MiR-135a-5p represses proliferation of HNSCC by targeting<i>HOXA10</i>

Guo, Linghong; Ding, Guozhong; Xu, Wencai; Ge, Hong; Chen, Xijuan; Lu, Yufei

doi:10.1080/15384047.2018.1450112

Cited by 42 publications

(33 citation statements)

References 28 publications

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“…The tumor suppressive function of miR-135a in LUAD has been consistently demonstrated in previous studies. For instance, miR-135a-5p promoted the progression of head and neck squamous cell carcinoma by targeting HOXA10 (Guo et al, 2018), the progression of thyroid carcinoma by VCAN (Zhao et al, 2017), and the progression of gastric cancer by KIFC1 (Zhang et al, 2016). Conversely, miR-135a was found to target SIAH1 to promote cell transformation in cervical cancer via the b-catenin pathway (Leung et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA RAET1K Enhances CCNE1 Expression and Cell Cycle Arrest of Lung Adenocarcinoma Cell by Sponging miRNA-135a-5p

Zheng

Ren

et al. 2020

Front. Genet.

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Molecular dysregulation is believed to participate in the onset and progression of lung adenocarcinoma (LUAD). This study aimed to identify and evaluate the potential key long noncoding RNAs (lncRNAs) involved in the significant dysfunctional process of LUAD. We found that lncRNA retinoic acid early transcript 1K (RAET1K) was upregulated in tumor tissues and were correlated with a poor prognosis of patients with LUAD; further, for the first time, we detected the biological roles of RAET1K. Weighted gene correlation network and gene set enrichment analysis revealed that high RAET1K expression is related to cell cycle dysfunction through upregulated cyclin E1 (CCNE1) by targeting miR-135. The dualluciferase reporter gene assay was performed to clarify the binding relationship between RAET1K and miR-135a-5p in transgenic A549 and H1299 cells. Real-time PCR and Western blot analyses showed that RAET1K overexpression and miR-135a-5p inhibition exerted a strong synergistic effect on CCNE1 expression, and cell cycle flow cytometry analysis was used to confirm the arrest of A549 and H1299 cells at the G1/S phase. The lncRNA RAET1K/miR-135a-5p axis might participate in the regulation of LUAD progression by influencing CCNE1 expression and the accumulation of cells arrested at the G1/S phase boundary.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA RAET1K Enhances CCNE1 Expression and Cell Cycle Arrest of Lung Adenocarcinoma Cell by Sponging miRNA-135a-5p

Zheng

Ren

et al. 2020

Front. Genet.

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“…Several researchers have been reported that miR-135a-5p act as a putative tumor suppressor in many cancers by regulating targets expression. For instance, miR-135a-5p inhibited proliferation of neck squamous cell carcinoma via targeting HOXA10 [29]. Moreover, miR-135a-5p regulated cell proliferation, migration and invasion in thyroid carcinoma cells by targeting VCAN 3′UTR [30].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA DANCR knockdown inhibits proliferation, migration and invasion of glioma by regulating miR-135a-5p/BMI1

et al. 2020

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Background: Glioma is the most common and aggressive primary brain tumor with high mortality rate around the world. LncRNAs have been identified to play key roles in tumorigenesis in various cancers, including glioma. However, the precise mechanism of DANCR in progression of glioma remains poorly defined. Methods:The expression levels of DANCR, miR-135a-5p and BMI1 were measured by qRT-PCR in glioma tissues and cells. Cell proliferation, migration and invasion were detected by CCK-8 assay and transwell assay, respectively. The possible binding sites of miR-135a-5p and DANCR or BMI1 were predicted by online software and verified using luciferase report assay and RNA immunoprecipitation (RIP) assay. Western blot analysis was carried out to detect the protein of BMI1 expression. A xenograft tumor model was established to investigate the functions of DANCR in glioma progression in vivo.Results: DANCR was upregulated and miR-135a-5p was downregulated in glioma tissues and cells. Knockdown of DANCR inhibited cell proliferation, migration and invasion in glioma cells. In addition, miR-135a-5p was a direct target of DANCR, and its elevated expression could reverse miR-135a-5p inhibition-mediated progression of glioma. Moreover, miR-135a-5p could specially bind to BMI1, and the expression of BMI1 was obviously elevated in glioma tissues and cells. Furthermore, DANCR acted as a ceRNA to regulate BMI1 expression and BMI1-mediated effects on progression of glioma by sponging miR-135a-5p. Besides, inhibition of DANCR limited tumor growth by regulating miR-135a-5p and BMI1 expression in vivo.Conclusion: DANCR knockdown inhibited cell proliferation, migration and invasion in glioma cells through regulating miR-135a-5p/BMI1 axis, providing viable therapeutic avenues for treatment of glioma.

