&lt;p&gt;MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/&amp;beta;-catenin pathway&lt;/p&gt;

Wang, Shuai; Du, Shanshan; Lv, Yong; Zhang, Fengyan; Wang, Wenzhan

doi:10.2147/cmar.s200566

Cited by 19 publications

(23 citation statements)

References 43 publications

(50 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the field of RB research, a variety of different miRNAs have been revealed to be aberrantly expressed, and their anomalous expression plays important roles in the regulation of multiple cancer-related processes, including cell survival, proliferation, apoptosis, metastasis, angiogenesis and epithelial-mesenchymal transition (10). For instance, miR-98 (11), miR-186 (12) and miR-665 (13) are weakly expressed in RB and restrain tumor progression; on the contrary, miR-93 (14), miR-106b (15) and miR-198 are overexpressed in RB and promote tumor aggressiveness. miR-936 has been reported to exert important effects on the progression of non-small cell lung cancer (16) and glioma (17).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway

Shi³

et al. 2020

Oncol Rep

View full text Add to dashboard Cite

MicroRNA-936 (miR-936) has been reported to play important roles in the progression of non-small cell lung cancer and glioma. However, the expression and functions of miR-936 in retinoblastoma (RB) remain elusive and need to be further elucidated. Herein, the aims were to measure miR-936 expression in RB, identify the functional importance of miR-936 in the oncogenicity of RB, and investigate the underlying molecular mechanisms. Reverse-transcription quantitative PCR was carried out to determine miR-936 expression in RB tissues and cell lines. Cell proliferation, colony formation, apoptosis, migration, and invasion in vitro and tumor growth in vivo were examined respectively by Cell Counting Kit-8, colony formation, flow cytometric, and Transwell migration and invasion assays and a subcutaneous heterotopic xenograft experiment. The potential target of miR-936 was predicted by bioinformatic analysis and was subsequently validated by luciferase reporter assay, reverse-transcription quantitative PCR, and western blotting. miR-936 expression was weak in both RB tissues and cell lines and was correlated with differentiation, lymph node metastasis and TNM staging in RB. RB cell proliferation, colony formation, migration, and invasion in vitro and tumor growth in vivo were attenuated by exogenous miR-936, whereas apoptosis was enhanced by miR-936 overexpression. Further molecular investigation identified histone deacetylase 9 (HDAC9) as a direct target gene of miR-936 in RB cells. HDAC9 depletion had effects similar to those of miR-936 overexpression in RB cells. Recovery of HDAC9 expression counteracted the tumor-suppressive action of miR-936 on the oncogenicity of RB cells. Ectopic miR-936 expression deactivated the PI3K/AKT pathway in RB cells in vitro and in vivo by decreasing HDAC9 expression. Downregulated miR-936 is related to poor prognosis in RB, and its upregulation inhibits RB aggressiveness via direct targeting of HDAC9 mRNA and thereby inactivation of the PI3K/AKT pathway.

show abstract

Section: Introductionmentioning

confidence: 99%

MicroRNA‑936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway

Shi³

et al. 2020

Oncol Rep

View full text Add to dashboard Cite

show abstract

“…Recent research has revealed that miR-665 can regulate EMT-related proteins by targeting mRNAs in various cancers. 16,17 It has also been reported that miR-665 is down-regulated in osteosarcoma, 18 retinoblastoma, 19 and ovarian cancer, 20 but is up-regulated in non-small cell lung cancer 21 and breast cancer. 22 However, the functional role of miR-665 in GC remains unclear.…”

Section: Introductionmentioning

confidence: 97%

<p>miR-665 Suppresses the Epithelial–Mesenchymal Transition and Progression of Gastric Cancer by Targeting <em>CRIM1</em></p>

