Identification of eight key miRNAs associated with renal cell carcinoma: A meta‑analysis

Ying, Guanghui; Wu, Ruilan; Xia, Min; Fei, Xiapei; Zha, Chenqin; Wu, Fengyuan

doi:10.3892/ol.2018.9384

Cited by 17 publications

(24 citation statements)

References 36 publications

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“…Increasing numbers of studies indicate that miR-362-5p promotes cell proliferation, tumor growth, and metastasis in hepatocellular carcinoma, human breast cancer, and lung cancer (Ni et al, 2015;Ni et al, 2016;Luo et al, 2018). However, miR-362-5p inhibits proliferation and migration of neuroblastoma cells and it is downregulated in renal cell carcinoma (Wu et al, 2015;Ying et al, 2018). It indicates that miR-362-5p could play oncogenic or suppressive roles in progression of these cancers.…”

Section: Introductionmentioning

confidence: 99%

MiR-362-5p, Which Is Regulated by Long Non-Coding RNA MBNL1-AS1, Promotes the Cell Proliferation and Tumor Growth of Bladder Cancer by Targeting QKI

Wei

Wang

et al. 2020

Front. Pharmacol.

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In this study, we found miR-362-5p was upregulated in bladder cancer tissues and we predicted that QKI is potential a target of miR-362-5p and MBNL1-AS1 might be able to directly target to miR-362-5p. We attempted to evaluate whether miR-362-5p could play its roles in bladder cancer through regulating QKI (quaking) and whether the expression and function of miR-362-5p could be mediated by lncRNA MBNL1-AS1. We performed the gain-and loss-function experiments to explore the association between miR-362-5p expression and bladder cancer proliferation. In vivo, the nude mice were injected with miR-362-5p knockdown SW780 cells to assess the effects of miR-362-5p on tumor growth. The results showed upregulation of miR-362-5p promoted cell proliferation of bladder cancer cells. MBNL1-AS1 and QKI could directly bind with miR-362-5p, and knockdown of MBNL1-AS1 or QKI could abrogate the regulatory effects of miR-362-5p on bladder cancer cell proliferation. Furthermore, downregulation of miR-362-5p inhibited bladder tumor growth and increased QKI expression. Our data unveiled that miR-362-5p may play an oncogenic role in bladder cancer through QKI and MBNL1-AS1 might function as a sponge to mediate the miR-362-5p expression and function.

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Section: Introductionmentioning

confidence: 99%

MiR-362-5p, Which Is Regulated by Long Non-Coding RNA MBNL1-AS1, Promotes the Cell Proliferation and Tumor Growth of Bladder Cancer by Targeting QKI

Wei

Wang

et al. 2020

Front. Pharmacol.

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“…Another inhibitor for PD-L1 expression is miR-138-5p, which can be considered as a tumor suppressor that is commonly deficient in colorectal cancer (CRC) and linked to poor clinical outcomes [18]. miR-138-5p was recently identified as one of the key miR-NAs dysregulated in renal cell carcinoma (RCC) [21]. The expression of miR-138 is also reduced in squamous cell carcinoma of the head and neck, thyroid, and ovarian tumors [19,20].…”

Section: Mirnas Direct Regulation Of Pd-l1 Expressionmentioning

confidence: 99%

“…The expression of miR-138 is also reduced in squamous cell carcinoma of the head and neck, thyroid, and ovarian tumors [19,20]. miR-138-5p was recently identified as one of the key miR-NAs dysregulated in renal cell carcinoma (RCC) [21]. miR-138-5p mimics were shown to inhibit the cell proliferation and invasion of RCC cell lines [22].…”

