MiR-205 suppresses epithelial–mesenchymal transition and inhibits tumor growth of human glioma through down-regulation of HOXD9

Dai, Bin; Zhou, Guangyou; Hu, Zhiqiang; Zhu, Guangtong; Mao, Beibei; Su, Housheng; Jia, Qingbin

doi:10.1042/bsr20181989

Cited by 19 publications

(18 citation statements)

References 29 publications

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“…These results suggest that miR-205 may be involved in the regulation of cell proliferation and migration of TC as a tumor inhibitor in TC. This is also consistent with the results of Dai et al (17) and Lu et al (19), which fully indicates that miR-205 may inhibit the proliferation and migration of TC cells. Previous studies have shown that miR-205 is usually an upstream regulator.…”

Section: Discussionsupporting

confidence: 92%

“…Previous studies have shown that miR-205 is usually an upstream regulator. The studies of Dai et al (17) and Lu et al (19) also confirmed that miR-205 plays a role in tumor by regulating its target genes. However, the mechanism of miR-205 inhibiting the proliferation and migration of TC cells is not clear.…”

Section: Discussionmentioning

confidence: 84%

“…miR-30a may be a new therapeutic target for TC. miR-205 is misexpressed in many tumors, Dai et al (17) reported that miR-205 is often underexpressed in glioma tissues. miR-205 can inhibit the growth, invasion and reverse the EMT process of glioma by downregulating its target gene HOXD9.…”

Section: Discussionmentioning

confidence: 99%

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Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

et al. 2020

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This study explored the target of miR-205 and the effect of miR-205 on the proliferation and migration regulating its target in thyroid cancer cells (TC). Twenty-five pairs of TC and adjacent tissues were collected after surgical resection. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the expression of miR-205 in TC tissues and cells (SW579, B-CPAP, TPC-1, WRO). SW579 cells were transfected with miR-205 mimic, and SW579 cells with overexpression of miR-205 were constructed. The effects of miR-205 overexpression on the proliferation and migration of SW579 cells were observed by cell counting kit-8 (CCK-8) and Transwell assays, respectively. Luciferase reporter assay was further used to look for the target of miR-205 and to study the mechanism of miR-205 in the proliferation and migration of TC cells. Compared with normal tissues and cells, the expression of miR-205 was significantly reduced in TC tissues (t=3.47, P= 0.031) and cells (t=5.41, P= 0.016). Overexpression of miR-205 inhibited the proliferation (t=4.12, P= 0.035) and migration (t= 4.47, P= 0.027) of SW579 cells. Luciferase reporter assays found that CCNB2 was a target gene of miR-205 (t= 4.63, P= 0.024), qRT-PCR and western blot assays confirmed there was negatively correlation between CCNB2 and miR-205 (t=3.55, P= 0.029; t=2.86, P= 0.043). CCNB2 overexpression reversed the inhibition of miR-205 on the proliferation (t=3.70, P=0.031) and migration (t=4.12, P=0.022) of SW579 cells. In conclusion, miR-205 inhibits the proliferation and migration of TC cells by targeting CCNB2, which may be a potential target of TC therapy.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 84%

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Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

et al. 2020

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“…MiR-205-5p expression was reduced in pulmonary arterial hypertension and miR-205-5p suppressed the proliferation of pulmonary vascular smooth muscle by binding MICAL2 mRNA [28]. Also, miR-205 could down-regulate HOXD9 expression to suppress EMT and tumor development [29]. In keloid, An et al demonstrated that miR-205-5p up-regulation noticeably hindered cell viability, triggered cell apoptosis, and blocked cell invasion and migration ability in human keloid fibroblasts [22].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA CACNA1G-AS1 promotes proliferation and invasion and inhibits apoptosis by regulating expression of miR-205 in human keloid fibroblasts

