MicroRNA-145 promotes esophageal cancer cells proliferation and metastasis by targeting SMAD5

Zhang, Qiong; Gan, Hui-Li; Song, Wenqing; Chai, Damin; Wu, Shiwu

doi:10.1080/00365521.2018.1476913

Cited by 25 publications

(21 citation statements)

References 26 publications

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“…Next, 38 overlapping genes were selected through intersecting the predicted target genes scoring over 75 in the miRDB database, scoring over 0.85 in the mirDIP database and the top 50% in the other databases (Figure 1G). Furthermore, it has been previously reported that the SMAD5 gene plays an important regulatory role in a variety of tumors (15,16). The KEGG database indicates that SMAD5 is closely associated with the TGF-β signaling pathway (map04350), which is considered to be one of the key pathways in the regulation of NPC progression (17)(18)(19).…”

Section: Resultsmentioning

confidence: 99%

Silencing of Long Non-coding RNA SMAD5-AS1 Reverses Epithelial Mesenchymal Transition in Nasopharyngeal Carcinoma via microRNA-195-Dependent Inhibition of SMAD5

Zhao

Shang

et al. 2019

Front. Oncol.

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Long non-coding RNAs (lncRNAs) have gained widespread attention in recent years as a key regulator of diverse biological processes, but the knowledge of the mechanisms by which they act is still very limited. Differentially expressed lncRNA SMAD5 antisense RNA 1 (SMAD5-AS1) in nasopharyngeal carcinoma (NPC) and normal samples shown by in silico analyses were selected as the main subject, and then was suggested to bind to SMAD5-AS1 and SMAD5. Therefore, the purpose of the present study was to investigate the effects of SMAD5-AS1/miR-195/SMAD5 on epithelial-mesenchymal transition (EMT) in NPC cells. High expression of SMAD5-AS1 and SMAD5 but low miR-195 expression was determined in NPC tissues and NPC cell lines by RT-qPCR and western blot analysis. SMAD5-AS1 could upregulate SMAD5 expression by competitively binding to miR-195 in NPC cells. Loss-and gain-of-function investigations were subsequently conducted in NPC cells (CNE-2 and CNE-1) to explore the role of SMAD5-AS, miR-195 and SMAD5 in NPC progression by assessing cellular biological functions and tumorigenic ability in vivo as well as determining the expression of EMT markers. Downregulation of SMAD5-AS1 or SMAD5 or overexpression of miR-195 led to inhibited NPC cell proliferation, invasion and migration and reversed EMT, enhanced apoptosis in vitro as well as restrained tumor growth in vivo. In conclusion, our findings indicate that silencing of lncRNA SMAD5-AS1 induces the downregulation of SMAD5 by miR-195, eventually repressing EMT in NPC. Hence, SMAD5-AS1 may represent a potential therapeutic target for NPC intervention.

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Section: Resultsmentioning

confidence: 99%

Silencing of Long Non-coding RNA SMAD5-AS1 Reverses Epithelial Mesenchymal Transition in Nasopharyngeal Carcinoma via microRNA-195-Dependent Inhibition of SMAD5

Zhao

Shang

et al. 2019

Front. Oncol.

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“…miR‐145 is a newly discovered miRNA, which is significantly less expressed in breast cancer (Ding et al, ), cervical cancer (Sathyanarayanan et al, ), glioma (Xu et al, ), colon cancer (Li et al, ), esophageal cancer (Zhang et al, ), and non‐small‐cell lung cancer (Yin et al, ). The genes regulated by miRNA‐145 are different in different tumors, and the molecular mechanisms of their anti‐cancer effects are also different.…”

Section: Discussionmentioning

confidence: 99%

miR‐145 inhibits glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells

et al. 2019

Cell Biology International

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miR‐145 has been found to be a participant in cancer metastasis and glucose metabolism in ovarian cancer. However, the role of glutamine metabolism in ovarian cancer remains unclear. In this study, we aim to elucidate the molecular mechanism underlying the regulation of glutamine metabolism by miR‐145 in ovarian cancer cells. The messenger RNA (mRNA) levels of miR‐145 and glutaminase 1 (GLS1) were examined by quantitative real‐time polymerase chain reaction (qRT‐PCR). The protein levels of c‐myc and GLS1 were detected by western blot analysis. Luciferase reporter assays were used to validate c‐myc was a target of miR‐145. Glutamine metabolism was analyzed using assay kits. In addition, we performed luciferase reporter assays and chromatin immunoprecipitation assay to validate c‐myc transcription activated GLS1 and promoted GLS1 expression. The qRT‐PCR demonstrated that the mRNA level of miR‐145 and GLS1 was negatively correlated in ovarian cancer tissues and cell lines. Kaplan–Meier survival analysis and the log‐rank test showed that patients with high miR‐145 expression had significantly increased the overall survival. The overexpression of miR‐145 inhibited glutamine consumption, α‐ketoglutarate production, and cellular ATP levels. Furthermore, we found miR‐145 inhibited glutamine metabolism by targeting c‐myc. Moreover, c‐myc could promote GLS1 expression by transcription activated. Together, our results revealed that miR‐145 inhibited glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells, which may improve the current strategy of ovarian cancer diagnosis and therapy.

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“…[ 38 ] For SMAD5, it has been reported that miR-145 can promote the migration and migration of esophageal cancer cells by inhibiting theexpression of SMAD5. [ 39 ] Fstl1 can promote glioma growth through SMAD1/SMAD5/SMAD8. [ 40 ] At the same time, SMAD5 expression increases in prostate cancer, which is closely related to postoperative survival.…”

Section: Discussionmentioning

confidence: 99%

Integrated TCGA and GEO analysis showed that SMAD7 is an independent prognostic factor for lung adenocarcinoma

et al. 2020

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MicroRNA-145 promotes esophageal cancer cells proliferation and metastasis by targeting SMAD5

Abstract: Our study uncovered the crucial role of miR-145/SMAD5 in esophageal cancer and highlighted its target potential for diagnostic and therapeutic purpose.

Cited by 25 publications

References 26 publications

Silencing of Long Non-coding RNA SMAD5-AS1 Reverses Epithelial Mesenchymal Transition in Nasopharyngeal Carcinoma via microRNA-195-Dependent Inhibition of SMAD5

Silencing of Long Non-coding RNA SMAD5-AS1 Reverses Epithelial Mesenchymal Transition in Nasopharyngeal Carcinoma via microRNA-195-Dependent Inhibition of SMAD5

miR‐145 inhibits glutamine metabolism through c‐myc/GLS1 pathways in ovarian cancer cells

Integrated TCGA and GEO analysis showed that SMAD7 is an independent prognostic factor for lung adenocarcinoma

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