Section: Mirnas Direct Regulation Of Pd-l1 Expressionmentioning

confidence: 99%

Immunomodulatory MicroRNAs in cancer: targeting immune checkpoints and the tumor microenvironment

et al. 2019

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Cancer immunotherapy represents a promising new era in cancer management due to the relatively high safety margins and selectivity, compared to the classical cancer chemotherapeutic agents. However, there is an imperative need to overcome tumor resistance in order to improve clinical outcomes and maximize the benefits of cancer immunotherapy. The interaction between the programmed cell death‐1 (PD‐1) receptor and its ligand PD‐L1 is a vital immune checkpoint that is often adopted by cancer cells to undergo immune evasion. PD‐1/PD‐L1 signaling is regulated at multiple levels through the crosstalk with other immune targets or relevant signaling partners involved in the cancer progression. Among the significant epigenetic players that are implicated in modulating the immune system are microRNAs (miRNAs). A complex system of these noncoding RNAs regulates the gene expression at the post‐transcriptional level and plays a significant role in the modulation of both innate and the adaptive immune systems. The expression profile of immune‐modulatory miRNAs might be useful as a predictive biomarker for the response and clinical outcomes in cancer immunotherapy. Therefore, in the current review, we highlighted the role of miRNAs in cancer immune evasion through a critical discussion of their impact on key immune checkpoints as well as the role of miRNAs in cancer progression and resistance.

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“…MicroRNAs (miRNAs) are small non-coding RNAs (~22 nucleotides in length) that regulate gene expression on a post-transcriptional level through base-pairing with complementary sequences of the 3'untranslated region (UTR) of mRNAs (8). Recent studies demonstrated that miR-720 and eight other miRNAs serve crucial roles in RCC (9,10). For example, miR-92a-3p has been reported to serve a crucial role in the progression of various types of cancer, including lung cancer, esophageal squamous cell carcinoma, colorectal, breast, ovarian, and cervical cancer (11)(12)(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Cell proliferation is induced in renal cell carcinoma through miR‑92a‑3p upregulation by targeting FBXW7

et al. 2020

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Renal cell carcinoma (RCC) is the most common type of kidney cancer whose incidence has gradually increased worldwide. MicroRNAs (miRNAs) represent a type of short endogenous non-coding RNA containing approximately 22 nucleotides, which are capable of regulating mRNAs at the post-transcriptional level in human cells. miRNAs have been demonstrated to mediate gene expression by influencing important regulatory genes. Accumulating evidence indicates that certain miRNAs are involved in RCC development. The present study investigated the underlying mechanism and functional role of miR-92a-3p in RCC cells using reverse transcription-quantitative polymerase chain reaction, western blotting, 3' UTR luciferase assay, cell proliferation assay and soft agar assay. The results demonstrated that miR-92a-3p expression level is significantly upregulated in RCC tissues and cell lines; however, F-box and WD repeat domain containing 7 (FBXW7) expression level was significantly downregulated in RCC tissues and cell lines. Subsequently, whether FBXW7 could be considered as a direct target of miR-92a-3p in RCC cells was investigated. The results demonstrated that miR-92a-3p overexpression significantly promoted RCC cell proliferation and colony formation. Conversely, miR-92a-3p downregulation significantly inhibited RCC cell proliferation and colony formation. In addition, FBXW7 knockdown significantly enhanced RCC cell proliferation and colony formation. Conversely, FBXW7 overexpression significantly inhibited RCC cell proliferation and colony formation. Collectively, these results demonstrated that miR-92a-3p/FBXW7 pathway may represent a novel strategy and therapeutic target for RCC.

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Identification of eight key miRNAs associated with renal cell carcinoma: A meta‑analysis

Cited by 17 publications

References 36 publications

MiR-362-5p, Which Is Regulated by Long Non-Coding RNA MBNL1-AS1, Promotes the Cell Proliferation and Tumor Growth of Bladder Cancer by Targeting QKI

MiR-362-5p, Which Is Regulated by Long Non-Coding RNA MBNL1-AS1, Promotes the Cell Proliferation and Tumor Growth of Bladder Cancer by Targeting QKI

Immunomodulatory MicroRNAs in cancer: targeting immune checkpoints and the tumor microenvironment

Cell proliferation is induced in renal cell carcinoma through miR‑92a‑3p upregulation by targeting FBXW7

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