MicroRNA‑496 suppresses tumor cell proliferation by targeting BDNF in osteosarcoma

Ye, Jing; Xie, Wenli; Zuo, Yunxia; Jing, Guang-Wu; Tong, Jie

doi:10.3892/etm.2019.8356

Cited by 5 publications

(6 citation statements)

References 33 publications

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“…50 An earlier study showed that Bdnf mRNA can be targeted by miR-496a-3p. 51 Our data showed that removal of TRAX caused an elevation of miR-496a-3p and a reduction in Bdnf (Fig. 2F,G), indicating that miR-496a-3p is a substrate of the TRAX/Translin complex, which negatively regulates the expression of Bdnf.…”

Section: Discussionmentioning

confidence: 58%

“…[44][45][46][47] Levels of these four miRNAs and their corresponding target mRNAs that have previously been implicated in either HD or/and neurons were validated using qRT-PCR assays (Table 1; Supplementary Appendix S1). [44][45][46][47][48][49][50][51][52][53] The detailed rationale underlying the selection of target miRNAs for validation is described in the Materials and Methods section of the Supplementary Appendix S3. TRAX ablation elevated all four miRNAs in the context of HD mice.…”

Section: Trax Regulated the Mirna-mrna Axis In Hdmentioning

confidence: 99%

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TRAX Provides Neuroprotection for Huntington's Disease Via Modulating a Novel Subset of MicroRNAs

et al. 2022

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A BS TRACT: Background: Huntington's disease (HD) is a neurodegenerative disease caused by CAG-repeat expansions (>36) in exon 1 of HTT, which dysregulates multiple cellular machineries. Translin-associated protein X (TRAX) is a scaffold protein with diverse functions, including suppressing the microRNA (miRNA)mediated silencing by degrading pre-miRNA. To date, the role of TRAX in neurodegenerative diseases remains unknown. Objectives: We delineated the role of TRAX upregulation during HD progression. Methods: Expression of TRAX in the brains of humans and three mouse models with HD were analyzed by immunohistochemistry staining, western blot, and quantitative reverse transcription-polymerase chain reaction. Adeno-associated viruses harboring TRAX short hairpin RNA were intrastriatally injected into HD mice to downregulate TRAX. HD-like symptoms were analyzed by behavioral and biochemical assessments. The miRNAsequencing and RNA-sequencing analyses were used to identify the TRAX-regulated miRNA-messenger RNA (mRNA) axis during HD progression. The identified gene targets were validated biochemically in mouse and human striatal cells. Results: We discovered that TRAX was upregulated in the brains of HD patients and three HD mouse models. Downregulation of TRAX enhanced 83 miRNAs (including miR-330-3p, miR-496a-3p) and subsequently changed the corresponding mRNA networks critical for HD pathogenesis (eg, DARPP-32 and brain-derived neurotrophic factor). Disruption of the TRAX-mediated miRNA-mRNA axis accelerated the progression of HD-like symptoms, including the degeneration of motor function, accumulation of mHTT aggregates, and shortened neurite outgrowth. Conclusions: We demonstrated that TRAX upregulation is authentic and protective in HD. Our study provides a novel layer of regulation for HD pathogenesis and may lead to the development of new therapeutic strategies for HD.

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Section: Discussionmentioning

confidence: 58%

Section: Trax Regulated the Mirna-mrna Axis In Hdmentioning

confidence: 99%

TRAX Provides Neuroprotection for Huntington's Disease Via Modulating a Novel Subset of MicroRNAs

et al. 2022

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“…The present study revealed that NNT-AS1 acted as a sponge of miR-496, which acted as a tumor suppressor in CRC cells. Previous studies have suggested that miR-496 functions as a tumor suppressor in various cancers, such as CRC, lung cancer and osteosarcoma (18,39,40). A recent study identified that miR-496 acted as an oncogene and promoted malignancy in CRC cells (41).…”

Section: Discussionmentioning

confidence: 99%

Serum long non‑coding RNA NNT‑AS1 protected by exosome is a potential biomarker and functions as an oncogene via the miR‑496/RAP2C axis in colorectal cancer