et al. 2020

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Background: Keloid is a fibrous tissue proliferative disease in which proliferative scars grow beyond the boundary of the original wound skin. Long non-coding RNAs (lncRNAs), as competing endogenous RNAs (ceRNAs), bind to microRNAs (miRNAs) to regulate various biological processes. The present study was aim to illuminate the mechanism of calcium voltage-gated channel subunit alpha1 G antisense RNA 1 (CACNA1G-AS1) in human keloid fibroblasts. Methods: CACNA1G-AS1 and miR-205 levels were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Cell Counting Kit-8 (CCK-8) assay was used to measure the proliferation and transwell assay was performed to evaluate cell invasion. Furthermore, the apoptosis rates of cells were evaluated by flow cytometry analysis, and the activity of caspase-3 in keloid fibroblasts was tested by Caspase-3 activity assay. Dual luciferase reporter assay was carried out to examine the relationship between CACNA1G-AS1 and miR-205 and RNA immunoprecipitation (RIP) assay was conducted to further confirm the relation. Results: CACNA1G-AS1 level was up-regulated in keloid tissues and keloid fibroblasts. CACNA1G-AS1 overexpression promoted proliferation and invasion and suppressed apoptosis of keloid fibroblasts. Moreover, miR-205 was targeted by CACNA1G-AS1 and miR-205 was markedly decreased in keloid tissues and keloid fibroblasts. Also, miR-205 expression was negatively regulated by CACNA1G-AS1 and miR-205 silencing enhanced proliferation and invasion and inhibited apoptosis. Furthermore, CACNA1G-AS1 and miR-205 played the antagonistic role in miR-205 expression, proliferation, invasion, and apoptosis of keloid fibroblasts. Conclusion: CACNA1G-AS1 suppressed miR-205 expression to promote proliferation and invasion and inhibit apoptosis in human keloid fibroblasts.

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“…Bao et al 19 discovered through a bioinformatic analysis that the HOXD gene family is specifically upregulated in human lung squamous carcinoma, including HOXD9. In another glioma study, 20 it was discovered that miR-205 could downregulate HOXD9, suppress epithelial-mesenchymal transition in tumor cells, and inhibit growth of human glioma. However, the relationship between HOXD9 and GC has not yet been reported.…”

Section: Discussionmentioning

confidence: 99%

<p>HOXD9 Activates the TGF-β/Smad Signaling Pathway to Promote Gastric Cancer</p>

Xiong¹,

Yin²,

Gao³

et al. 2020

OTT

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Background: Gastric cancer (GC) is the most common malignant tumor of the digestive tract and its molecular mechanism is not clear. HOXD9 plays an important role in tumor progression as transcription factor. In the current study, we explored the role of HOXD9 in GC. Methods: We predicted the expression and potential mechanism of HOXD9 in GC through an online database. The expression of HOXD9 was detected in GC and adjacent tissues, and then we analyzed the relationship between HOXD9 and the prognosis of patients with GC. In vitro, we investigated the effects of HOXD9 on malignant biological behaviors such as proliferation, migration, and invasion of the GC cell line MCG-803. In addition, we have initially studied the underlying mechanism by Western blot. Results: High expression of HOXD9 in GC was predicted by online database prediction and implied poor prognosis. In the clinical sample, we confirmed the above predictions. In vitro, we found that knockdown of HOXD9 could effectively inhibit the proliferation, migration, and invasion of GC cells. In terms of mechanism, HOXD9 may activate the TGF-β/Smad signaling pathway. Conclusion: HOXD9 promotes the malignant biological process of GC, which may be a potential therapeutic target for GC.

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MiR-205 suppresses epithelial–mesenchymal transition and inhibits tumor growth of human glioma through down-regulation of HOXD9

Cited by 19 publications

References 29 publications

Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

Effect of miR‑205 on proliferation and migration of thyroid cancer cells by targeting CCNB2 and the mechanism

Long non-coding RNA CACNA1G-AS1 promotes proliferation and invasion and inhibits apoptosis by regulating expression of miR-205 in human keloid fibroblasts

<p>HOXD9 Activates the TGF-β/Smad Signaling Pathway to Promote Gastric Cancer</p>

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