Zhang

Pei

et al. 2020

CMAR

View full text Add to dashboard Cite

Background: Gastric cancer (GC) is one of the most common aggressive cancers and is characterized by high mortality. Increasing evidence has shown that microRNA-665 (miRNA-665) serves as inhibiting-miRNA in cancers. However, the role of miR-665 in GC is yet unclear. Methods: miR-665 was first analyzed using bioinformatics. Subsequent quantitative realtime PCR was used to detect miR-665 expression levels in different GC cell lines and tissues. The function of miR-665 in GC cells was determined via Cell Counting Kit 8, colony formation, wound healing, and transwell assays. Furthermore, Western blotting was utilized to measure the expression level of epithelial-mesenchymal transition (EMT)-related proteins. The target prediction and luciferase reporter assays were performed to confirm the binding between miR-665 and 3ʹ-UTR of the CRIM1 gene. In addition, rescue assays were used to determine whether CRIM1 upregulation abolished the inhibitory effect of miR-665. Results: The expression of miR-665 was significantly decreased in GC patients and GC cell lines. Clinical and pathological analyses showed that the low expression of miR-665 was significantly associated with high TNM stage (P = 0.007), distant metastasis (P = 0.031), and poor differentiation (P = 0.029). Endogenic mimics of miR-665 remarkably suppressed GC cell proliferation, migration, invasion, and EMT in in vitro experiments. Inhibition of miR-665 expression induced the opposite effects. The results of the bioinformatics analysis and dual-luciferase assay showed that miR-665 targeted the 3ʹ-UTR of the CRIM1 gene. Rescue assays revealed that overexpression of CRIM1 attenuated the inhibitory effects of miR-665 in GC progression and EMT. Conclusion: The overall study results demonstrated that miR-665 inhibits tumor progression and EMT in GC by targeting CRIM1, indicating that miR-665 might be a potential therapeutic target in the treatment of GC patients.

show abstract

“…Accumulated evidence has confirmed the crucial regulatory role of miRNAs in diverse physiological and pathological processes, including cell proliferation, cell death, differentiation, metabolism, and even carcinogenesis [12][13][14]. A number of miRNAs are aberrantly expressed during the genesis and progression of RB [15][16][17]. Thus, it is urgently necessary to examine the specific functions of miRNAs in RB and to delineate their mechanism of action.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC00324 promotes retinoblastoma progression by acting as a competing endogenous RNA for microRNA-769-5p, thereby increasing STAT3 expression

Dong

Wan

Yan

et al. 2020

Aging

View full text Add to dashboard Cite

Long intergenic non-protein-coding RNA 324 (LINC00324) is abnormally expressed in multiple human cancer types and plays an important role in cancer initiation and progression. This study showed that LINC00324 was expressed at higher levels in retinoblastoma (RB) tumors and cell lines than in control samples. Increased LINC00324 expression closely correlated with the TNM stage, optic nerve invasion, and shorter overall survival among patients with RB. The knockdown of LINC00324 decreased RB cell proliferation, colony formation, migration, and invasion, and promoted apoptosis and cell cycle arrest in vitro as well as hindered tumor growth in vivo. With respect to the mechanism, LINC00324 acted as a competing endogenous RNA for microRNA-769-5p (miR-769-5p) in RB cells. The mRNA of signal transducer and activator of transcription 3 (STAT3) was identified as a direct target of miR-769-5p in RB cells. Rescue experiments indicated that restoration of STAT3 expression attenuated the tumor-suppressive actions of miR-769-5p in RB cells. Downregulation of miR-769-5p or restoration of STAT3 almost completely reversed the effects of LINC00324 knockdown on RB cells. Our findings describe a novel RB-related LINC00324-miR-769-5p-STAT3 axis that is implicated in the malignancy of RB in vitro and in vivo. This study may point to innovative therapeutic targets in RB.

show abstract

<p>MicroRNA-665 inhibits the oncogenicity of retinoblastoma by directly targeting high-mobility group box 1 and inactivating the Wnt/β-catenin pathway</p>

Cited by 19 publications

References 43 publications

MicroRNA‑936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway

MicroRNA‑936 inhibits the malignant phenotype of retinoblastoma by directly targeting HDAC9 and deactivating the PI3K/AKT pathway

<p>miR-665 Suppresses the Epithelial–Mesenchymal Transition and Progression of Gastric Cancer by Targeting <em>CRIM1</em></p>

Long noncoding RNA LINC00324 promotes retinoblastoma progression by acting as a competing endogenous RNA for microRNA-769-5p, thereby increasing STAT3 expression

Contact Info

Product

Resources

About