RETRACTED: miR-613 inhibits proliferation and invasion of breast cancer cell via VEGFA

Wu, Jin‐Lei; Yuan, Peng; Mao, Qixin; Lü, Peng; Xie, Tian; Yang, Hanzhao; Wang, Chengzheng

doi:10.1016/j.bbrc.2016.07.031

Cited by 29 publications

(24 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…VEGFA is a member of the PDGF/VEGF growth factor family which encodes a heparin-binding protein that plays predominant roles in angiogenesis by inducing proliferation and migration of vascular endothelial cells. It is upregulated in many known tumors and its expression is correlated with tumor stage and progression (28)(29)(30). Cdc42 is a small GTPase of the Rho-subfamily which regulates cytoskeletal dynamics, cell shape, and numerous other cellular processes including polarity, migration, cell cycle progression and cell fate determination.…”

Section: Snhg15 Affects the Growth Of Glioma Microvascular Endotheliamentioning

confidence: 99%

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

Xue

Liu

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

Malignant glioma, the most common intracranial primary tumor, is characterized by increased angiogenesis. Accumulating evidence has shown that long non-coding RNAs (lncRNAs) play an important role in a variety of biological behaviors of tumors. However, the role of lncRNAs in the regulation of glioma vascular endothelial cell function remains to be investigated. To simulate the glioma microenvironment, we applied glioma conditioned medium (GCM) to human cerebral microvascular endothelial cells (hCMECs). In the present study, the lncRNA SNHG15 was found to be highly expressed in glioma vascular endothelial cells. Cell Counting Kit-8 (CCK-8), migration and tube formation assays demonstrated that knockdown of SNHG15 inhibited glioma vascular endothelial cell proliferation, migration and tube formation in vitro. Furthermore, knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42, which are known to promote angiogenesis. Bioinformatics software and dual-luciferase system analysis confirmed that SNHG15 affected endothelial cell function by targeting miR-153. Additionally, the present study showed that miR-153 targeted the 3'‑untranslated region of VEGFA and Cdc42 and downregulated their expression. In conclusion, knockdown of SNHG15 downregulated the expression of VEGFA and Cdc42 by targeting miR-153, consequently suppressing glioma vascular endothelial cell proliferation, migration and tube formation. Therefore, SNHG15 and miR-153 are new potential therapeutic targets for anti-angiogenesis treatment of glioma.

show abstract

Section: Snhg15 Affects the Growth Of Glioma Microvascular Endotheliamentioning

confidence: 99%

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

Xue

Liu

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

show abstract

“…26,30,31 Currently, increasing studies suggested that miR-613 played pivotal roles in the initiation and progression of some tumors. [32][33][34][35][36][37][38][39] For examples, Li et al 36 found that miR-613 expression level was downregulated in the osteosarcoma cell lines and samples. Elevated expression of miR-613 suppressed osteosarcoma cell proliferation and colony formation through regulating c-MET expression.…”

Section: Discussionmentioning

confidence: 99%

“…**P < 0.01carcinoma cell proliferation, migration, and invasion by suppressing sphingosine kinase 2 (SphK2) expression. Wu et al39 showed that overexpression of miR-613 suppressed breast cancer cell invasion, migration, and proliferation through targeting VEGFA. However, the function and expression of miR-613 in the LSCC remain unknown.…”

mentioning

confidence: 99%

MiR‐613 suppressed the laryngeal squamous cell carcinoma progression through regulating PDK1

Wang

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are aberrantly expressed in several tumors and play important role in tumorigenesis. However, little is known about the role of miR-613 in laryngeal squamous cell carcinoma (LSCC). We determined the expression of miR-613 in a panel of 30 LSCC specimens. Compared with the adjacent normal samples, 20 cases of LSCC tissues exhibited decreased expression of miR-613. The average expression of miR-613 in LSCC tissues was lower than in normal samples. Moreover, we demonstrated that exogenous expression of miR-613 suppressed LSCC cell proliferation, invasion, and blocked G1/S phase transition. We identified that 3-phosphoinositide-dependent protein kinase-1 (PDK1) was a direct target gene of miR-613 in LSCC cell. Overexpression of miR-613 suppressed PDK1 expression in LSCC cell. Furthermore, we demonstrated that PDK1 was upregulated in LSCC tissues. MiR-613 expression was inversely correlated with the expression of PDK1 in LSCC tissues. Moreover, we showed that PDK1 was involved in the miR-613-mediated cancer suppression of LSCC cell. These results suggested that miR-613 played as a tumor suppressor gene in LSCC partly by inhibiting PDK1 expression.

show abstract

“…14 Zhang et al proved that miR-155-3p reversed PTX resistance through the negative interaction with MYD88 in BC. 15 Previous reports demonstrated that miR-613 was down-regulated in BC 16 and impeded the production of PTX resistance in triple-negative BC. 17 However, it needs further exploration of the molecular mechanism behind miR-613 in PTX resistance of BC.…”

Section: Introductionmentioning

confidence: 98%

<p>Long Non-Coding RNA UCA1 Modulates Paclitaxel Resistance in Breast Cancer via miR-613/CDK12 Axis</p>

Liu¹,

Jiang²,

Zhang³

et al. 2020

CMAR

View full text Add to dashboard Cite

Background: Paclitaxel (PTX) occupies a considerable status in the chemotherapies of breast cancer (BC), but the drug resistance keeps an obstructive factor of PTX treatment. This study was designed to explore the molecular mechanism of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) in PTX resistance of BC. Methods: UCA1, microRNA-613 (miR-613) and cyclin-dependent kinase 12 (CDK12) expression was assayed through quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay was implemented for evaluating the half inhibitory concentrations (IC 50) of PTX and cell viability. Cell apoptosis was examined by flow cytometry. The target relationship was explored using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. CDK12 protein level was detected through Western blot. Xenograft tumor assay was applied for assessing the influence of UCA1 on PTX resistance of BC in vivo. Results: UCA1 expressed highly in PTX-resistant BC tissues and cells and regulated PTX resistance in BC cells by affecting cell viability and apoptosis in part. UCA1 negatively interacted with miR-613 and modulated PTX resistance via sponging miR-613. CDK12 was a downstream gene of miR-613 and miR-613 exerted the modulation of PTX resistance via targeting CDK12. Furthermore, UCA1 regulated CDK12 level through interacting with miR-613. The regulatory role of UCA1 in PTX resistance of BC was achieved by miR-613/ CDK12 axis in vivo. Conclusion: UCA1 mediated PTX resistance in BC through the miR-613/CDK12 axis, manifesting that UCA1 might improve the PTX treatment of BC as a significant therapeutic biomarker.

show abstract

RETRACTED: miR-613 inhibits proliferation and invasion of breast cancer cell via VEGFA

Cited by 29 publications

References 21 publications

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153

MiR‐613 suppressed the laryngeal squamous cell carcinoma progression through regulating PDK1

<p>Long Non-Coding RNA UCA1 Modulates Paclitaxel Resistance in Breast Cancer via miR-613/CDK12 Axis</p>

Contact Info

Product

Resources

About