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“…As an oncogene, miR-135a-5p promotes cell proliferation and metastasis in hepatocellular carcinoma (32,33) and breast cancer (34). However, miR-135a-5p served as an anti-oncogene and targeted HOXA10 to suppress the proliferation of head and neck squamous cell carcinoma (35). Thus, miR-135a-5p may serve a dual role in cancers.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of miRNA‑135a‑5p ameliorates TGF‑β1‑induced human renal fibrosis by targeting SIRT1 in diabetic nephropathy

Zhang

Zha

2020

Int J Mol Med

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miRNA-135a-5p upregulation has been identified in renal fibrosis in diabetic nephropathy (DN) with an incompletely known mechanism. Previous data showed that Sirtuin 1 (SIRT1) serves as a novel therapeutic target for DN and interact with the transforming growth factor-β/mothers against decapentaplegic homolog (TGF-β/Smad) signaling pathway. The aim of this study was to investigate the regulatory relationship between miR-135a-5p and SIRT1. The expression of miR-135a-5p and SIRT1 was detected using reverse transcription-quantitative PCR and western blotting. The renal fibrosis and Smad3 signaling pathway were assessed by western blotting, by analyzing protein expression of collegen1A1, α-smooth muscle actin (α-SMA), fibronectin (FN), epithelial-cadherin, Smad3 and phosphorylated Smad3 (p-Smad3). The target binding between miR-135a-5p and SIRT1 was predicted on TargetScan Human software, and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation. The results demonstrated miR-135a-5p is upregulated and SIRT1 was downregulated in the serum and renal tissue of DN patients, and TGFβ1-induced DN cell models in human HK-2 and HMCs. Knockdown of miR-135a-5p and overexpression of SIRT1 could inhibit TGFβ1-induced renal fibrosis in vitro. Moreover, SIRT1 was a downstream target for miR-135a-5p. Silencing of SIRT1 could abolish the suppressive role of miR-135a-5p knockdown in TGFβ1-induced HK-2 and HMCs. The TGFβ1 induced p-Smad3 expression in HK-2 and HMCs, which could be attenuated by miR-135a-5p knockdown via SIRT1. In conclusion, knockdown of miR-135a-5p inhibits TGFβ1-induced renal fibrosis by targeting SIRT1 and inactivating Smad3 signaling, providing a novel insight into miR-135a-5p as a potential therapeutic approach for DN.

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MiR-135a-5p represses proliferation of HNSCC by targetingHOXA10

Abstract: MiR-135a-5p could repress HNSCC cells proliferation and enhance apoptosis by directly targeting HOXA10, implying miR-135a-5p's significance on HNSCC treatment.

Cited by 42 publications

References 28 publications

Long Noncoding RNA RAET1K Enhances CCNE1 Expression and Cell Cycle Arrest of Lung Adenocarcinoma Cell by Sponging miRNA-135a-5p

Long Noncoding RNA RAET1K Enhances CCNE1 Expression and Cell Cycle Arrest of Lung Adenocarcinoma Cell by Sponging miRNA-135a-5p

Long noncoding RNA DANCR knockdown inhibits proliferation, migration and invasion of glioma by regulating miR-135a-5p/BMI1

Inhibition of miRNA‑135a‑5p ameliorates TGF‑β1‑induced human renal fibrosis by targeting SIRT1 in diabetic nephropathy

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