Yin

et al. 2021

Mol Med Rep

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Increasing evidence has indicated that long non-coding RNAs (lncRNAs) serve an essential role in carcinogenesis and cancer development. It has been reported that lncRNA nicotinamide nucleotide transhydrogenase antisense RNA 1 (NNT-AS1) serves a crucial role in several types of cancer. However, the clinical significance of circulating NNT-AS1 expression in colorectal cancer (CRC) remains to be elucidated. The current study aimed to investigate the potential role of NNT-AS1 and the clinical significance of its serum expression levels in patients with CRC. The expression of NNT-AS1 was measured in 40 pairs of tumor and adjacent normal tissues from patients with CRC via reverse transcription-quantitative PCR. The serum expression levels of NNT-AS1 were assayed in an independent cohort of healthy controls and patients with CRC. The levels of NNT-AS1 were also compared between paired preoperative and postoperative serum samples. In addition, the presence of exosomal NNT-AS1 in serum was explored. Furthermore, the biological roles of NNT-AS1 were investigated in CRC cells in vitro. The expression of NNT-AS1 was significantly upregulated in tumor tissues compared with adjacent normal tissues (P<0.05). A higher level of NNT-AS1 was associated with an advanced CRC stage. The serum levels of NNT-AS1 were significantly upregulated in patients with CRC compared with healthy subjects (P<0.05). Furthermore, the NNT-AS1 levels were significantly decreased in postoperative samples compared with preoperative samples (P<0.01). In addition, it was also identified that NNT-AS1 was upregulated in CRC exosomes (P<0.01), whereas no significant difference was observed in NNT-AS1 levels between serum and exosomes. Silencing of NNT-AS1 inhibited the proliferation, migration and invasion of CRC cells. It was also identified that NNT-AS1 exerted its effects via regulation of the microRNA-496/Ras-related protein Rap-2c axis. The present study demonstrated that circulating NNT-AS1, which may be protected by exosomes, could be a novel potential biomarker and therapeutic target in CRC.

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“…Abnormal proliferation is a unique feature of tumor cells andthe inhibition of tumor cell proliferation is controversial (23). miRNA serves an important role in tumorigenesis and the development of malignant tumors and regulates the proliferation and invasion of tumor cells by combining with target genes (24)(25)(26).…”

Section: Discussionmentioning

confidence: 99%

miR‑224‑5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN

Peng

Guo

et al. 2021

Mol Med Rep

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Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)-224-5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription-quantitative PCR was used to explorethe expression of miR-224-5p and the PTEN gene. MTT, wound healing, Transwell and tumorigenesis assays were conducted to investigate the proliferation, migration and invasion of MCC1 cells in vitro and in vivo. Western blot analysis was employed to test the protein expression of PTEN. The target gene of miR-224-5p was assessed and verified by luciferase assay. miR-224-5p expression was notably higher, while PTEN expression was lower, in MCC1 cells compared with normal tissues and cells. Overexpression of miR-224-5p promoted the proliferation, migration and invasion of MCC and knockdown of miR-224-5p inhibited these functions. Bioinformatics analysis and luciferase assay indicated that PTEN was the direct target gene of miR-224-5p. The negative correlation between miR-224-5p and PTEN was confirmed both in vitro and in vivo. PTEN reversed the effects of miR-224-5p on proliferation, migration and invasion of MCC1 cells. The present study revealed for the first time, to the best of the authors' knowledge, that miR-224-5p was highly expressed and served an oncogenic role in MCC. miR-224-5p not only regulated the proliferation, migration and invasion of pancreatic MCC but may also be a potential therapeutic target for MCC.

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MicroRNA‑496 suppresses tumor cell proliferation by targeting BDNF in osteosarcoma

Cited by 5 publications

References 33 publications

TRAX Provides Neuroprotection for Huntington's Disease Via Modulating a Novel Subset of MicroRNAs

TRAX Provides Neuroprotection for Huntington's Disease Via Modulating a Novel Subset of MicroRNAs

Serum long non‑coding RNA NNT‑AS1 protected by exosome is a potential biomarker and functions as an oncogene via the miR‑496/RAP2C axis in colorectal cancer

miR‑224‑5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN

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