miR-615 Fine-Tunes Growth and Development and Has a Role in Cancer and in Neural Repair

Godínez-Rubí, Marisol; Ortuño-Sahagún, Daniel

doi:10.3390/cells9071566

Cited by 19 publications

(12 citation statements)

References 94 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Then, we found circRNA_100146 may be a target of miR-615-5p. Previously, many studies have reported miR-615-5p served as a tumor promoter in several tumors ( Guan et al, 2019 ; Godínez-Rubí and Ortuño-Sahagún, 2020 ). In PCa, miR-615-5p was shown to suppress the ability of proliferation and metastasis of tumor cells ( Li et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Hsa_circRNA_100146 Promotes Prostate Cancer Progression by Upregulating TRIP13 via Sponging miR-615-5p

Zeng

Liu

Yang

et al. 2021

Front. Mol. Biosci.

View full text Add to dashboard Cite

Objective: This study was conducted for investigating the functions of circular RNA circRNA_100146 (circRNA_100146) in the development of prostate cancer (PCa) and identifying the underlying mechanisms of the circRNA_100146/miR-615-5p/TRIP13 axis.Materials and Methods: Under the support of RT-PCR, the expression of circRNA_100146 in PCa cells was examined. Cell Counting Kit-8 (CCK-8) assays and clone formation assays were applied to the assessment of cell proliferation. We then determined cell invasion and migration through transwell assays and wound healing assays. RNA pull-down assays and luciferase reporter assays were performed for the exploration of the regulatory effects of potential molecules on the expressions of the targeting genes. In addition, a nude mouse xenograft model was applied to demonstrate the oncogenic roles of circRNA_100146 in PCa.Results: CircRNA_100146 expression was distinctly upregulated in PCa cells. Silencing of circRNA_100146 suppressed PCa cells’ invasion, migration, and proliferation. CircRNA_100146 sponged miR-615-5p to suppress its expressions, while miR-615-5p targeted the 3’-UTR of TRIP13 to repress the expression of TRIP13. In addition, we observed that knockdown of miR-615-5p reversed the suppression of circRNA_100146 silence on the proliferation and invasion of PCa cells. In addition, the tumor growth was also suppressed by silencing circRNA_100146 in vivo.Conclusion: CircRNA_100146 is a tumor promoter in PCa, which promoted progression by mediating the miR-615-5p/TRIP13. CircRNA_100146 can be a potential candidate for targeted therapy of PCa.

show abstract

Section: Discussionmentioning

confidence: 99%

Hsa_circRNA_100146 Promotes Prostate Cancer Progression by Upregulating TRIP13 via Sponging miR-615-5p

Zeng

Liu

Yang

et al. 2021

Front. Mol. Biosci.

View full text Add to dashboard Cite

show abstract

“…MiRNAs are upstream mediators of a variety of molecular pathways due to their role in coordinating detailed biological mechanisms [128][129][130][131][132][133][134][135]. As occurs in different pathological events, miRNA dysregulation leads to alterations in normal cellular events [136,137]. Increasing evidence demonstrates that Nrf2 signaling is under surveillance of miRNAs in different pathological events for regulating response of cells to oxidative stress [138,139].…”

Section: Nrf2 Modulationmentioning

confidence: 99%

Nrf2 Signaling Pathway in Chemoprotection and Doxorubicin Resistance: Potential Application in Drug Discovery

et al. 2021

View full text Add to dashboard Cite

Doxorubicin (DOX) is extensively applied in cancer therapy due to its efficacy in suppressing cancer progression and inducing apoptosis. After its discovery, this chemotherapeutic agent has been frequently used for cancer therapy, leading to chemoresistance. Due to dose-dependent toxicity, high concentrations of DOX cannot be administered to cancer patients. Therefore, experiments have been directed towards revealing underlying mechanisms responsible for DOX resistance and ameliorating its adverse effects. Nuclear factor erythroid 2-related factor 2 (Nrf2) signaling is activated to increase levels of reactive oxygen species (ROS) in cells to protect them against oxidative stress. It has been reported that Nrf2 activation is associated with drug resistance. In cells exposed to DOX, stimulation of Nrf2 signaling protects cells against cell death. Various upstream mediators regulate Nrf2 in DOX resistance. Strategies, both pharmacological and genetic interventions, have been applied for reversing DOX resistance. However, Nrf2 induction is of importance for alleviating side effects of DOX. Pharmacological agents with naturally occurring compounds as the most common have been used for inducing Nrf2 signaling in DOX amelioration. Furthermore, signaling networks in which Nrf2 is a key player for protection against DOX adverse effects have been revealed and are discussed in the current review.

show abstract

“…MiR-615-5p also participates in regulating cell growth, proliferation and migration, and has been shown to act as a tumour promoter or tumour suppressor, for example, through post transcriptional inhibition of oncogenes involved in essential biological processes, mainly by preventing invasiveness and metastasis, the main causes of tumour reappearance. 17…”

Section: Discussionmentioning

confidence: 99%

Potential mechanism of circRNA_000585 in cholangiocarcinoma

Xin

Lin

2021

J Int Med Res

View full text Add to dashboard Cite

Objective Circular RNA (circRNA) plays a vital role in the development and progression of malignancies, however, the function of circRNAs in cholangiocarcinoma (CCA) remains unexplored. The aim of this study was to investigate circRNA expression in CCA versus para-cancer tissues, and elucidate any potential associated mechanisms. Methods Differential expression of circRNAs between CCA and para-cancer tissue was analysed by microarray hybridization, and validated by real-time quantitative reverse transcription–polymerase chain reaction (qRT–PCR). The downstream pathway was investigated using bioinformatics and qRT–PCR. Results Microarray hybridization revealed 10 circRNAs with > 3-fold increased expression versus para-cancer (circRNA_002172, circRNA_002144, circRNA_001588, circRNA_000166, circRNA_000585, circRNA_000167, circRNA_402608, circRNA_006853, circRNA_001589, circRNA_008882), and three circRNAs with > 3-fold decreased expression (circRNA_406083, circRNA_104940, circRNA_006349). CircRNA_000585 was shown by qRT-PCR to be upregulated in tumour versus paired para-cancer tissue from 15 patients with CCA. Bioinformatics analysis revealed a potential pathway comprising circRNA_000585/microRNA-615-5p/angiomotin (AMOT)/Yes associated protein 1 (YAP) in CCA. RT–PCR validation of crucial molecule expression showed downregulation of miR-615-5p, and upregulation of AMOT and YAP in CCA tumours. Conclusion Multiple circRNAs are dysregulated in CCA. CircRNA_000585 is upregulated in CCA, and may function by a circRNA_000585/miR-615-5p/AMOT/YAP pathway, which may be a novel CCA pathway.

show abstract

miR-615 Fine-Tunes Growth and Development and Has a Role in Cancer and in Neural Repair

Cited by 19 publications

References 94 publications

Hsa_circRNA_100146 Promotes Prostate Cancer Progression by Upregulating TRIP13 via Sponging miR-615-5p

Hsa_circRNA_100146 Promotes Prostate Cancer Progression by Upregulating TRIP13 via Sponging miR-615-5p

Nrf2 Signaling Pathway in Chemoprotection and Doxorubicin Resistance: Potential Application in Drug Discovery

Potential mechanism of circRNA_000585 in cholangiocarcinoma

Contact Info

Product

Resources

About