSCLC malignant progression at least in part through targeting the miR-212-3p/ADAM10 axis, illuminating a novel understanding of circRNA regulation in NSCLC.

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“…It is well known that NFIA plays a carcinogenic role in many human cancers. [35][36][37] For example, high NFIA expression was reported to be firmly related to lymph node metastasis in patients with ESCC. 35 NFIA leads to adverse prognosis and recurrence for GBM patients.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LINC00511 Acts as an Oncogene in Colorectal Cancer via Sponging miR-29c-3p to Upregulate NFIA

Zhang

Ding

et al. 2021

OTT

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Background Colorectal cancer (CRC), characterized by high mortality and incidence rate, is one of the most common types of rectum tumors in the gastrointestinal tract worldwide. An increasing number of investigations indicated that long noncoding RNAs (lncRNAs) have been implicated in the growth of a wide range of cancers. Although it has obtained general acceptance that lncRNA LINC00511 plays a significant role in numerous cancers, the regulatory mechanism of LINC00511 in CRC still needs to be explored. Materials and Methods Bioinformatics analysis and a wide range of experiments of sphere formation assay, cell proliferation assay, RT-qPCR, colony formation assay, Transwell assay and Western blot assays investigated the function and mechanism of LINC00511 in CRC tissues and cells. Results Our results manifested that the expression level of LINC00511 was obviously upregulated in CRC tissues and cells and it accelerated CRC development through facilitating cell proliferation, metastasis and stemness. Molecular mechanism exploration uncovered that LINC00511 acted as a ceRNA competing with NFIA to bind with miR-29c-3p. Through rescue experiments, we discovered that NFIA upregulation partly counteracted the inhibitive effect induced by LINC00511 silencing on CRC progression. Conclusion These results revealed that LINC00511 participated in the progression of CRC by targeting the LINC00511/miR-29c-3p/ NFIA axis, indicating that LINC00511 may be a potential therapeutic target for CRC treatment.

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MiR-212-3p inhibits cell proliferation and promotes apoptosis by targeting nuclear factor IA in bladder cancer

Cited by 22 publications

References 31 publications

ZLM-7 inhibits the occurrence and angiogenesis of breast cancer through miR-212-3p/Sp1/VEGFA signal axis

ZLM-7 inhibits the occurrence and angiogenesis of breast cancer through miR-212-3p/Sp1/VEGFA signal axis

<p>CircNFIX Acts as a miR-212-3p Sponge to Enhance the Malignant Progression of Non-Small Cell Lung Cancer by Up-Regulating ADAM10</p>

LncRNA LINC00511 Acts as an Oncogene in Colorectal Cancer via Sponging miR-29c-3p to Upregulate NFIA

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