Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

Chen, Peijie; Zhao, Liwen; Pan, Xiang; Jin, Lü; Lin, Cheng-Yuan; Xu, Weijie; Xu, Jinling; Guan, Xin; Wu, Xueling; Wang, Yong; Yang, Shangqi; Wang, Tao; Lai, Yongqing

doi:10.3892/ol.2018.8081

Cited by 27 publications

(23 citation statements)

References 33 publications

(37 reference statements)

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“…Taheriazam et al (33) demonstrated that miRNA-130b expression was increased in OS tissues, whereas, the level of miRNA-218 expression was downregulated; these miRNAs may serve as potential biomarkers in the early detection of OS. In this study, it was indicated that the expression of miR-136 was downregulated in the patients with OS, which is consistent with the results in previous studies (34,35). For instance, miR-136 was downregulated and acted as a tumor suppressor in colon cancer (34).…”

Section: Discussionsupporting

confidence: 92%

“…For instance, miR-136 was downregulated and acted as a tumor suppressor in colon cancer (34). In renal cell carcinoma, miR-136 was reported to be downregulated and associated with renal cell carcinoma cellular functions (35). To improve the understanding of the role of miR-136 in OS, its expression patterns and association with the clinicopathological features of the patients with OS were investigated.…”

Section: Discussionmentioning

confidence: 99%

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Downregulation of miR‑136 promotes the progression of osteosarcoma and is associated with the prognosis of patients with osteosarcoma

Chu

Wang

et al. 2019

Oncol Lett

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Osteosarcoma (OS) is the most common bone tumor in children and young adults, and is an aggressive tumor with poor prognosis. MicroRNAs (miRNAs) are aberrantly expressed in various types of cancer, and contribute to cancer tumorigenesis and progression. In the present study, the potential prognostic value and biological function of miRNA-136 (miR-136) in OS was investigated. Reverse transcription-quantitative polymerase chain reaction analysis was used to evaluate the expression of miR-136 in OS tissues and cell lines. Kaplan-Meier survival analysis and Cox regression analysis were conducted to investigate the prognostic significance of miR-136. Various in vitro cell based assays were used to evaluate the effects of miR-136 on the biological behavior of OS cells. A luciferase assay was performed to determine the key miR-136 targets associated with OS. The expression of miR-136 was significantly downregulated in osteosarcoma tissues and cells compared with the normal controls (all P<0.05). Decreased miR-136 expression was significantly associated with Enneking staging (P=0.030) and distant metastasis (P=0.016). Decreased miR-136 expression in patients was associated with shorter overall survival compared with patients with increased expression levels (log-rank test; P<0.05). The expression of miR-136 was indicated as an independent prognostic factor for the patients (hazard ratio= 0.496; 95% confidence interval=0.250-0.987; P=0.046). MTT, transwell and Matrigel assays demonstrated that upregulation of miR-136 decreased proliferation, migration and invasion of OS cells. Bioinformatics and luciferase assays demonstrated that migration and invasion enhancer 1 (MIEN1) is a direct target of miR-136. Together, the results suggested that miR-136 functions as a tumor suppressor gene to regulate proliferation, migration and invasion of OS cells. MIEN1 was a potential target of miR-136. Additionally, miR-136 may serve as a prognostic biomarker for OS.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Downregulation of miR‑136 promotes the progression of osteosarcoma and is associated with the prognosis of patients with osteosarcoma

Chu

Wang

et al. 2019

Oncol Lett

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“…miR-136-5p was reported to serve as a tumor-suppressive miRNA in renal cell carcinoma and has the potential to be used as biomarker for early detection and prognosis prediction. 16 In addition, miR-136-5p was found decreased expression in lung squamous cell cancer and it may interact with UGT1A7 and ADH7 to regulate cellular metabolism processes. 17 We validated the direct connection of FOXP4-AS1 and miR-136-5p using luciferase activity reporter assay.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA FOXP4-AS1 Is Involved in Cervical Cancer Progression via Regulating miR-136-5p/CBX4 Axis</p>

Zhao¹,

Yang²,

Long³

2020

OTT

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Introduction: Cervical cancer (CC) is a major health threat to women worldwide. Long non-coding RNA (lncRNA) has been reported to play crucial roles in regulating carcinogenesis, including CC. Methods: In this work, levels of lncRNA forkhead box P4 antisense RNA 1 (FOXP4-AS1) in CC cell lines and normal cell lines were analyzed with quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) method. Effects of FOXP4-AS1 on CC cellular behaviors including proliferation, migration, and invasion were explored. Bioinformatic prediction tools and luciferase activity reporter assay were conducted to explore the downstream molecules for FOXP4-AS1. Results: We found FOXP4-AS1 expression was significantly higher in CC cell lines than in normal cell line. Functionally, force FOXP4-AS1 expression increased CC cell proliferation, migration, and invasion, while FOXP4-AS1 knockdown caused opposite effects. Mechanistically, we found FOXP4-AS1 acts as competing endogenous RNA (ceRNA) for microRNA-136-5p (miR-136-5p) to regulate chromobox 4 (CBX4) expression. Discussion: These findings indicated FOXP4-AS1 plays an oncogenic role in CC, which may provide novel therapeutic biomarker against CC.

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“…Moreover, the expression of this micro-RNA is inversely correlated with the stage/grade and the metastatic potential of tumors and mammary cell lines. Hsa-miR-136-5p is also described for its tumor suppressor role in the context of prostate cancer, renal carcinomas, pulmonary adenocarcinomas or osteosarcomas [91][92][93][94][95].…”

Section: Post-transcriptional Regulation Of the Expression Of Erα36 Bmentioning

confidence: 99%

The Role of ERα36 in Development and Tumor Malignancy

Thiébaut

Konan

Guerquin

et al. 2020

IJMS

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Estrogen nuclear receptors, represented by the canonical forms ERα66 and ERβ1, are the main mediators of the estrogen-dependent pathophysiology in mammals. However, numerous isoforms have been identified, stimulating unconventional estrogen response pathways leading to complex cellular and tissue responses. The estrogen receptor variant, ERα36, was cloned in 2005 and is mainly described in the literature to be involved in the progression of mammary tumors and in the acquired resistance to anti-estrogen drugs, such as tamoxifen. In this review, we will first specify the place that ERα36 currently occupies within the diversity of nuclear and membrane estrogen receptors. We will then report recent data on the impact of ERα36 expression and/or activity in normal breast and testicular cells, but also in different types of tumors including mammary tumors, highlighting why ERα36 can now be considered as a marker of malignancy. Finally, we will explain how studying the regulation of ERα36 expression could provide new clues to counteract resistance to cancer treatments in hormone-sensitive tumors.

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Tumor suppressor microRNA‑136‑5p regulates the cellular function of renal cell carcinoma

Cited by 27 publications

References 33 publications

Downregulation of miR‑136 promotes the progression of osteosarcoma and is associated with the prognosis of patients with osteosarcoma

Downregulation of miR‑136 promotes the progression of osteosarcoma and is associated with the prognosis of patients with osteosarcoma

<p>LncRNA FOXP4-AS1 Is Involved in Cervical Cancer Progression via Regulating miR-136-5p/CBX4 Axis</p>

The Role of ERα36 in Development and Tumor Malignancy

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